BLOCK 3 - ALL SLIDES - STUDENT COPY 2023.pptx

Block 3 NEUROPHYSIOLOGY Copyright © 2011 by Saunders, an imprint of Elsevier Inc. UNIT 9 Chapter 46: Organization of the Nervous System, Basic Functions of Synapses, and Neurotransmitters Slides by Thomas H. Adair, PhD Copyright © 2021 by Saunders, an imprint of Elsevier Inc. Four lobes of cer...

Block 3 NEUROPHYSIOLOGY Copyright © 2011 by Saunders, an imprint of Elsevier Inc. UNIT 9 Chapter 46: Organization of the Nervous System, Basic Functions of Synapses, and Neurotransmitters Slides by Thomas H. Adair, PhD Copyright © 2021 by Saunders, an imprint of Elsevier Inc. Four lobes of cerebral cortex Frontal lobe: (higher mental functions) •Anterior cerebral art. •Middle cerebral art. Parietal lobe: (integrates sensory information from different modalities) •Anterior cerebral art. •Middle cerebral art. Temporal lobe: (auditory perception, semantics, memory) •Middle cerebral art. •Posterior cerebral art. Occipital lobe: (visual processing center – visual cortex) •Middle cerebral art. Surface anatomy of brain Primary motor cortex Somatosensory cortex Cranial nerves Cranial nerves Organization of the nervous system Anatomical stuff Spinal cord Organization of Nervous System • Sensory Division – tactile, visual, auditory, olfactory • Integrative Division – process information, creation of memory • Motor Division – respond to and move about in our environment Somatosensory Axis of Nervous System Figure 46-2 Skeletal Motor Nerve Axis of Nervous System Figure 46-3 3 Major Levels of CNS Function Spinal cord level Lower brain level Higher brain or cortical level Spinal Cord Level • The spinal cord level: – more than just a conduit for signals from periphery of body to brain and vice versa – cord contains: • walking circuits • withdrawal circuits • support against gravity circuits • circuits for reflex control of organ function Lower Brain Level • Contains: – medulla, pons, mesencephalon, hypothalamus, thalamus, cerebellum and basal ganglia • Controls subconscious body activities: – arterial pressure, respiration, equilibrium, feeding reflexes, emotional patterns Higher Brain or Cortical Level • Cortex never functions alone, always in association with lower centers. • Large memory storehouse. • Essential for thought processes. • Each portion of the nervous system performs specific functions, but it is the cortex that opens the world up for one’s mind. Neuron Structure 3 major components: • Soma • Axon terminal. - main body of neuron. - extends from soma to synaptic - the effector part of neuron. • Dendrite - projections from soma. - the sensory portion of neuron. Figure 46-1 Anterior motor neuron Posterior horn receives sensory information. anterior root anterior horn Also called (anterior column or ventral horn) - contains motor neurons that affect axial muscles. Figure 45-6 Review of membrane potential Vm -65 0 mV EK -86 ENa +61 ECl -70 Fig 46-8 Electrotonic potentials Subthreshold potential change vs. action potential Recap: how membrane potential and excitability relate Synaptic responses - EPSP Note the following: • no action potentials occurred in postsynaptic neuron because a threshold potential was not achieved • the excitatory post synaptic potential (EPSP) is an electrotonic response that decays with an exponential time course • the last EPSP is larger because it ?Which channels and ions can create occurs before the previous EPSP an EPSP? has decayed fully. Glutamate • opens cation channels • chief excitatory transmitter in CNS ?What type of summation is shown? Presynaptic neuron + Postsynaptic neuron Presynaptic neuron 0 mV -70 threshold -60 mV -70 epsp 10 ms Postsynaptic neuron With spatial summation, EPSP’s created by distant synapses overlap. A single neuron can have more than one synaptic terminal Spatial summation can occur with a single presynaptic neuron. Copyright © 2011 by Saunders, an imprint of Elsevier Inc. Synaptic responses - IPSP Note the following: • The post-synaptic cell is hyperpolarized. – Remember that hyperpolarization depresses excitability - inhibitory – This is an inhibitory post synaptic potential (IPSP) • IPSPs can summate too!! • IPSPs result from increases in ?Which ions are involved in membrane permeability creating an IPSP? Presynaptic neuron - Postsynaptic neuron 0 mV Presynaptic neuron -70 -60 GABA (γ-Aminobutyric acid), opens Clchannels. • chief inhibitory transmitter in adult CNS • could be an excitatory transmitter during development (because of Postsynaptic neuron mV -70 ipsp -80 10 ms Summation of Postsynaptic Potentials Spatial Summation excitation of a single presynaptic neuron on a dendrite will almost never induce an AP in the neuron. each terminal on the dendrite accounts for about a 0.5 - 1.0 mV EPSP. when multiple terminals are excited simultaneously the EPSP generated may exceed the threshold for firing and induce an AP. Summation of Postsynaptic Potentials Temporal Summation A neurotransmitter opens a membrane channel for about 1 msec, but a postsynaptic potential (EPSP or IPSP) lasts for about 15 msec A second opening of the same membrane channel can increase the postsynaptic potential to a greater level. Therefore, the more rapid the rate of terminal stimulation, the greater the postsynaptic potential. Rapidly repeating firings of a small number of terminals can summate to reach the threshold for an AP. Electrotonic potentials EPSP = IPSP = Figure 45-9 Simultaneous firing of many synapses is required to reach threshold • Often the summated postsynaptic potential is excitatory in nature but has not reached threshold levels. • This neuron is said to be facilitated because the potential is nearer the threshold for firing compared to the resting level, but not yet to the firing level. • It is easier to stimulate this neuron with subsequent input. threshold Figure 46-10 Facilitation at the squid giant synapse A Presynaptic Membrane Potential (mV) Postsynaptic Membrane Potential (mV) 0 0.5 Ca++ concentration in synaptic end of neuron 0.4 Amount of facilitation Action potentials 0.3 Facilitation B 0.2 0.1 EPSPs 0.0 10 20 Time (ms) 30 0 10 20 30 40 50 Interval between stimuli (ms) Redrawn after Purves, Neuroscience. 5th ed., Sinauer, 2012. Facilitation: • Definition – The increased transmitter release produced by an action potential that follows closely upon a preceding action potential. Note: This is not temporal summation. • Mechanism – prolonged elevation of presynaptic calcium levels following synaptic activity. Function of Dendrites in Stimulating Neurons  Dendrites allow signal reception from a large spatial area providing opportunity for summation of signals from many presynaptic neurons.  