Biopsychology Midterms Reviewer

The “where” versus “what” and the “control of behavior” versus “conscious perception” theories make BIOPSYCHOLOGY MIDTERMS...

The “where” versus “what” and the “control of behavior” versus “conscious perception” theories make BIOPSYCHOLOGY MIDTERMS different predictions. REVIEWER Datorin, Tanato, Virgilio DORSAL AND VENTRAL STREAMS Two Theories and What They Predict SENSATION AND PERCEPTION Threshold, Senses, and Sensory Problems A. “Where” vs. “What” Theory Dorsal stream specializes in visual spatial perception 1) Sight - light waves Ventral stream specializes in visual pattern recognition 2) Hearing - sound waves 3) Tasting - liquid substances Predicts 4) Smelling - gaseous particles ➔ Damage to dorsal stream disrupts visual spatial 5) Touch - touch perception ➔ Damage to ventral stream disrupts visual pattern recognition Topic 5 THE SENSORY SYSTEMS B. “Control of Behavior” vs. “Conscious Perception” Theory A. SENSE OF SIGHT Dorsal stream specializes in visually guided behavior How we see Ventral stream specializes in conscious visual perception Predicts ➔ Damage to dorsal stream disrupts visually guided behavior but not conscious visual perception ➔ Damage to ventral stream disrupts conscious visual perception but not visually guided behavior Detailed Sequence (following the basic process) 1) Object 2) Light waves 3) Pupil -> Lens (focus) 4) Retina (converts the light to neural signals) BASIC PROCESS 5) Neurons 1) Object 6) Brain 2) Stimulus 3) Sensory Organ 4) Neurons VISUAL PROBLEMS 5) Brain 6) Interpretation 1) Nearsightedness or Myopia ➔ A condition where a person is capable of seeing nearby objects with greater activity Sequence than distant objects. 1) Light enters eyes and reaches the retina 2) Translation of light to neural signals 2) Farsightedness or Hyperopia 3) From retina to the primary visual cortex ➔ A condition where a person can see distant objects with greater activity than nearby ★ Light, sometimes defined as waves of electromagnetic objects. energy between 380 and 760 nanomeneter in length.  3) Presbyopia 5) Sensory Neurons ➔ A condition characterized by the brittleness of 6) Brain and Interpretation the lens (permits us to focus on objects at a varying distance) which usually begins at abour 38-46 years old. AUDITORY PROBLEMS ➔ Due to old age (decline) 1) Conduction deafness ➔ Damage to the structures of the middle ear 4) Strabismus or Cross-eyed (eardrum or bone that conduct and amplify ➔ A visual disorder in which both eyes cannot sound waves from the outer ear to the inner focus on the same point at the same time. ear) ➔ They profit from hearing aids 5) Astigmatism ➔ Caused by abnormal curvature of the lens, so that images are distorted 2) Sensory Neural Deafness ➔ Loss of hair cells which will not regenerate 6) Color Blindness ➔ People who suffer from this condition are ➔ Monochromats and sensitive to light and dark sensitive to sounds of some pitches than only others. a) Partial Color Blindness - sex-linked trait (men); dichromats and can 3) Stimulation deafness discriminate only 2 colors (red & ➔ Stems from exposure to very loud sounds green or blue & yellow) ➔ Hair cells might have been damaged. ➔ Men - genetically manifested ➔ Women - Carrier (recessive) C. SENSE OF SMELL B. SENSE OF HEARING How we smell How we hear Detailed Sequence (following the basic process) 1) Object 2) Gaseous Particles Detailed Sequence (following the basic process) 3) Olfactory Mucosa (receptor cells) 1) Object Olfactory Bulbs (they synapse with the neuron) 2) Sound waves 4) Sensory Neurons 3) Tympanic Membrane (vibration) 5) Amygdala (medial nucleus involved in the sense f 4) Oval window - Round window smell) Cochlea (encoder) Auditory Nerve  Thalamus (receives sensory signals and sends them to 4) Neuron - carries signals away from taste buds, while the associated primary cortical area) receiving input from many receptors 6) Interpretation Solitary Nucleus of the Medulla (they synapse on neurons that project to the ventral posterior nucleus of OLFACTORY PROBLEMS the thalamus) 1) Anosmia or Smell Blindness 5) Brain ➔ A condition developed for a particular odor 6) Interpretation which suggests that one kind of receptor has been damaged or degenerated. ➔ Note that the nose is sensitive to various basic TASTE PROBLEMS odors. 