Quiz 1 Phisology.pdf

The neuron is the major functional unit of the nervous system. Neurons vary in shape depending on location and role. Basic neuron structure includes: Dendrites (information-receiving area) Cell body (soma) with organelles for metabolic activity Axon (carries informa...

The neuron is the major functional unit of the nervous system. Neurons vary in shape depending on location and role. Basic neuron structure includes: Dendrites (information-receiving area) Cell body (soma) with organelles for metabolic activity Axon (carries information) Presynaptic terminal (transmits information to other cells) Axons are often covered with a myelin sheath that speeds up information transfer. Neurons are interconnected within neural circuits/pathways serving specific functions. Neural pathways with similar functions form neural systems (e.g., visual system pathways). Glial cells support neuron structure and function: Produce myelin sheaths Aid neuron growth and repair Regulate extracellular potassium and neurotransmitters Form synapses and participate in immune responses Glial cells do not produce action potentials but modulate neural communication. Some glial-mediated responses contribute to neurodegenerative diseases and chronic pain. The mammalian nervous system is divided into: 1. Central Nervous System (CNS) – includes the brain and spinal cord, protected by the skull and vertebrae. 2. Peripheral Nervous System (PNS) – composed of spinal and cranial nerves carrying action potentials to and from the CNS. PNS nerves are categorized into: Afferent axons – carry signals toward the CNS. Efferent axons – carry signals away from the CNS. The PNS has two subsystems: 1. Sensory subsystem – afferent axons from sensory receptors transmit signals to the CNS (e.g., photoreceptors, tactile receptors). 2. Motor subsystem – efferent axons transmit signals from the CNS to muscles and glands. o Somatic efferent neurons – control skeletal muscles. o Visceral efferent neurons – control smooth muscle, cardiac muscle, and glands. Visceral afferent neurons – carry signals from receptors in visceral organs to the CNS (e.g., chemoreceptors, stretch receptors).  Autonomic nervous system (ANS) – part of the PNS and CNS responsible for involuntary control of smooth muscle, cardiac muscle, and physiological functions like heart rate and digestion. Spinal nerves – formed by afferent and efferent axons converging in the spinal canal. Dorsal roots – entry point for afferent sensory axons into the spinal cord. Ventral roots – exit point for efferent motor axons from the spinal cord. Cranial nerves – connect the brain to the face and head through openings in the skull. Regenerative ability: PNS axons can regenerate slowly after injury and reconnect. CNS axons do not regenerate effectively due to inhibitory factors in their environment. Research on glial cells offers hope for improving axonal regeneration in both CNS and PNS. The CNS is divided into six major regions: spinal cord, medulla, pons, midbrain, diencephalon, and telencephalon. The brainstem includes the medulla, pons, and midbrain; the forebrain consists of the diencephalon and telencephalon. Spinal cord: Receives sensory input and sends motor output to the trunk and limbs. Handles simple reflexes like muscle stretch and limb withdrawal. Medulla: Manages life-support functions (respiration, cardiovascular system). Handles sensory input and motor output for the head and neck via cranial nerves. Pons: Relays information between the cerebral cortex and cerebellum. Involved in orofacial touch and motor control of chewing. Cerebellum: Coordinates smooth, accurate movements and motor learning. Midbrain: Processes visual and auditory information via superior and inferior colliculi. Controls eye movement, pupil constriction, and pain modulation (periaqueductal gray).  Diencephalon: Includes the thalamus (relay and modulator for sensory information) and hypothalamus (regulates autonomic nervous system, controls hormone secretion, maintains homeostasis). Telencephalon (cerebral hemispheres): Contains the cerebral cortex (sensory integration, voluntary movement) and subcortical structures like basal ganglia (modulates motor function) and hippocampus (memory and spatial learning). The hippocampus is one of the few brain regions where new neurons are generated in adulthood. The CNS is protected by three layers called meninges: 1. Pia mater – the innermost layer, attached to the surface of the brain and spinal cord. 2. Arachnoid – the middle layer, with a spiderweb appearance, containing cerebrospinal fluid (CSF) in the subarachnoid space. 