Dendrites do not transmit action potentials. They have few voltage gated Na+ channels. Figure 46-11  Dendrites transmit signals by electrotonic conduction. Transmission of current by conduction in the fluids of the dendrites. Special Characteristics of Synaptic Transmission Synaptic facilitation – enhanced responsiveness following repetitive stimulation. – mechanism is build-up of calcium ions in presynaptic terminals. – build-up of calcium causes more vesicular release of Synaptic fatigue (or short-term synaptic depression) transmitter. – excitatory synapses are repetitively stimulated at a rapid rate until rate of postsynaptic discharge becomes progressively less. – It’s a protective mechanism for excessive neuronal activity – Possible mechanism for causing epileptic seizure to end – Mechanism: See Reverberatory Circuit below. Synaptic delay – the process of neurotransmission takes time, from the time delay one can calculate the number of chemically connected series neurons in a circuit. Actions of transmitter substances on postsynaptic membrane Ion channels: o Cation channels / Anion channels o Rapid response – short lived o Small molecule transmitters (Ach, NE, etc) 2nd messenger system o Multiple responses o Prolonged responses o Neuropeptides Synaptic transmission: ion channels Synaptic transmission: 2nd messenger Figure 46-7 Neurotransmitters: 2 main types 1. Small molecule, rapidly acting transmitters 2. Neuropeptides, slowing acting transmitters Small molecule, rapidly acting transmitters Function: small molecule Usually excitatory in CNS transmitters mediate most acute responses of nervous system. Usually inhibitory GABA: Chief inhibitory transmitter in CNS Glycine: inhibitory transmitter, mainly in cord Glutamate: Chief excitatory transmitter in CNS. Accounts for >90% of the synaptic connections in CNS. Synthesized on demand; does not use vesicles – diffuses through membrane Table 45-1 What does this have to do with chicken eggs? 113 mg choline Neuropeptides, slowing acting transmitters, GFs Act on Metabotropic receptors Cause long-term changes  Changes in number of neuron receptors • Often co-released with small molecule  Long-term opening or closure of ion channels  Changes in number and sizes of synapses transmitters • Some neurons make several different peptides Table 45-1 Environmental Changes and Synaptic Transmission • Acidosis. – depresses neuronal activity. – diabetic coma – pH change from 7.4 to 7.0 usually will induce coma. • Alkalosis. – increases neuronal excitability. – Can initiate petit mal seizure – pH change from 7.4 to 8.0 usually will induce seizures. • Hypoxia. – brain highly dependent on oxygen – interruption of brain blood flow for 3 to 7 sec can lead to unconsciousness. END UNIT 9 Chapter 47: Sensory Receptors, Neuronal Circuits for Processing Information Slides by Thomas H. Adair, PhD Copyright © 2021 by Saunders, an imprint of Elsevier Inc. Types of Sensory Receptors • Mechanoreceptors - detect deformation • Thermoreceptors - detect change in temperature • Nociceptors - detect damage (pain receptors) Noci - is derived • Electromagnetic - detect light from the Latin term for “hurt” • Chemoreceptors - taste, smell, CO2, O2 etc. Types of Sensory Receptors Figure 47-1 Locations of skin sensory receptors in the fingertip Glabrous skin (non-hairy skin) Epidermis Dermis Subcutaneous layer Purves. Neuroscience. 5th ed, 2012. Figure 9.5 Sensation • Each of the principal types of sensation: touch, pain, sight, sound, is called a modality of sensation. • How the sensation is perceived is determined by the characteristics of the receptor and the central connections of the axon connected to the receptor. • Specificity of nerve fibers for transmitting only one modality of sensation is called Labeled-line principle refers to a the concept each receptor responds to a labeled linethat principle. limited range of stimuli and has a direct line to the brain. What factors generate receptor potentials? • Mechanical deformation - stretches the membrane and opens ion channels. • Application of chemicals - also opens ion channels. • Change in temperature - alters membrane permeability. • Electromagnetic radiation - changes membraneNote permeability tostimuli ions. lead to that all these changes in membrane permeability to ions; this can cause either hyperpolarization or hypopolarization (i.e., depolarization). Generation of receptor potential by mechanism distortion Mechanical distortion increases Na+ conductance causing a receptor potential. The receptor potential is an electrotonic potential. ? Why is there no AP except in the axon? Figure 47-3 Pacinian corpuscle Relationship between receptor potentials and action potentials - APs occur when receptor potential (green line) rises above threshold Figure 47-2 - Increased stimulus intensity causes increased receptor potential, which increases AP frequency. Stimulus strength and receptor potential in Pacinian corpuscle Only larges changes in stimulus strength can be discerned when stimulus strength is high Small changes in stimulus strength can be discerned when stimulus strength is low This relationship allows receptors to have a wide range of response Figure 47-4 Adaptation of Receptors Figure 47-5 Adaptation of Receptors (cont.) Rate of adaptation varies with type of receptor. Adapted from Kandel, Schwartz And Jessell 4th addition 2000 Rapidl y adapti ng Slowly adapti ng Rapidl y adapti ng Slowly adapti ng Mechanism of Adaptation - varies with the type of receptor. • Mechanoreceptors – fluid redistribution in Pacinian corpuscle decreases distorting force. • Photoreceptors – the amount of light sensitive chemicals is changed. Slowly Adapting (Tonic) Receptors • Continue to transmit impulses to brain for long periods of time while stimulus is present. S • Keep brain apprised of the status of the body with respect to its surroundings. • Will adapt to extinction if stimulus is present but this may take hours or days. • These receptors include muscle spindle, Golgi tendon apparatus, Ruffini endings, Merkel discs, Macula, pain, temperature, chemo- and baroreceptors. Rapidly Adapting (Phasic) Receptors • Respond only when change is taking place. S • Rate and strength of response is related to rate and intensity of stimulus. • Important for predicting future position or condition of body. • Very important for balance and movement. • Types of rapidly adapting receptors: Pacinian corpuscle, Meissner’s corpuscle, semicircular canals. Slowly and rapidly adapting mechanoreceptors provide different information Stimulus Slowly adapting 0 1 2 Time (s) 3 Rapidly adapting 0 Slowly adapting receptors (aka, tonic receptors) continue to respond to a stimulus. 4 Rapidly adapting receptors (aka, phasic receptors) – respond only at the onset (and often the offset) of stimulation. 1 2 Time (s) 3 4 Sensory Nerve Classification Transmission of receptor information to brain by different types of neurons Figure 47-6 Somatic sensory afferents that link receptors to CNS Purves. Neuroscience. 