1) Ageusia a) Flowery ➔ Temporary loss of taste by eating hot food and b) Misty (soft) scraping the tongue. c) Musky (strong-smelling ➔ The number of taste cells declines with age; reddish-brown substance) taste loss can be closely associated by the d) Ethereal (delicate and light) elderly who already suffer from the decline of e) Pungent (strong smell – frying sense of smell. onions) f) Putrid decaying (rotting) g) Burnt E. SENSE OF TOUCH How we touch D. SENSE OF TASTE How we taste Detailed Sequence (following the basic process) Detailed Sequence (following the basic process) 1) Object 1) Object 2) Touch 2) Liquid Substances 3) Skin Receptors (Free nerve endings, Pacinian 3) Taste Receptors - taste buds in the papillae corpuscles, Merkel’s disks, Ruffin endings) Primary Taste 4) Pressure evokes a burst of firing in all receptors, which a) Sweet corresponds to the sensation of being touched b) Sour 5) Neural Fibers (dermatomes) that carry information c) Bitter from cutaneous receptors and other somatosensory d) Salty receptors gather together in nerves and enter the spinal e) Umami (taste produced by a different cord via dorsal roots combination of activity in these five kinds of 6) Brain (somatosensory cortex in the forebrain) receptors) 7) Interpretation  Topic 6 SKIN PROBLEMS SENSORIMOTOR SYSTEM 1) Pain ➔ pain message to the brain is initiated by the Three Principles of Sensorimotor Function release of various chemicals including Prostaglandins which not only facilitate 1. The Sensorimotor System is Hierarchically transmission to the brain but also heighten Organized circulation to the injured area causing redness 2. Motor Input is Guided by Sensory Inputs and swelling called Inflammation. 3. Learning Changes the Nature and Locus of ➔ Analgesics (aspirin or ibuprofen) work by Sensorimotor Control preventing prostaglandin production. 2) Acne ➔ Occurrence of inflamed or infected sebaceous 1. The Sensorimotor System is Hierarchically glands in the skin Organized ➔ A condition characterized by red pimples on the face, prevalent chiefly among teenagers. ➔ The operation of both the sensorimotor system and a large efficient company is directed by commands that 3) Psoriasis cascade down through the levels of a hierarchy. ➔ A skin disease marked by red, itchy, scaly ➔ It works from the association cortex or the company patches president (the highest levels) to the muscles or the workers (lowest levels) 4) Ezcema ➔ The main advantage of this hierarchical organization is ➔ Patches of skin become rough and inflamed that the higher levels of the hierarchy are left free to perform more complex functions. 5) Dermatitis ➔ Both the sensorimotor system and a large, efficient ➔ Skin becomes red and swollen company are parallel hierarchical systems; that is, they ➔ It can result in symptoms such as redness, are hierarchical systems in which signals flow between itching, swelling, and sometimes blistering or levels over multiple paths. oozing. ➔ This parallel structure enables the association cortex to exert control over the lower levels of the hierarchy in more than one way. ➔ The sensorimotor and company hierarchies are also characterized by functional segregation. ➔ Functional segregation- means that each level of the sensorimotor and company hierarchies tends to be composed of different units (neural structures or departments), each of which performs a different function. 2. Motor Input is Guided by Sensory Inputs ➔ Just like efficient companies, sensorimotor systems are also flexible. They continuously monitor the effects of their own activities, and use this information to fine-tune their activities. ➔ The eyes, the organs of balance, and the receptors in the skin, muscles, and joints all monitor the body’s  responses, and they feed their information back into sensorimotor circuits. ➔ This sensory feedback plays an important role in directing the continuation of the responses that produced it. ➔ But there is an exception, as the only responses that are not normally influenced by the sensory feedback are ballistic movements—brief, all-or-none responses, high-speed movements, such as swatting a fly. 3. Learning Changes the Nature and Locus of Sensorimotor Control ➔ During the initial stages of the motor learning process, each individual response is performed under conscious control, then, after much practice, individual responses become organized into continuous integrated sequences of action that flow smoothly and A. SENSORIMOTOR ASSOCIATION CORTEX are adjusted by sensory feedback without conscious regulation. Association cortex is at the top of a person’s ➔ Simply stated, mura siya ug practiced or learned sensorimotor hierarchy. There are two major areas of behavior kumbaga. For example, if naga learn palang ka sensorimotor association cortex: the posterior parietal mag bicycle, you’ll make sure na every step from riding association cortex and the dorsolateral prefrontal the bicycle to balancing should be thought of. But association cortex. Both of them perform different with practice, it becomes automatic. Eventually, your functions. brain organizes these steps into smooth, flowing 1. Posterior Parietal Association Cortex actions that adjust naturally based on how it feels, ➔ Plays an important role in integrating two kinds of without you having to think about