3. Dura mater – the thick outer layer, often fused with the skull's inner surface. Cerebrospinal fluid (CSF): A clear fluid found in the subarachnoid space, spinal cord, and brain ventricles. Produced in brain ventricles and flows to bathe the CNS, exchanging with extracellular fluid. Removes waste, provides micronutrients, and is a diagnostic tool for CNS infections, inflammation, or tumors. Acts as a shock absorber, protecting the CNS during sudden movements. The nervous system has three main functions: 1. Collect sensory information from the external or internal environment. 2. Integrate inputs (consciously or unconsciously) to formulate a response plan. 3. Produce motor output to change or maintain the environment. PNS is responsible for collecting sensory information and executing motor output. CNS is primarily responsible for integrating sensory inputs. These functions occur at both the system and individual neuron levels. Four distinct anatomical regions of a neuron: Dendrites: Receive signals from other neurons. Cell body (soma): Manufactures essential proteins for neuron function.  Axon: Transmits action potentials (electrical impulses). Presynaptic terminals: Transmit chemical signals to other cells at synapses. Cell body functions: Contains organelles for protein synthesis (nucleus, ribosomes, rough ER, Golgi apparatus). Degrades surplus proteins (lysosome, proteasome). Axon structure and function: Conducts action potentials from the cell body to the presynaptic terminals. Lacks ribosomes, relies on axoplasmic transport for protein delivery. Large axons are insulated by myelin (produced by Schwann cells in PNS, oligodendrocytes in CNS), increasing signal conduction speed. Presynaptic terminals and synapses: Transmit chemical signals (neurotransmitters) to adjacent cells at synapses. Synapses consist of the presynaptic terminal, postsynaptic receptor, and synaptic cleft. Signal transmission process: Dendrites receive neurochemical signals. Signals are integrated at the initial axon segment. Action potential is generated and transmitted to presynaptic terminals. Neurotransmitters are released, affecting the next neuron or muscle cell. Resting membrane potential: Neurons have an electrical potential (voltage) across their cell membrane, known as the resting membrane potential. Unique to neurons and muscle cells: Unlike most other cells, neurons and muscle cells can change the magnitude and sign of their membrane potential in response to synaptic signaling or environmental stimuli. Action potential: When the membrane potential reaches a certain threshold, it triggers an action potential that travels rapidly along the axon. Ion gradients: The resting membrane potential results from the differential separation of ions, particularly sodium (Na+) and potassium (K+), across the membrane. Charge distribution: An excess of positive charges accumulates outside the membrane, while negative charges accumulate inside, making the inside of the cell negatively charged relative to the outside. Typical voltage: The resting membrane potential in mammalian neurons is usually around −70 mV, with the extracellular fluid considered at 0 mV. Na+/K+ pump: This pump actively moves Na+ out of the cell and K+ into the cell against their concentration gradients, maintaining the ion distribution. It contributes to the resting membrane potential by pushing three Na+ out for every two K+ brought in, leading to more positive charge outside the cell.  Dynamic equilibrium of ions: Ions, like K+, move across the membrane toward dynamic equilibrium. K+ tends to flow out due to its concentration gradient, but the negative charge left behind pulls K+ back inside, leading to a balance between the chemical and electrical forces. This balance creates the ion's equilibrium potential, contributing to the resting membrane potential. Differential permeability: The membrane is much more permeable to K+ than to Na+ due to a higher number of K+ leak channels. This allows K+ to approach its equilibrium potential (about −90 mV) more easily than Na+, which has a lesser impact on the resting potential, resulting in a typical resting membrane potential of −70 mV. Energy requirement: The Na+/K+ pump requires energy from ATP, consuming 50% to 70% of the brain’s energy, making glucose and oxygen crucial for its function. Clinical importance: Impaired glucose or oxygen supply can affect the pump, leading to neurological deficits. The body carefully regulates serum Na+ and K+ levels, and any