5th ed, 2012. Table 9.1 Importance of Signal Intensity • Signal intensity is critical for interpretation of signal by brain (e.g., pain). • Gradations in signal intensity can be achieved by: 1) Spatial summation - increasing the number of fibers stimulated. An example of spatial summati on 2) Temporal summation - increasing the rate of firing in a given number of fibers. Figure 47-7 Excitation and Facilitation Figure 47-9 Neuron ‘1’ excites neuron ‘a’, and facilitates neurons ‘b’ and ‘c’ Figure 47-10 Neuronal Pools • Groups of neurons with special characteristics of organization. • Comprise many different types of neuronal circuits. – converging – diverging – reverberating – inhibitory Divergence in neuronal pathways Figure 47-11 Amplifying type of divergence. Signal is transmitted in two directions. Example: single pyramidal cell in motor cortex can stimulate several hundred Example: information from dorsal columns of spinal cord takes two directions (1) cerebellum, (2) Convergence of multiple input fibers Figure 47-12 - Multiple terminals from single incoming fiber terminate on same neuron. - Provides spatial summation - Allows summation of information from multiple sources. - Correlates, summates, and sorts information. Inhibitory circuit excite no AP Figure 47-13 Important for controlling all antagonistic pairs of muscles… called the reciprocal inhibition circuit. Important in preventing over-activity in brain Reverberatory or Oscillatory Circuits Output signals from reverberatory circuit after single input stimulus Hall, Guyton. Figure 47-15 Figure 47-14 • A single input stimulus (1 msec) causes a prolonged output (msec to minutes). • Caused by Positive feedback within neuronal circuit (the input to the circuit is re-excited). • What Note: causes the circuit can cessation be facilitated sudden of or inhibited as shown. reverberation? Reverberatory circuits (cont.) This is positive feedback - What stops it? fatigue of synaptic junctions What is the mechanism of fatigue? A. Transmitter depletion B. Receptor inactivation C. Abnormal ion concn in axon D. All of the above Control of synaptic sensitivity Underactivity leads to upregulation of membrane receptors Overactivity leads to downregulation of membrane receptors. ot all reverberatory circuits fatigue Shows continuous output from reverberating circuit that can be enhanced or suppressed ANS uses this type of information transmission to control vascular tone, gut tone, heart rate, etc. Figure 47-16 END UNIT 9 Chapter 48: Somatic Sensations: I. General Organization, the Tactile and Position Senses Slides by Thomas H. Adair, PhD Copyright © 2021 by Saunders, an imprint of Elsevier Inc. assification of somatic sensations Mechanoreceptive - stimulated by mechanical displacement. Tactile: touch, pressure, vibration, tickle, itch Proprioceptive: static position, rate of change Thermoreceptive. detect heat and cold. Nociceptive. detect pain and any factor that damages tissue. Tactile receptors – small field Meissner corpuscles • Location: non-hairy skin close to surface (fingertips, lips, eyelids, nipples and external genitalia). • Function: motion detection, grip control Stimuli: skin motion, low frequency Meissner corpuscles vibration Merkel discs • Adaptation: rapid adaptation • Location: tip of epidermal ridges • receptive field: 22 mm2 • Function: form and texture perception • type Aβ nerve fibers • Stimuli: edges, points, corners, curvature • Adaptation: slow adaptation • receptive field: 9 mm2 • type Aβ nerve fibers • Merkel discs Purves. Neuroscience. 5th ed, 2012. Figure 9.5 Activity patterns recorded from mechanosensory afferents in fingertip Each dot is an action potential Small field, slow adaptation Larger field, fast adaptation Very large field, slow adaptation Huge field, very fast adaptation Purves. Neuroscience. 5th ed, 2012. Figure 9.6 Tactile receptors – large field Pacinian corpuscle (~ 1 mm) • Location: dermis and deeper tissues • Function: perception of distant events through transmitted vibrations; tool use • Stimuli: vibration (250 Hz is optimal) Ruffini corpusclevery rapid • Adaptation: • adaptation Location: dermis force; hand •• Function: Receptive tangential field: entire finger or shape; hand motion detection • type Aβ nerve fibers • Stimuli: skin stretch • Adaptation: slow adaptation • receptive field: 60 mm2 • type Aβ nerve fibers Pacinian corpuscles Purves. Neuroscience. 5th ed, 2012. Figure 9.5 Free nerve endings Free nerve endings (myelinated). • Location: surface of body and elsewhere • Function/stimuli: pain, temperature • Adaptation: slow adaptation • type Aδ nerve fibers, i.e., A-delta Free nerve endings (unmyelinated). • Location: surface of body and elsewhere • Function/stimuli: pain, temperature, itch • Adaptation: slow adaptation • type C Purves. Neuroscience. 5th ed, 2012. Figure 9.5 Pathways for the Transmission of Sensory Information Anterolateral system Dorsal columnmedial lemniscal system Purves. Neuroscience. 5th ed, 2012. Figure 9.1B Almost all sensory information enters spinal cord through dorsal roots of spinal nerves. Two pathways for sensory afferents. Anterolateral system Dorsal column-medial lemniscal system Dorsal Column-medial lemniscal System • Contains large myelinated nerve fibers (30-110 m/sec). A-beta • Three neurons to sensory cortex / decussates in medulla oblongata • High degree of spatial orientation maintained throughout the tract. • Transmits information rapidly and with a high degree of spatial fidelity (i.e., discrete types of mechanoreceptor information). • Transmits touch, vibration, Figure 48-3 The Anterolateral System • Contains smaller myelinated and unmyelinated fibers for slow transmission (0.5-40 m/sec). (A-delta, C) • three neurons to sensory cortex / decussates in spinal cord • low degree of spatial orientation. • transmits a broad spectrum of modalities. • pain, thermal sensations, crude touch and pressure, tickle and Figure 47-13 Dermatomes Dermatome – area of skin supplied by sensory neurons that arise from a spinal nerve ganglion. Clinical significance • Localizing cord lesion • Viruses such as varicella zoster hibernate in ganglia causing rash in associated dermatome. • Referred pain (discussed later) Figure 48-14 Shingles follows the dermatome Years or decades after a chickenpox infection, the virus (varicella zoster virus) may break out of nerve cell bodies and travel down nerve axons to cause viral infection of skin associated with nerve. The rash occurs in the dermatome of the infected nerve cell. The Somatosensory Cortex • Located in the postcentral gyrus. • Highly organized distinct spatial orientation. • Each side of cortex receives information from opposite side of body. • Unequal representation of the body. – lips have greatest area of representation followed by face and thumb. – trunk and lower body have least area of representation. Figure 48-6 Sensory homunculus Homunculus – (latin) little human Figure 47-7 Brodmann areas Brodmann areas show cytoarchitectural organization of neurons (cell size, packing density, lamination) that he observed in cerebral cortex using Nissl stain (1909). Figure 48-5 Figure 48-6 Somatosensory area 1 (primary somatosensory area) Brodmann’s areas: 1, 2, 3 Somatosensory association area Brodmann’s areas: 5,7 Lesions of somatosensory cortex Destruction of somatosensory area I causes: loss of vibration, fine touch, and proprioception. discrete localization ability. inability to judge the degree of pressure. inability to determine the weight of an object. inability to judge texture. Also: Hemineglect (unilateral neglect, hemispatial neglect or spatial neglect): patients are unaware of items to one side of space. Astereognosis: inability to recognize objects by touch Agraphesthesia: a disorientation of the skin’s sensation across its space (e.g., hard to identify a number or letter traced on the hand) Figure 47-7 Somatosensory association area • Areas 5 and 7 in parietal area. • Receives input from somatosensory cortex, ventrobasal nuclei of thalamus, visual and auditory cortex. • Function is to decipher complex sensory associations. • Loss of these areas • inability to recognize complex objects • neglect of contralateral world and even refusal to acknowledge ownership of contralateral