it. information: directing behavior by providing spatial information, and in directing attention. ➔ It receives information from the three sensory systems General Model of Sensorimotor System Function that play roles in the localization of the body and external objects in space: the visual system, auditory system, and the somatosensory system. ➔ Assigned to know the original positions of the part of the body that are to be moved, and must know the position of the external objects in which the body is going to react. Damage/s to the Posterior Parietal Association Cortex 1. Apraxia- disorder of voluntary movement– problem only becomes evident when the patient is instructed to perform an action– usually a consequence of damage to the left posterior parietal cortex, or its connections. The model illustrates several principles of sensorimotor system 2. Contralateral Neglect- disturbance of a patient’s organization; it is the framework of this chapter. ability to respond to stimuli on the side of the body opposite to the side of a brain lesion in the absence of simple sensory or motor deficits.  ➔ The disturbance is often associated with large lesions IDENTIFYING THE AREAS OF SECONDARY of the right posterior parietal cortex. MOTOR CORTEX ➔ Neuroanatomical research has made a case for at least eight areas of secondary motor cortex in each hemisphere, each with its own subdivisions: ❖ Three different supplementary motor areas (SMA, preSMA, and supplementary eye field) ❖ Two premotor areas (dorsal and ventral) ❖ Three small Cingulate Motor Areas 2. Dorsolateral Prefrontal Association Cortex ➔ It receives projections from the posterior parietal cortex, ➔ To qualify as a secondary motor cortex, an area must and it sends projections to areas of the secondary be appropriately connected with association and motor cortex, to primary motor cortex, and to the secondary motor area. frontal eye field. ➔ In general, areas of the secondary motor cortex are ➔ Evaluates external stimuli and initiates voluntary thought to be involved in the programming of reactions— supported by neuronal responses. specific patterns of movements after taking general instructions from the dorsolateral prefrontal cortex. MIRROR NEURONS ➔ Are neurons that fire when an individual performs a particular goal-directed hand movement or when they observe the same goal-directed movement performed by another. ➔ Neurons that grow active when performing an action or watching another perform the same action ➔ In monkey studies, mirror neurons fired while grasping or watching another grasp a particular object but not other objects; or for a specific purpose and not for other purposes. B. SECONDARY MOTOR CORTEX C. PRIMARY MOTOR CORTEX Areas of secondary motor cortex are those that receive much of their input from association cortex, and send much of their Primary motor cortex is located in the precentral gyrus of the output to primary motor cortex. For many years, only two areas frontal lobe. It is the major point of convergence of cortical were known: the supplementary motor area and the sensorimotor signals, and it is the major, but not the only, point premotor cortex. of departure of sensorimotor signals from the cerebral cortex. 1. Supplementary motor area- wraps over the top of the frontal lobe and extends down its medial surface into the longitudinal fissure. 2. Premotor Cortex- runs in a strip from the supplementary motor area to the lateral fissure.  CEREBELLUM ➔ 10% of the brain’s mass but 50% of its neurons ➔ receives information from primary and secondary motor cortex, information about descending motor signals from brain stem motor nuclei, and feedback from motor responses via the somatosensory and vestibular systems. CONVENTIONAL VIEW OF PRIMARY MOTOR BASAL GANGLIA CORTEX ➔ Unlike the cerebellum, which is organized ➔ The somatotopic layout of the human primary systematically in lobes, columns, and layers, the basal motor cortex is commonly referred to as the motor ganglia are a complex heterogeneous collection of homunculus. interconnected nuclei. ➔ Motor homunculus- individual response when a ➔ Modulate motor output and cognitive functions specific area is stimulated. including learning and memory. ➔ It is important to note that each site in the primary motor cortex receives sensory feedback from receptors D. DESCENDING MOTOR PATHWAYS in the muscles and joints that the site influences. Neural signals are conducted from the primary motor cortex to CURRENT VIEW OF PRIMARY MOTOR CORTEX the motor neurons of the spinal cord over four different ➔ Recent efforts to map the primary motor cortex have pathways. Two pathways descend in the dorsolateral region of used new stimulation techniques—rather than the spinal cord, and the other two descend in the ventromedial stimulating with brief impulses that are just above