disruption can cause severe neurological issues. Neurons and muscle cells can change their membrane potential in response to synaptic signals from a presynaptic cell. Neurotransmitters from the presynaptic terminal bind to receptors on the postsynaptic membrane, opening or closing ion-selective channels, altering the postsynaptic membrane potential. Postsynaptic potential changes can be either: More negative (hyperpolarization), leading to inhibitory postsynaptic potentials (IPSPs). More positive (depolarization), leading to excitatory postsynaptic potentials (EPSPs). EPSP (Excitatory Post-Synaptic Potential) occurs when the postsynaptic potential becomes more positive, increasing the likelihood of an action potential. Depolarization is caused by opening of Na+ channels, allowing Na+ to enter the cell and making the membrane potential more positive. IPSP (Inhibitory Post-Synaptic Potential) occurs when the membrane potential becomes more negative (hyperpolarized), reducing the likelihood of an action potential. Hyperpolarization occurs when K+ channels open, allowing K+ to exit the cell, making the membrane potential more negative. Postsynaptic potentials are transient, lasting only a few milliseconds, and diminish in magnitude as they spread away from the synapse. Chemical synaptic transmission involves ligand-gated ion channels, which respond to neurotransmitter binding to produce EPSPs or IPSPs.  Action potentials begin at the axon’s initial segment and propagate down the entire axon. EPSPs and IPSPs result from action potentials and synaptic transmissions, but decrease in magnitude as they spread along the postsynaptic membrane. Summation of EPSPs and IPSPs at the axon’s initial segment determines whether an action potential will be triggered. If enough EPSPs occur to reach the threshold potential, an action potential is generated, involving sequential opening of voltage-gated sodium (Na+) and potassium (K+) channels. The action potential involves a rapid depolarization (Na+ influx), followed by repolarization (K+ efflux), and can lead to brief hyperpolarization before returning to the resting state. Action potentials spread along the axon without decreasing in magnitude due to the opening of voltage-gated channels in adjacent membrane regions. Conduction velocity of the action potential depends on axon diameter and degree of myelination. Larger, more myelinated axons conduct faster. Saltatory conduction occurs in myelinated axons, where action potentials jump between the nodes of Ranvier, speeding up conduction. Diseases that attack myelin, like polyradiculoneuritis, slow down nerve conduction, but there is evidence that myelin may remodel with learning. Toxins and anesthetics, like tetrodotoxin and lidocaine, can block Na+ channels and interfere with action potential generation. Neurons communicate with other cells (e.g., muscle, secretory) via synaptic transmission. Synapses are specialized junctions where communication between cells occurs, which can be either electrical or chemical. In electrical synapses, ionic current flows directly between cells, while in chemical synapses, neurotransmitters mediate the communication. Chemical synaptic transmission involves neurotransmitter release from presynaptic terminals that bind to postsynaptic receptors, initiating changes like postsynaptic potentials. The neuromuscular junction (NMJ) is a specialized chemical synapse between a motor neuron and skeletal muscle fiber.  Motor neurons have their cell bodies in the CNS (spinal cord or brainstem), and their axons synapse with multiple muscle fibers. Each muscle fiber receives input from one motor neuron, allowing controlled contraction. The NMJ structure has three components: Presynaptic terminals (synaptic boutons) with vesicles storing acetylcholine (ACh), Synaptic cleft containing extracellular fluid and a basal lamina, Postsynaptic membrane with ACh receptors located in junctional folds. The release of acetylcholine from presynaptic terminals occurs at active zones, which align with ACh receptors on the postsynaptic membrane, ensuring efficient transmission. Transmission at the NMJ is one-way, from neuron to muscle, promoting muscle contraction. Evidence suggests molecules in muscle may influence the development and function of presynaptic motor neuron terminals during muscle growth. The neuromuscular junction transmits a chemical message unidirectionally from a motor neuron to a skeletal muscle cell, initiating muscle contraction. An action potential travels along the motor neuron axon to the presynaptic