body. Figure 48-5 Figure 47-6 Structure of Cerebral Cortex Diffuse lower input Related brain areas Incoming signals To brainstem and cord To thalamus Figure 48-8 Cellular Organization of the Cortex • Six separate layers of neurons with layer I near the surface of the cortex and layer VI deep within the cortex. • Incoming signals enter layer IV and spread both up and down. • Layers I and II receive diffuse input from lower brain centers. • Layers II and III neurons send axons to closely related portion of the cortex presumably for communicating between similar areas. • Layer V and VI send axons to more distant parts of the nervous system, layer V to the brainstem and spinal cord, layer VI to the thalamus. Cellular Organization of the Cortex (cont’d) • Within the layers the neurons are also arranged in columns. • Each column serves a specific sensory modality (i.e., stretch, pressure, touch). • Different columns interspersed among each other. – interaction of the columns occurs at different cortical levels which allows the beginning of the analysis of the meaning of the sensory signals. 6 Layers of cerebral cortex Vertical columns detect a different sensory spot on body with a specific sensory modality Incoming sensory signal excites layer IV I molecular layer II external granular layer III layer of small pyramidal cells IV internal granular layer V large pyramidal cell layer VI layer of fusiform or polymorphic cells Two-point discrimination • • The two-point discrimination threshold measures the minimum distance at which two stimuli are resolved as distinct; it reflects how finely innervated an area of skin is. The spatial resolution of stimuli on the skin varies throughout the body because the density of mechanoreceptors varies. Lateral inhibition improves twopoint discrimination Lateral inhibitio n present Figure 48-10 • Lateral inhibition is the capacity of an excited neuron to reduce activity of neighboring neurons; it improves degree of contrast – Occurs at every synaptic level (for dorsal column system): dorsal column nuclei, ventrobasal nuclei of thalamus, cortex END UNIT 9 Chapter 49: Somatic Sensations: II. Pain, Headache, and Thermal Sensations Slides by Thomas H. Adair, PhD Copyright © 2021 by Saunders, an imprint of Elsevier Inc. Pain Protective mechanism Occurs whenever tissue is being damaged. Causes individual to remove painful stimulus. two types of pain (fast pain and slow pain). fast pain (body surface) felt within 0.1 s after stimulus sharp pain: (knife cut, needle poke, burn). Not felt in most deeper tissues slow pain (body surface and deeper tissues) felt after 1 s or more throbbing or aching pain Usually associated with tissue destruction (bradykinin). Pain is perceived at 45◦ C at 45◦ C Pain is perceived Distribution curve obtained from large group of people showing minimal skin temperature that will cause pain Figure 49-1 Copyright © 2011 by Saunders, an imprint of Elsevier Inc. Do females have a higher pain threshold than males? Pain perception threshold is the minimum amount of pain that evokes a report of pain. Pain tolerance threshold is reached when the subject acts to stop the pain. Males have higher pain perception threshold than females, and some studies show that males also have a higher pain tolerance threshold; another way of thinking, is that females show more sensitivity to pain. "It makes sense that the female reaction to pain would be stronger than that of a male since the female is more important to the survival of the species, especially if she cares for the young." Pain Receptors and Their Stimulation Pain receptors are free nerve endings Widespread in skin, arterial walls, joint surfaces, periosteum, falx and tentorium of cranial vault Lower density in internal structures Pain receptors do not adapt to the stimulus. Intensity of pain is correlated with rate of tissue damage (not total amount of damage). Extracts from damaged tissue cause pain when injected under skin. Bradykinin is main cause of pain resulting from tissue damage (slow pain). Also, potassium and proteolytic enzymes contribute. Ischemia causes pain What is ischemia? What is hypoxia? Time course: arterial occlusion of limb causes pain in 15-20 s. Cause of ischemic pain. Lactic acid buildup Bradykinin Proteolytic enzymes Dual Pain Pathways 1. Fast pain (first pain) a. transmitted by type A-delta fibers (velocity 6-30 m/sec). b. transmitted in neospinothalamic tract 2. Slow pain (second pain) c. transmitted by type C fibers (0.5 - 2 m/sec). d. transmitted in the paleospinothalamic tract. Ad fiber C fiber 1st pain 2nd pain Subjective perception of pain time Because of these dual pathways, a double sensation of pain often occurs: sharp pain followed seconds later by slow pain. Neospinothalamic Tract Fast, sharp pain: A-delta fiber On entering cord, pain fibers may travel up or down 13 segments and terminate on neurons in dorsal horn. Glutamate is excitatory transmitter of A-delta pain fiber nerve ending. 2nd neuron crosses immediately to the opposite side and passes to the brain in the anterolateral columns. Figure 49-2 Some neurons terminate in the reticular substance but most go all the way to the ventrobasal complex of the thalamus. 3rd order neurons go to the cortex. Fast, sharp pain can be localized well when other tactile receptors are simultaneously stimulated. Figure 49-3 Paleospinothalamic Tract Slow, burning pain: C fiber Type C pain fibers terminate in laminae II & III of spinal cord. 2nd neuron crosses immediately to the opposite side and passes to the brain in the anterolateral columns. Substance P is excitatory transmitter of type C pain fiber nerve ending. Figure 49-2 Only 10 to 25 % of fibers terminate in thalamus. Most terminate diffusely in reticular nuclei of medulla, pons and mesencephalon; tectal area of mesencephalon; periaqueductal gray region. Poor localization of slow pain, often to just the affected limb or part of body. Figure 49-3 Substance P The P stand for “preparation” or “powder” • Substance P is a peptide composed of 11 amino acids • Thought to mediate lower back pain, arthritis, fibromyalgia. • Over-the-counter creams containing capsaicin (made from chili peppers) can deplete Substance P from local nerve endings and relieve pain. The Appreciation of Pain • Removal of somatic sensory areas of cortex does not destroy the ability to perceive pain. • Pain impulses to lower areas can cause conscious perception of pain. • Therefore, cortex is probably important for determining the quality of pain. • Stimulation of reticular areas of brain stem and intralaminar nuclei of thalamus (where pain fibers terminate) causes widespread arousal of the nervous system. Recall that C fibers that transmit slow pain terminate mainly in the reticular formation. What does this tell you? Endogenous Analgesia System Naloxone (aka, Narcan) is used to counter the effects of opiate overdose (heroin, morphine, etc) Naloxone is an opioid antagonist— meaning that it binds to opioid receptors and can reverse and block the effects of other opioids, such as heroin, morphine, and oxycodone. It's been called the Lazarus drug for its ability to revive people dying from overdoses. It can be injected or simply administered through a nasal spray. (The spray form of the drug is known by the brand name, Narcan.) Figure 