the region of the spinal cord. threshold of producing reaction, investigators used longer bursts of current—higher intensity, which are Dorsolateral Regions similar to the duration of a motor response (e.g., 0.5 to ➔ One group of axons that descend from the primary 1 second) motor cortex does so through the medullary ➔ Rather than eliciting the contractions of individual pyramids— two bulges on the ventral surface of the muscles, these currents elicited complex medulla–then decussate and continue to descend in natural-looking response sequences e.g. feeding the contralateral dorsolateral spinal white matter. response. ➔ This group of axons constitutes the dorsolateral ➔ Extensive damage to the human primary motor cortex corticospinal tract. has less effect than expected ➔ A second group of axons is the ones that descend from ➔ Large lesions to the primary motor cortex may disrupt the primary motor cortex synapses in the red nucleus of a patient’s ability to move one body part the midbrain. This pathway is called the dorsolateral independently of others corticorubrospinal tract (rubro refers to the red ➔ Large lesions may also produce astereognosia or nucleus). deficits in stereognosis— ability to identify the shape and form of a 3-dimensional object. CEREBELLUM AND BASAL GANGLIA The cerebellum and the basal ganglia are both important sensorimotor structures, but neither is a major part of the pathway by which signals descend through the sensorimotor hierarchy. Basically, both structures coordinate and modulate with each other to produce activities. Ventromedial Region fingers and face– permit the highest degree of selective ➔ Corticospinal tracts- descends ipsilaterally. Axons motor control. branch and innervate interneuron circuits bilaterally in ➔ A skeletal muscle comprises hundreds of thousands multiple spinal segments of threadlike muscle fibers bound together in a tough ➔ Cortico-brainstem-spinal tract- interacts with membrane and attached to a bone by a tendon. various brain stem structures and descends bilaterally ➔ Acetylcholine released by motor neurons at the carrying information from both hemispheres. neuromuscular junction causes contraction Moreover, synapse on interneurons of multiple spinal ➔ Fast muscle fibers– contract and relax quickly; segments controlling proximal trunk and limb fatigue quickly due to being poorly vascularized muscles. (meaning they have few blood vessels) - appear to have pale color. Dorsolateral vs. Ventromedial ➔ Slow muscle fibers– capable of sustained contraction due to vascularization. They usually appear to be ➔ The descending dorsolateral and ventromedial motor redder in color. pathways are similar in that each is composed of two ➔ Muscles are a mixture of fast and slow fibers. major tracts– one whose axons descend directly to ➔ Many skeletal muscles belong unambiguously to one the spinal cord and another whose axons synapse in of two categories: flexors and extensors. the brain stem on neurons that in turn descend to the Flexors- bend or flex a join spinal cord. Extensors- acts to straighten or extend a joint ➔ Any two muscles whose contraction produces the same movement, be it flexion or extension, are said to be synergistic muscles; those that act in opposition, like the biceps and triceps, are said to be antagonistic muscles. RECEPTOR ORGANS OF TENDONS AND MUSCLES GOLGI TENDON ORGANS ➔ Embedded in the tendons, which connect each skeletal muscle to the bones. ➔ They detect and respond muscle tension ➔ The function of golgi tendon organs is to provide the central nervous system with information about muscle tension, but they also serve a protective function. MUSCLE SPINDLES ➔ Embedded in the muscle tissue itself SENSORIMOTOR SPINAL CIRCUITS ➔ Respond to changes in muscle length, but they do not respond to changes in the muscle tension. The motor circuits of the spinal cord show considerable complexity in their functioning, independent of signals from REFLEXES the brain. ➔ Stretch Reflex: monosynaptic, serves to maintain limb stability e.g., patellar tendon reflex is MUSCLES monosynaptic ➔ Motor Units- smallest units of motor activity. Each ➔ Withdrawal Reflex: Unlike stretch reflex, withdrawal motor unit comprises a single motor neuron and all of reflex is not monosynaptic. When a painful stimulus is the individual skeletal muscle fibers that it innervates. applied to the hand, the first responses are recorded in ➔ When the motor neuron fires, all the muscle fibers the motor neurons of the arm flexor muscles about 1.6 contain; the units with the fewest fibers–those of the milliseconds later.  ➔ Reciprocal Innervation: antagonistic muscles interact so that movements are smooth– flexors are excited while extensors are inhibited. ➔ Recurrent Collateral Inhibition: feedback loop through Renshaw cells that gives muscle fiber that gives muscle fiber a rest after every contraction A. INDUCTION OF THE NEURAL PLATE ➔ Walking: a complex reflex in some animals Neural plate - a patch of tissue on the dorsal surface of the embryo becomes the neural plate TOPIC 7 Visible three weeks after conception, tissue that is destined to develop into the human nervous system DEVELOPMENT OF THE NERVOUS SYSTEM Development induced by chemical signals from the mesoderm (the “organizer”) Neurodevelopment Three layers of embryonic cells Neural development – an ongoing process in Ectoderm (outermost response to its genetic programs and environment; Mesoderm (middle) the nervous system is plastic, not static Endoderm (innermost) A complex process (phases of neurodevelopment) Neural plate cells are often referred to as embryonic Experience plays a key role stem cells. Dire consequences of neurodevelopmental errors Stem cells - cells that meet two specific criteria: 1. unlimited capacity for self-renewal The case of Genie 2. Develop into many different kinds of cells At age 13, Genie weighed 62 pounds (28.1 kg), was (totipotent, pluripotent or multipotent) 1.35 meters tall, and could not chew solid food Can become any kind of mature cell beaten, starved, restrained, kept in a dark room, 1. Totipotent – earliest cells have the ability to denied normal human interactions become any type of body cell Even with special care and training after rescue, her 2. Multipotent – with development, neural behavior never became normal plate cells are limited to becoming one of the Case of Genie illustrates the impact of severe range of mature nervous system cells deprivation on development How the neural plate develops into the neural tube during the third Five Phases of Neurodevelopment and fourth weeks of human embryological development. Ovum + sperm = zygote Developing neurons accomplish these things in five phases a. Induction of the neural plate b. Neural proliferation c. Migration and aggregation (alignment) d. Axon growth and synapse formation e. Neuron death and synapse rearrangement Totipotent - the fertilized egg is a cell that has the ability to develop into any class of cell in the body Pluripotent - tend to be specialized due to cell division and no longer totipotent Multipotent - develop into different cells of only one class (different kinds of blood cells) Unipotent - can develop into only one type of cell.  Neural plate folds to form the neural groove, and then the lips of the neural groove fuse to form the neural tube. The inside of the neural tube becomes eventually becomes the cerebral ventricles and spinal canal 40 days after conception three swellings (forebrain, midbrain, and hindbrain) are visible at the anterior end of the neural tube. Neural tube defects – develops into severe birth defects of the CNS resulting from errors in this folding process. B. NEURAL PROLIFERATION Neural plate folds to form the neural groove, which then fuses to form the neural tube Inside will be the cerebral ventricles and neural tube Neural tube cells proliferate in species-specific ways: three swellings at the anterior end in humans will become the forebrain, midbrain, and hindbrain Most cell division in the neural tube occurs in the ventricular zone— the region adjacent to the ventricle (the fluid-filled center of the tube) Proliferation is chemically guided by the organizer areas – the roof plate and the floor plate Aggregation The cells of the tube begin to proliferate, responsible After migration, cells align themselves with others for a pattern of swelling and folding that gives the cells and form structures brain of each member of species the characteristic Aggregation is mediated by cell-adhesion molecules shape. (CAMs) located on the surfaces of the neurons and other cells: C. MIGRATION AND AGGREGATION Aid both migration and aggregation CAMs recognize and adhere to molecules Migration elimination of just type of CAM can cause Once cells have been created through cell division in devastating effect on brain development the ventricular zone of the neural tube, they migrate Gap junctions pass cytoplasm between cells to the appropriate target location. Prevalent in brain development Migrating cells are immature, lacking axons and `May play a role in aggregation and other dendrites processes Two types of neural tube migration Radial migration (moving out) – usually by D. AXON GROWTH AND SYNAPSE FORMATION moving along radial glial cells Tangential migration (moving up) Axon growth Two methods of migration Once migration is complete and structures have Somal – an extension develops that leads formed (aggregation), axons and dendrites begin to migration, cell body follows grow Glial-mediated migration – cell moves along Growth cone – at the growing tip of each axon or a radial glial network dendrite, extends