terminal, causing the release of acetylcholine (ACh). The arrival of the action potential opens voltage-gated Ca²⁺ channels, allowing Ca²⁺ to enter the presynaptic terminal, triggering ACh release. Synaptic vesicles containing ACh dock at the presynaptic membrane through a complex of proteins (SNARE complex), preparing for rapid ACh release. The protein synaptotagmin, acting as a Ca²⁺ sensor, binds Ca²⁺ and triggers vesicle fusion with the membrane, releasing ACh into the synaptic cleft. ACh binds to nicotinic acetylcholine receptors on the postsynaptic muscle membrane, opening ligand-gated ion channels. This leads to Na⁺ influx, depolarizing the muscle membrane and generating an end-plate potential (EPP), sufficient to initiate an action potential and muscle contraction. Acetylcholinesterase, located in the synaptic cleft, breaks down ACh into acetate and choline, terminating the signal. Choline is recycled back into the presynaptic terminal for ACh synthesis.  Chemicals like organophosphate insecticides and nerve gases can inhibit acetylcholinesterase, leading to prolonged ACh presence, causing harmful effects. There is a 1:1 ratio between neuronal and muscle action potentials, meaning each motor neuron action potential generates one muscle action potential. Neuron-to-neuron synaptic transmission involves greater variety than transmission at the neuromuscular junction. Acetylcholine is the primary neurotransmitter at the neuromuscular junction, while neuron-to- neuron synapses use a variety of neurotransmitters, including nontraditional ones like endocannabinoids and nitric oxide. Neuron-to-neuron synapses may not release neurotransmitters directly into the synaptic cleft, leading to a wider distribution of the transmitter. Some nontraditional neurotransmitters are produced postsynaptically and affect presynaptic terminals, indicating that neuron-to-neuron communication is not strictly one-way. The postsynaptic membrane of neuron-to-neuron synapses can include the soma, dendrites, or terminals, and may contain dendritic spines that increase surface area and support local protein synthesis. Dendritic spines can change shape and size, contributing to synaptic function, learning, and memory. Excitatory and inhibitory effects occur in neuron-to-neuron synapses, while neuromuscular junctions always produce excitatory responses. Neuron-to-neuron synapses have a wider variety of receptor types compared to the nicotinic acetylcholine receptors found at the neuromuscular junction. Neurotransmitter action termination at neuron-to-neuron synapses can involve transporter- mediated reuptake, enzymatic degradation, diffusion, or spontaneous decay. Summation of presynaptic inputs is required to generate a postsynaptic action potential in neuron-to-neuron synapses, unlike the neuromuscular junction where a single action potential is sufficient. In muscle cells, action potentials lead to contraction, which, combined with contractions of many muscle cells, results in body movement. 1. Neurons communicate with muscles and other cells through synapses, which are specialized junctions for rapid signal transfer.  2. Synaptic transmission can be either electrical (direct ionic current between cells) or chemical (release of neurotransmitters). 3. Electrical synapses are less common but present in the mammalian nervous system, with ionic currents flowing directly between cells. 4. Chemical synapses involve the release of neurotransmitters from the presynaptic terminal upon action potential arrival. 5. At the neuromuscular junction, the primary neurotransmitter is acetylcholine, responsible for triggering muscle contraction. 6. Motor neurons originate in the central nervous system (CNS), either in the spinal cord or the brainstem, and send signals to muscles through their axons. 7. Each motor neuron controls multiple muscle fibers, but each muscle fiber receives input from only one motor neuron. 8. The presynaptic terminal is comprised of multiple synaptic boutons, which are swollen, button-like endings packed with synaptic vesicles containing acetylcholine. 9. Synaptic vesicles are organized in rows near active zones on the presynaptic terminal, where they release acetylcholine into the synaptic cleft. 10. Mitochondria in the presynaptic terminal support the high energy demands of the cell, providing materials like acetyl-CoA and ATP for neurotransmitter synthesis and vesicle movement. 11. The synaptic cleft is a narrow gap (~50 nm wide) between the presynaptic terminal and the postsynaptic muscle membrane, filled with extracellular fluid and a basal lamina that helps in synaptic adhesion. 