49-04 Analgesia system of brain and spinal cord • Electrical stimulation of periaqueductal gray area relieves pain (and inhibits nociceptive projection neurons in dorsal horn of cord). • Analgesic effects are mediated through 4 brainstem sites shown. • These centers harbor multiple transmitters that can both facilitate and inhibit neurons in dorsal horn. • Serotonin, from the Raphe nuclei stimulates interneurons in dorsal column, that, in turn secrete enkephalin. • Enkephalin (an opioid peptide) can cause both presynaptic and postsynaptic inhibition of incoming type C and type Aδ pain fibers where they synapse in dorsal horn. Somatic sensory cortex Amygdala Hypothalamus Anterolateral system Midbrain periaqueductal gray Parabrachial nucleus Medullary Reticular formation Raphe nuclei Dorsal horn of spinal cord Locus coeruleus Higher centers can control pain Somatic sensory cortex Amygdala Hypothalamus Midbrain periaqueductal gray • The placebo effect (Placebo means “I will please.”) Imaging studies: Placebo administration with expectation of an analgesic effect is associated with activation of opioid receptors in cortical and subcortical regions that are part of pain control system. Endogenous Opiate Systems • Early 1970’s it was discovered that injection of minute quantities of morphine into area around third ventricle produced a profound and prolonged analgesia. • This started the search for “morphine receptors” in the brain. • Several “opiate-like” substances have been identified. Endogenous Opiate Systems (cont.) Major endogenous opiates: beta-endorphin, met-enkephalin, leuenkephalin, dynorphin. Enkephalins and dynorphin - found in brain stem and spinal cord Beta-endorphin - found in hypothalamus and pituitary Function of opiate system Pain suppression during stress. Response to emergency (reduction in responsiveness to pain). Effective in defense, predation, dominance and adaptation to environmental challenges. Gate theory of pain Stimulation of type A-beta fibers from peripheral tactile receptors can decrease transmission of pain signals. Mechanism: a type of lateral inhibition of pain fiber by mechanosensory fiber. Probably the mechanism of action of massage, liniments, electrical stimulation of skin. Audioanalgesia can reduce Pain and Suffering During Labor Referred Pain from visceral sources Visceral tissues have few pain fibers. Hence, highly localized organ damage causes little pain; however, widespread damage can cause severe pain. Common causes of visceral pain ischemia. chemical irritation. spasm of a hollow viscus. over-distension of a hollow viscus. Often, pain from internal organ is perceived to originate from a distant area of skin. Mechanism: intermingling of second order neurons in dorsal horn of spinal cord from skin and viscera as shown. These are pain fibers Figure 49-5 Referred Pain Localized to dermatome of embryological origin. Heart localized to the neck, left shoulder and arm. Stomach localized above umbilicus. Colon localized below umbilicus. Understanding referred pain can lead to astute diagnoses that might otherwise be missed. Figure 49-6 Referred Pain (cont.) Right tip of scapula Some clinical abnormalities of pain and other somatic sensations • • Hyperalgesia: altered perception of pain such that stimuli which would normally induce a trivial discomfort causes significant pain. Often caused by damage to nociceptors or peripheral nerves. Tic Douloureux (painful tic): (aka, trigeminal neuralgia) disorder of trigeminal nerve (5th CN) can cause paroxysmal (sudden onset) facial pain. Can be triggered by touch or cold. Late onset: 60-70’s. • Brown-Sequard syndrome: Ipsilateral symptoms: loss of motor function (i.e. hemiparaplegia), vibration sense, fine touch proprioception (position sense), two-point discrimination, and weakness. Contralateral symptoms: loss of pain, temperature sensation, and crude touch. Hemiparaplegia: paralysis of one side of of the body Level of injury Dark area shows injury Headache Pain Brain tissue itself is insensitive to pain. Pain sensitive structures include membranes that cover brain and blood vessels: dura. blood vessels of the dura. venous sinuses. middle meningeal artery. Origin of Headache Pain Figure 49-9 Intracranial Headache Meningitis inflammation of meninges cause severe headache. Migraine results from abnormal vascular phenomenon. vasospasm followed by prolonged vasodilation. Vasodilation stretches coverings of blood vessels. Hangover irritation of meninges by alcohol breakdown products and additives. Extracranial Headache Muscular spasm, tension headache emotional tension may cause tension of muscles attached to neck and scalp which causes irritation of scalp coverings. Sinus headache irritation of nasal structures. Eye strain excessive contraction of the ciliary muscle in an attempt to focus, contraction of facial muscles. Substance P and Capsaicin • • • • • • Thought to mediate lower back pain, arthritis, fibromyalgia. Over-the-counter creams containing capsaicin (made from chili peppers) can deplete Substance P (by causing its release) from local nerve endings and hence relieve pain. Capsaicin selectively binds to a protein called TRPVI (transient receptor potential cation channel subfamily, member 1) or simply capsaicin receptor, that resides on membranes of pain and heat sensing neurons. The capsaicin receptor is a heat activated calcium channel, which normally opens between 37 and 45°C; hence, when capsaicin binds to its receptor, a sensation of heat is felt. Prolonged activation of neurons by capsaicin depletes presynaptic substance P, one of the body's neurotransmitters for pain and heat. Birds are not affected by capsaicin… mix with bird END UNIT 10 Chapter 50: The Eye: I. Optics of Vision Slides by Thomas H. Adair, PhD Copyright © 2021 by Saunders, an imprint of Elsevier Inc. Physiological Anatomy of the Eye Suspensory fibers that connect ciliary muscle with lens White outer layer. Continuous with cornea at front. Transparent, jellylike tissue. Contains photosensitive cells. 2/3 of refractive power of eye. Resculptured in LASEKS/LASIKS surgery Visual acuity is highest. Cones only. Optic disc Aka, Optic nerve head or blind spot. Exit point for axons. Entry point for retinal blood vessels. Nasal to fovea. Free flowing, watery fluid. Fills anterior and posterior chambers Needed for accommodatio n. Vascular layer between retina and sclera. Feeds outer layers of retina, ciliary body, and iris. CN II. Contains retinal ganglion cell axons and glial cells. About 1.5 million axons. Refractive Index Speed of light in air 300,000 km/sec. Light speed decreases when it passes through a transparent substance. The refractive index is the ratio of speed in air to speed in the substance. For example, if speed in a substance = 200,000 km/sec, R.I. = 300,000/200,000 = 1.5. Light rays bend when passing through an angulated interface with a different refractive index. The degree of refraction increases as the difference in R.I. increases and the degree of angulation increases. Structures of the eye have different R.I. and cause light rays to bend. These light rays are eventually focused on retina. Polycarbonate RI: 1.58 Figure 50-1 Refractive Principles of a Lens Convex lens focuses light rays Concave lens diverges light rays. TMP14, Figure 50-2 TMP14, Figure 50-3 Note that a point source of light has a longer focal length compared to light from a distant source; this is why an object comes into focus as it moves closer to the eye in a person with myopia (nearsightedness, long eyeball). Refractive Power of the eye - Diopter • • 2/3 of refractive power of eye resides in anterior surface of cornea. This refraction is virtually eliminated when swimming under water since water has refractive index close to that of cornea; hence, you get a blurry image underwater. Lens has less refractive power, but it’s adjustable. – a diopter is a measure of the power of a lens. – 1 diopter is the ability to focus parallel light rays at 1 meter. – the retina is about 17 mm behind refractive center of eye. – hence, the eye has a total refractive power of 59 diopters (1000/17). 