and retracts filopodia (fingerlike Most cells engage in both types of migration cytoplasmic extension) as if finding its correct route Chemoaffinity hypothesis – postsynaptic targets release a chemical that guides axonal growth, but this  does not explain the often circuitous routes often Necrotic cells break apart and spill their contents observed into extracellular fluid, and the consequence is Mechanisms underlying axonal growth are the same potentially harmful inflammation across species Apoptosis is safer than necrosis – does not promote A series of chemical signals exist along the way – inflammation attracting and repelling In apoptotic cell death, DNA and other internal Such guidance molecules are often released by glia structures are cleaved apart and packaged in Adjacent growing axons also provide signals membranes before the cell breaks apart. Pioneer growth cones – the first to travel a route, if genetic programs for apoptotic cell death are interact with guidance molecules blocked, consequence is cancer Fasciculation – the tendency of developing axons to if programs are inappropriately activated, grow along the paths established by preceding axons consequence is neurodegenerative disease Topographic gradient hypothesis – seeks to explain cause of apoptotic cell death - genetically topographic maps programmed for early death and failure to obtain life preserving chemicals supplied by targets Synapse Formation Neurotrophins – promote growth and survival, After axons reach their intended sites, formation of guide axons, stimulate synaptogenesis new synapses happen. Nerve growth factor (NGF) Synapse – connection between two neurons that allows them to communicate. Synapse Rearrangement Depends on the presence of glial cells – especially Neurons that fail to establish correct connections are astrocytes particularly likely to die High levels of cholesterol are needed – supplied by Space left after apoptosis is filled by sprouting axon astrocytes terminals of surviving neurons Chemical signal exchange between presynaptic Ultimately leads to increased selectivity of (sending) and postsynaptic (receiving) neurons is transmission needed A variety of signals act on developing neurons E. NEURON DEATH & SYNAPSE REARRANGEMENT Neuron Death Many more neurons—about 50 percent more—are produced than required, and large-scale neuron death occurs in waves in various parts of the brain throughout development Neurons die due to failure to compete for chemicals provided by targets The more targets, the fewer cell deaths Destroying some cells increases survival rate Effects of Experience on Postnatal Development of of remaining cells Neural Circuits Increasing number of innervating axons Neurodevelopment = interaction between neuron decreases the proportion that survives and the environment Genetic programs inside neurons are triggered and Permissive experiences: those that are necessary for cause them to actively complete suicide information in genetic programs to be manifested Passive cell death is called necrosis Instructive experiences: those that contribute to the Active cell death is called apoptosis direction of development  Effects of experience on development are Effects of Experience on Topographic Sensory Cortex time-dependent Maps Critical period – experience that occurs Cross-modal rewiring experiments demonstrate the within a particular interval to influence plasticity of sensory cortexes – with visual input, the development auditory cortex can see Sensitive period – experience has great effect Change input, change cortical topography – shifted on development when it occurs during a auditory map in prism-exposed owls particular interval but still can have weak Early music training influences the organization of effect outside the interval human auditory cortex – fMRI studies Early Studies of Experience and Neurodevelopment: Experience Fine-Tunes Neurodevelopment Deprivation and Enrichment Neural activity regulates the expression of genes that direct the synthesis of CAMs Early visual deprivation Neural activity influences the release of Fewer synapses and dendritic spines in neurotrophins primary visual cortex Some neural circuits are spontaneously active and Deficits in depth and pattern vision this activity is needed for normal development Experience clearly has major effects on the Enriched environment development and maintenance of neural circuits Thicker cortices Greater dendritic development Neuroplasticity in Adults More synapses per neuron The mature brain changes and adapts Debate: neurogenesis does not occur in adults 1980 studies (adult birds) and 1990 studies (rat Competitive Nature of Experience and hippocampus) Neurodevelopment Neurogenesis (growth of new neurons) seen in Ocular Dominance Columns example: olfactory bulbs and hippocampuses of