12. The postsynaptic membrane on the muscle fiber has junctional folds, which increase the surface area for acetylcholine receptors and align with the active zones of the presynaptic neuron. 13. Acetylcholine receptors are densely packed at the mouth of these junctional folds, ensuring efficient neurotransmission. 14. The region containing junctional folds and acetylcholine receptors is referred to as the motor end plate of the neuromuscular junction. 15. Transmission is one-way at the neuromuscular junction, going from neuron to muscle with no reverse signaling. 16. Synaptic transmission at the neuromuscular junction is designed to ensure muscle contraction upon neurotransmitter release. 17. In addition to acetylcholine, other molecules in the muscle may influence the survival and development of presynaptic motor neurons during development. 18. Acetylcholine release causes postsynaptic depolarization, leading to the generation of an action potential in the muscle fiber. 19. The neuromuscular junction is specialized for precise and rapid communication, crucial for muscle function related to movement and posture. 20. The efficiency of synaptic transmission at the neuromuscular junction is critical for coordinated muscle contraction, which allows for locomotion and other motor functions. These expanded points highlight additional anatomical, functional, and biochemical aspects of the neuromuscular junction and neuron-to-muscle communication.  The neuromuscular junction transmits a chemical signal unidirectionally from a motor neuron to a skeletal muscle cell. An action potential on the motor neuron triggers the release of acetylcholine (ACh), which binds to receptors on the muscle fiber. The action potential travels down the axon, opening voltage-gated Ca2+ channels at the presynaptic terminal. Ca2+ influx causes synaptic vesicles, primed at active zones, to release acetylcholine into the synaptic cleft. SNARE proteins and synaptotagmin (Ca2+ sensor) facilitate vesicle docking and fusion with the presynaptic membrane. After ACh release, vesicles are recycled, refilled with newly synthesized ACh for future neurotransmission. ACh binds to nicotinic acetylcholine receptors (ligand-gated ion channels) on the postsynaptic muscle membrane, causing Na+ to enter and depolarize the cell. The resulting end-plate potential is sufficient to open voltage-gated Na+ channels, triggering an action potential on the muscle cell, leading to contraction. Acetylcholinesterase, anchored to the synaptic cleft, rapidly breaks down ACh into acetate and choline, terminating its action. Choline is transported back into the presynaptic terminal for recycling into new ACh molecules. Inhibitors of acetylcholinesterase, like organophosphate insecticides or nerve gases, prevent ACh breakdown, leading to prolonged muscle activation and potential harmful effects. The action potential-to-contraction sequence is precisely regulated, ensuring a 1:1 ratio between neuronal and muscle action potentials. 1. Neuron-to-neuron synaptic transmission differs significantly from transmission at the neuromuscular junction. 2. Unlike the neuromuscular junction where acetylcholine is the primary neurotransmitter, neuron-to-neuron synapses use a variety of neurotransmitters, including non-traditional ones like endocannabinoids and nitric oxide. 3. Some neurotransmitters in neuron-to-neuron synapses are not released from distinct active zones, and may diffuse more widely across the synaptic cleft. 4. Neuron-to-neuron communication can be bidirectional, where molecules from the postsynaptic neuron affect the presynaptic terminal.  5. The postsynaptic membrane in neuron-to-neuron synapses can be on the soma, dendrites, or terminals, without junctional folds, but may have dendritic spines that increase surface area and play a role in learning and memory. 6. Synaptic transmission at neurons can produce excitatory or inhibitory effects, unlike the neuromuscular junction, which is always excitatory. 7. Neuron-to-neuron synapses have a wider variety of receptors, including G-protein coupled receptors, while the neuromuscular junction predominantly uses nicotinic acetylcholine receptors. 8. Termination of neurotransmitter action at neuron-to-neuron synapses involves reuptake or enzymatic degradation, which can be slower and less specific than at the neuromuscular junction. 9. A single action potential in a presynaptic neuron rarely generates a full action potential in the postsynaptic neuron; summation of inputs is typically required. 