1000/17 = 59 diopters 17 mm TMP14, Figure 50-8 TMP14, Figure 50-9 Accommodati on Refractive power of lens is 20 diopters. Refractive power can be increased to 34 diopters by making lens thicker; this is called accommodation. Accommodation is necessary to focus image on retina. An untethered lens is almost spherical in shape. Lens is held in place by suspensory ligaments (zonule fibers) which under normal resting conditions causes the lens to be almost flat. Contraction of ciliary muscle decreases tension in the suspensory ligaments, allowing the lens to become more spherical (thicker); this increases the refractive power of lens. Under control of parasympathetic nervous system. Presbyopia: Also called age-related farsightedness. It’s the inability to accommodate. The lens gets harder and less flexible with age because of decreased levels of Power of accommodation α-crystallin. decreases with age: Child, 14 diopters (34-20) 50 years old, 2 diopters 70 years old, 0 diopters TMP14, Figure 50-8 TMP14, Figure 50-10 Errors of Refraction Normal vision corrected with convex lens Far sightedness Near sightedness Guyton, Figure 50-12 Astigmatism: unequal focusing of light rays due to an oblong shape of the cornea. corrected with concave lens Hyperopia and Myopia ciliary muscle relaxed “farsightedness” Ciliary muscle relaxed Ciliary muscle contracted HYPEROPIA (farsightness) caused by a short eyeball or sometimes a weak lens. contraction of ciliary muscle increases strength of lens (i.e., reduces focal distance). • So, a farsighted person can focus distant objects on retina because of accommodation. • If there is sufficient accommodation left, a farsighted person can also focus close objects on retina. MYOPIA (nearsightness) • caused by a long eyeball or sometimes too much refractive power in lens system. Genetic and ciliary muscle relaxed environmental factors contribute to myopia – too much close work can promote myopia. No mechanism to focus distant objects on retina (contraction of ciliary muscle would make distant “nearsightedness” objects even more out of focus). • Objects come into focus as they move closer to As an object moves toward the eye. eye, the rate of parasympathetic stimulation increases, causing the ciliary muscle to contract. What happens to the lens? Cataracts leading cause of blindness worldwide • Cataracts – cloudy or opaque area of the lens caused by coagulation of lens proteins – Accounts for about half the cases of blindness in the world. – UV solar radiation is major factor in production of cataracts Surgical implantation of plastic lens can usually restore vision. ~6 million per year. Visual Acuity • 20/20 – ability to see letters of a given size at 20 feet (normal vision) • 20/40 – what a normal person can see at 40 feet, this person must be at 20 feet to see. • 20/200 – what a normal person can see at 200 feet, this person must be at 20 feet to see. • 20/15 – Means what? Ans. can see at 20 feet what a person with 20/20 vision could only see at 15 feet Snellen chart Fluid System of the Eye Intraocular fluid keeps eyeball round and distended. 2 fluid chambers. aqueous humor, in front of lens. (freely flowing fluid). vitreous humor, behind lens (gelatinous mass with little fluid flow). Produced by ciliary body at rate of 2-3 microliters/min. (~3-4 mL/day) Flows through pupil into anterior chamber; then between cornea and iris, through meshwork of trabeculae to enter the canal of schlemm which empties into extraocular veins . TMP14, Figure 50-19 Intraocular Pressure Normally 15 mm Hg (range: 2-20 mm Hg). Level of pressure is determined by resistance to outflow of aqueous humor in canal of Schlemm. Rate of production of aqueous humor is constant under normal conditions (can be increased in systemic hypertension). Long-term hypertension is a risk factor for glaucoma. Increased pressure can cause blindness due to compression of axons of optic nerve as well as blood vessels. Hall, Figure 5021 Glaucoma 2nd leading cause of blindness worldwide (after cataracts) • Usually caused by high intraocular pressure (IOP). Increased IOP compresses blood vessels and axons of optic nerve at optic disc; this leads to poor nutrition of nerve fibers. Two main types of glaucoma • Open angle and closed angle (angle refers to area between iris and cornea). Open angle glaucoma (also called Chronic glaucoma) • 90% of cases in U.S. • Insidious – no pain initially • reduced flow through trabecular meshwork (tissue debris, WBC, deposition of fibrous material, etc). Types of Glaucoma Eye Drops Closed angle glaucoma • 10% of cases in U.S. – sudden closure of iridocorneal angle with sudden ocular pain. A medical emergency. • Treatment: Laser peripheral iridotomy (LPI), where an opening in the iris is made using a Prostaglandin analogs - increase outflow of fluid from eye. Beta blockers – decrease production of intraocular fluid. Alpha agonists - decrease fluid production and increase drainage. Carbonic anhydrase inhibitors (CAIs) – decrease UNIT 10 Chapter 51: The Eye: II. Receptor and Neural Function of the Retina Slides by Thomas H. Adair, PhD Copyright © 2021 by Saunders, an imprint of Elsevier Inc. Retina Light sensitive portion of eye. Contains cones for color vision. Contains rods for night vision. Contains neural architecture. Light must pass through neural elements to activate light sensitive rods and cones. But this is not so bad since neural elements are virtually transparent in vivo. • Each retina has 100 million rods; 3 million cones; and 1.6 million ganglion cells. TMP14, Figure 51-1 The Fovea It’s a small area at center of retina ~1 mm2. center of fovea, called “central fovea” or “fovea centralis” contains only cones. these cones have special structure. aid in detecting detail. In central fovea, neuronal cells and blood vessels are displaced to each side so light can strike cones with less obstruction. This is area of greatest visual acuity. At central fovea: no rods, and ratio of cones to ganglion cells is 1:1; this explains high degree of visual acuity in central retina. Figure 51-2 The Fovea Figure 51-2 Distribution of rods and cones Structure of Rods and Cones Pigment layer Guyton, Figure 51-4 Guyton, Figure 51-3 Rods and Cones RODS • high sensitivity; specialized for night vision (scotopic vision) • more photopigment • high amplification; single photon detection • saturate in daylight • slow response, long integration time • more sensitive to scattered light • low acuity; highly convergent retinal pathways, not present