adult Monocular deprivation changes the pattern of mammals – adult neural stem cells created in the synaptic input into layer IV of V1 (but not binocular ependymal layer lining in ventricles and adjacent deprivation) tissues Altered exposure during a sensitive period leads to enriched environments and exercise can promote reorganization neurogenesis Active motor neurons take precedence over inactive one Effects of Experience on the Reorganization of the Adult Cortex Tinnitus (ringing in the ears) – produces major reorganization of primary auditory cortex Adult musicians who play instruments fingered by left hand have an enlarged representation of the hand in the right somatosensory cortex Skill training leads to reorganization of motor cortex Brains adapt to abnormal environmental conditions; moreover, it acquires the ability to adapt more effectively if it encounters the same condition again. Experience has been shown to increase, decrease, or modify cortical synapses, buttons, and dendritic spines  For example, ASD patients who suffer from an Disorders of Neurodevelopment: Autism Spectrum intellectual disability often perform well on tests Disorder and Williams Syndrome involving rote memory, jigsaw puzzles, music, and art A. AUTISM SPECTRUM DISORDER ASD Savants Is a complex neurodevelopmental disorder. Savants – are persons with developmental Apparent before the age of 3 and typically does not disabilities who nevertheless display amazing and increase in severity specific cognitive or artistic abilities. Three core symptoms ~1/10 autistic individuals display savant abilities Reduced ability to interpret emotions and Perhaps a consequence of compensatory functional intentions improvement in one area following damage to Reduced capacity for social interaction another Preoccupation with a single subject or activity Genetic Bases of ASD Two core symptoms: (sa book) Siblings of the autistic have a 5% chance of being Reduced capacity for social interaction and autistic communication 60% concordance rate for monozygotic twins Restricted and repetitive patterns of Several genes interacting with the environment behavior, interests, or activities prevalence: 80% are male, 50% suffer from mental Neural Mechanisms of ASD retardation, 35% have seizures Understanding of brain structures involved in Asperger’s syndrome – mild ASD with cognitive autism is still limited, so far implicated: and linguistic functions well preserved ❖ Cerebellum older mothers are more likely to give birth to a child ❖ Amygdala with autism, mothers under age 30 but with a father ❖ Frontal cortex who is over 40 years old increases the probability Two lines of research on cortical involvement in Early warning sign: a delay in the development of autism: social interaction 1. Abnormal response to faces in autistic Decline in eye contact between 2 to 6 patients months - Spend less time than non-autistic No smiles or happy expressions by 9 months subjects looking at faces, especially No communicative gestures such as pointing eyes or waving by 12 months - Low fMRI activity in fusiform face Incidence is 1 in 68 births (sa book) area Incidence: 6.6 per 1,000 births (or 1 in 166) 2. Possibly deficient in mirror neuron 80% males, 60% mentally retarded, 35% epileptic, function ( secondary motor cortex) 25% have little or no language ability Intensive Behavioral Therapy can improve the lives B. WILLIAMS SYNDROME of some ASD individuals Williams Syndrome – neurodevelopmental disorder facial feature: square shaped ears positioned too low associated with intellectual disability and with a on the head with tops flopped over heterogeneous pattern of disabilities. medical advancements for ASD: broadening of Mental retardation and an uneven pattern of abilities diagnostic criteria, increasing public awareness, and disabilities improved methods of identifying cases People with williams syndrome are sociable, emphatic, talkative – exhibit language skills, music ASD is a Heterogeneous Disorder. skills, and an enhanced ability to recognize faces Affected individuals may be severely impaired in (opposite to ASD) some aspects but may be typical, or even superior in 1 in 7,500 births others. Profound impairments in spatial cognition; low IQ  Usually have heart disorders associated with a mutation in a gene on chromosome 7 – the gene (and others) is absent in 95% of those with Williams Chromosome 7 – controls the synthesis of elastin, a protein that imparts elasticity to many organs and tissues, including the heart Evidence for a role of chromosome 7 (as in autism) General thinning of cortex at juncture of occipital and parietal lobes, and at the orbitofrontal cortex “Elfin” appearance – short, small upturned noses, oval ears, broad mouths Mythical creatures like elves are said to be based on persons with Williams syndrome