in central fovea • Achromatic; one type of rod pigment (rhodopsin) •More common in the periphery CONES • lower sensitivity; specialized for day vision (photopic vision) • less photopigment • less amplification • saturate only with intense light • fast response, short integration time • more sensitive to direct axial rays • high acuity; less convergent retinal pathways, concentrated in central fovea • Trichromatic; three types of cones, each with a different pigment (photopsin) that is sensitive to a different part of visible spectrum • More common in the fovea and macula Pigment Layer of Retina Contains black pigment called melanin. Prevents light reflection in globe of eye. Without pigment, light would scatter diffusely; normal contrast between dark and light would be diminished. Albinos lack pigment layer poor visual acuity because of scattering of light. Even with corrective lenses, vision is rarely better than 20/200. Pigment epithelium/choroid contains high levels of vitamin A (needed for phototransduction). TMP14, Figure 51-1 Visual Phototransduction Rhodopsin resides in disk membrane of outer segment of rod and encloses light sensitive 11cis retinal molecule. Absorption of a photon of light by retinal leads to a change in configuration from 11-cis to all-trans retinal. The retinal then breaks away from rhodopsin, causing rhodopsin to be activated. The activated rhodopsin (aka, Metarhodopsin II) then begins the 2nd messenger cascade which leads to Conversion of light into electrical signals ROD Rhodopsi n 11-cis retinal light 11-cis retinal All-trans retinal • Occurs in rods, cones and photosensitive ganglion cells. • The pigment protein in rods is called rhodopsin; • The pigment protein in cones is called photopsin, a close analog of rhodopsin (there are 3 types of photopsin: types I (red), II (green), and III) (blue). • The pigment portion of photosensitive retinal ganglion cells is called melanopsin. • The transduction mechanism is similar for • The rods, cones, and probably light sensitive all-trans retinal is then reduced ganglion cells. retinol, which then to all-trans travels back to the retinal pigment epithelium layer to be “recharged” to become 11-cis retinal. • The 11-cis retinal travels back to the rod where it is conjugated to an opsin to form new rhodopsin or a new photopsin. Vitamin A1 is required for Phototransduction Vitamin A1 (aka, all-trans retinal) is converted into 11-cis retinal within the retinal pigment epithelium. Food source: two types found in diet. • Preformed vitamin A: animal products such as meat, fish, poultry and dairy foods. • Pro-vitamin A: plant-based foods such as fruits and vegetables. The most common type of provitamin A is beta-carotene. Pro-vitamin A is a Vitamin A deficiency precursor of vitamin A. • the leading cause of preventable childhood blindness worldwide in developing countries • Prolonged and severe vitamin A deficiency can produce total and irreversible blindness. • ~250,000–500,000 children become blind each year (with the highest prevalence in Southeast Asia and Africa). (nyctalopia): Lack of vitamin • Night blindness A1 causes a decrease in retinal, which results in decreased production of rhodopsin; and a lower sensitivity of retina light. Night blindness can to occur in patients with GI absorption problem, e.g., celiac disease, cholestasis. Why? Br J Ophthalmol. 2006 Aug; 90(8): 955–956. http://medical-dictionary.thefreedictionary.com/vitamin+A+deficiency TMP14, Figure 51-5 Rod Receptor Potential Normally about -40 mV (in dark). Normally, outer segment of rod is permeable to Na+ and Ca++ ions. Dark In the dark, an inward current (the dark current) carried by Na+ and Ca + + ions flows current into outer segment of rod. An outward current carried by K+ ions occurs in inner segment of rod. When rhodopsin decomposes, it causes hyperpolarization of rod by decreasing Na+ and Ca++ permeability of outer segment. Greater amounts of light produce greater electronegativity. So, photoreceptor cells depolarize in scotopic conditions (low light or no light) and hyperpolarize in photopic conditions (well-lit conditions). Na+ Ca++ TMP14, Figure 51-6 -40 mV Ca++ -70 mV Ca++ Phototransduction – Closure of cGMP-gated Na+ and Ca++ channels with subsequent hyperpolarization (1) Light activated rhodopsin (metarhodopsin II) activates transducin. (2) Transducin activates cGMP phospho- diesterase, which destroys cGMP. (3) cGMP levels decrease, (4) causing sodium channels to close. (5) Closure of sodium channels causes photoreceptors to hyperpolarize Metarhodopsin II is deactivated rapidly after activating transducin by rhodopsin kinase and arrestin. 1 2 4 3 5. -40 mV mV →-70 Na+, Ca++ channel TMP14, Figure 51-7 Duration and Sensitivity of Receptor Potential Rods: a single pulse of light activates receptor potential for more than 1 s. Cones: occurs 4 X faster. Receptor potential is proportional to logarithm of light intensity. Information within the neural elements of the retina is conveyed by electrotonic potentials, not action potentials. very important for discrimination of light intensity. Color Vision Color vision results from activation of cones. The pigment protein in cones is called photopsin, a close analog of rhodopsin (there are 3 types of photopsin: types I (red), II (green), and III) (blue). The retinal portion of the photopsins is the same as in rods. Each cone is receptive to a particular wavelength of light. Figure 51-8 Color Blindness Lack of a particular type of cone. Genetic disorder mostly passed along on X chromosome. Hence, occurs almost exclusively in males. Blue color blindness affects both men and women equally, because it is carried on a non-sex chromosome. Most color blindness results from lack of red or green cones. lack of a red cone, protanope lack of a green cone, deuteranope Lack of a blue cone, tritanopia What happens in hereditary color deficiency? Red or green cone peak sensitivity is shifted. Red or green cones absent. Normal cone sensitivity curves (TRICHROMAT) 437 nm B 533 nm 564 nm G R Deuteranomaly (green shifted toward red) 5% of Males 437 nm B 564 nm G R Deutan Dichromat (no green cones; only red and blue) 437 nm 1% of Males (there is no green curve) B 564 nm R Deuteranope Vision Normal Color Deuteranope, shades of orange, no yellow or green Protanomalous (red shifted toward green) 1% of Males 533 nm 437 nm B G R 152 Protan Dichromat (no red cones; only green and blue) 1% of Males (there is no red curve) 533 nm 437 nm B G Protanomaly Normal Protanomaly Protanope Vision Normal Vision Protanope, red-green colors are difficult to distinguish Neural Organization of Retina Direction of light Figure 51-12 Signal Transmission in the Retina Neural elements in retina use electrotonic potentials (aka, graded potentials) to move current along their membranes instead of action potentials (exceptions include ganglion cells and some of the amacrine cells). The electrotonic potentials allow graded conduction of signal strength proportional to light intensity. Ganglion cells have action potentials. send signals to brain via optic nerve (CN 2). spontaneously active with continuous action potentials. visual signals are superimposed on this background. many excited by changes in light intensity. respond to contrast borders, this is the way the pattern of the scene is transmitted to the brain. Figure 51-12 Lateral Inhibition Processing the visual image begins in the retina. One example is lateral inhibition. Horizontal cells provide inhibitory feedback to rods and cones and bipolar cells. Output of horizontal cells is always inhibitory. Prevents lateral spread of light excitation on retina. Contrast is enhanced with excitatory center and inhibitory surround. Enhances visual contrast. TMP14, Figure 51-12 TMP14, Figure 51-13 Lateral Inhibition (cont.) APs from ganglion cell 1. Area excited by spot of light. 2. Area adjacent to excited spot. Figure 51-14 Lateral inhibition, the function of horizontal cells Figure 51-15 The Optic Disc (also called the optic nerve head) What is it? • point where ganglion cell axons (~1 million) exit the eye to form the optic nerve (2nd cranial nerve). • entry point for retinal blood vessels • creates a blind spot since there are no rods or cones. • located 3-4 mm to nasal side of fovea. • size: 1.76mm (horizontally) x 1.92mm vertically • Has a central depression called the optic cup edematous optic disc Aka, papilledema Function of Amacrine Cells • • • • • • • About 30 different types. Their primary targets are ganglion cells Some are involved in the direct pathway from rods to bipolar cells to amacrine cells to ganglion cells. A few have action potentials Some amacrine cells respond strongly to the onset of the visual signal, some to the extinguishment of the signal. Some respond to movement of a light signal across the retina. Amacrine cells are a type of interneuron that aid in the beginning of visual signal analysis. Most (but not all) amacrine cells release inhibitory transmitters, GABA or glycine. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3 652807/ Figure 51-12 Copyright © 2011 by Saunders, an imprint of Elsevier Inc. Ganglion Cells • More than 20 different types • Different types respond to the following: • Specific directions of motion or orientation • Fine detail • Increases or decreases in light Two classes of ganglion cells: P and M • Particular colors cells P cells (parvocellular cells): • Project to parvocellular layers of lateral geniculate nucleus (LGN) of thalamus • Small receptive fields, slow impulse conduction, sensitive to color and fine details, relatively insensitive to lowM cells (magnocellular cells): contrast signals • Project to magnocellular layers of lateral geniculate nucleus of thalamus • Larger receptive fields • Fast impulse conduction • More sensitive to low contrast B&W stimuli Figure 50-12 Copyright © 2011 by Saunders, an imprint of Elsevier Inc. UNIT 10 Chapter 52: The Eye: III. Central Neurophysiology of Vision Slides by Thomas H. Adair, PhD Copyright © 2021 by Saunders, an imprint of Elsevier Inc. Visual Pathways to the Cortex Optic nerve - axons of ganglion cells of retina. Optic chiasm. all fibers from nasal halves of retina cross to opposite side and join fibers from opposite temporal retina to form optic tracks. Synapse in dorsal lateral geniculate nucleus (LGN) of thalamus. From LGN to primary visual cortex by way of optic radiation. Two principal functions of LGN. Relay information to primary visual cortex via optic radiation. “Gate control” of information to primary visual cortex. (of thalamus) Figure 52-1 Lateral Geniculate Nucleus: Relay Function Half of the fibers in each optic tract are derived from one eye, and half from the other eye. Signals from the two eyes are kept apart in the LGN. Layers 2, 3, and 5 receive input from ipsilateral eye Layers 1, 4, and 6 receive input from contralateral eye Kandel, Schwartz and Jessell 4th edition 2000, McGraw Hill fig 26-4 Lateral Geniculate Nucleus: Gate Function LGN controls (gates) how much signal passes to cortex. LGN receives gating control signals from corticofugal fibers originating in primary visual cortex (not shown) reticular areas of midbrain (not shown) Both inputs are inhibitory and can turn off signal transmission in select areas of LGN. So, both inhibitory inputs control the visual input that is allowed to pass to cortex. Also, signals are provided to: A. Control the vergence of the eyes so they converge at the object of interest. B. Control the focus of the eyes based on calculated distance to object of interest. • Information is also provided describing the velocity of major elements in central field of vision, and which way the organism (person) is moving relative to • Kandel, Schwartz and Jessell 4th edition 2000, McGraw Hill fig 26-4 Primary Visual Cortex • Primary visual cortex lies in calcarine fissure. • Distribution from eye is shown. • Note large area of representation of macula (which includes fovea). • Fovea has several 100x more representation in cortex compared to peripheral portions of retina. • Secondary visual areas are visual association areas, where the visual image is dissected and analyzed. Figure 52-2 Analysis of the Visual Image the visual signal in the primary visual cortex is concerned mainly with contrasts in the visual scene. the greater the sharpness of the contrast, the greater the degree of stimulation. also detects the direction of orientation of each line and border. for each orientation of a line, a specific neuronal cell is stimulated. Visual Perception is a Creative Process how the brain perceives a visual image is not understood well. visual perception is thought to be mediated by three parallel pathways that process information on motion, depth and form, and color. Autonomic innervation of eye • Parasympathetic preganglionic fibers arise from Edinger-Westphal nucleus and synapse with postganglionic fibers in ciliary ganglion as shown. • The postganglionic fibers send action potentials through ciliary nerves to eyeball to control: 1. ciliary muscle (lens focusing) 2. Sphincter of iris (constricts pupil) • Sympathetic preganglionic fibers originate in intermediolateral horn of 1st thoracic segment of cord and synapse with postganglionic fibers in superior cervical ganglion as shown. • The postganglionic fibers innervate radial fibers of iris (which open pupil), plus several extraocular Ciliary nerve Figure 51-11 Control of Accommodation Recall that accommodation is the mechanism that focuses the lens system. The lens system focused on a distant object can refocus on a close object in less than 1 s. • Parasympathetic control mechanism is poorly understood • Chromatic aberration: red light rays focus posteriorly compared to blue light rays. Eye can tell which is in better focus and relay information to accommodation mechanism. (seems unlikely since color blind people can still focus) • Convergence: neural signal for convergence cause simultaneous signal to strengthen lens. • Fovea lies in depression of retina. Differences between foveal image and image of surrounding retina may also give clues about which way lens should respond. • Oscillation of the degree of accommodation occurs all the time (2x per second). An image becomes better focused Figure 52-11 Control of Pupillary Diameter • Pupils constrict when the amount of light entering the eyes increases. Functions to help eyes adapt to extremely rapid changes in light conditions. Pupillary light reflex pupil • Parasympathetic nerves excite pupillary sphincter muscle, decreasing pupillary aperture (miosis). • Sympathetic nerves excite radial fibers