10. Muscle cell action potentials lead to contraction, and collective shortening of muscle fibers results in body movement. Body Movement: Caused by the contraction of skeletal muscles across movable joints. Muscles consist of a central muscle "belly" and two tendons that connect different bones, enabling joint movement. Muscle contraction shortens the distance between tendons, moving bones. Skeletal muscles contract by shortening; multiple muscles around joints control flexion (decreasing angle) or extension (increasing angle). Skeletal Muscle Structure: Muscles consist of muscle fibers, each containing nuclei, mitochondria, and other organelles. Muscle fibers range from 5 to 100 µm in diameter and are innervated by motor neurons at a neuromuscular junction. Muscle Fiber Components: Muscle fibers contain myofibrils arranged in parallel. Myofibrils consist of repeating sarcomeres, the basic contractile units. Sarcomeres contain actin (thin filaments) and myosin (thick filaments) responsible for contraction. The protein titin helps maintain alignment and elasticity in the sarcomere. Sarcomere Structure: Sarcomeres have Z disks at each end and contain actin, myosin, tropomyosin, and troponin. Actin and myosin filaments interact, with myosin heads forming cross-bridges to shorten the sarcomere during contraction.  Sarcoplasmic Reticulum and T Tubules: The sarcoplasmic reticulum surrounds myofibrils and stores calcium ions needed for muscle contraction. T tubules, invaginations of the sarcolemma, conduct action potentials deep into the muscle fiber, facilitating synchronized contractions. Action Potentials in Skeletal Muscle: Skeletal muscle cells have a resting membrane potential similar to neurons. At the neuromuscular junction, acetylcholine activates nicotinic receptors on the sarcolemma, causing an end-plate potential (EPP). The EPP opens voltage-gated sodium channels, triggering a muscle fiber action potential. Spread of Action Potential: The action potential spreads along the sarcolemma and into the interior of the muscle via transverse (T) tubules. This allows the action potential to reach the sarcoplasmic reticulum, essential for coupling excitation with muscle contraction. Excitation-Contraction Coupling: The action potential triggers the release of Ca²⁺ from the sarcoplasmic reticulum into the sarcoplasm, initiating contraction. Ca²⁺ is pumped back into the sarcoplasmic reticulum after the action potential passes, causing muscle relaxation. Mechanism of Ca²⁺ Release: Voltage-gated Ca²⁺ channels on the T tubules and Ca²⁺ release channels on the sarcoplasmic reticulum mediate Ca²⁺ release. Dihydropyridine (DHP) receptors (Ca²⁺ channels) on the T tubules mechanically couple with ryanodine receptors (Ca²⁺ release channels) on the sarcoplasmic reticulum to release Ca²⁺ into the sarcoplasm. Additional Factors: The release channels can also be opened by Ca²⁺ itself, a mechanism more relevant in cardiac muscle. Sarcomere Shortening: Actin slides along myosin, shortening the sarcomere when Ca²⁺ ions and ATP are available.  Myosin heads repetitively bind and pull the actin filaments in the presence of Ca²⁺, resulting in muscle contraction. When Ca²⁺ binds to troponin, it causes tropomyosin to move, exposing the myosin- binding sites on actin. Cross-Bridge Cycle: Myosin heads attach to actin, powered by ATP hydrolysis (ATP → ADP + phosphate). The heads extend and flex in a "cocked" state, producing the power stroke that moves actin filaments. Absence of Ca²⁺ causes myosin-binding sites on actin to be covered again, leading to sarcomere relaxation. Muscle Fiber Types: Fast-Twitch Fibers: Thicker, contract rapidly, have extensive sarcoplasmic reticulum, less blood and mitochondrial supply, fatigue quickly; suited for powerful, brief movements like sprinting and jumping. Slow-Twitch Fibers: Thinner, rich in blood, mitochondria, and myoglobin (red muscle); rely on oxidative metabolism, contract slower, fatigue less easily; adapted for sustained activities like antigravity muscle work. Intermediate Fibers: A subclass of fast-twitch fibers with properties between fast and slow fibers. Muscle Composition: Most muscles contain a blend of fast- and slow-twitch fibers, which can adapt with training. Muscle fibers exist along a continuum, not as distinct categories. 1. Motor Units: o A motor unit consists of one alpha motor neuron and all the muscle fibers it innervates. o Motor units have the same muscle fiber type (fast- or slow-twitch). o Small motor units have small neurons, innervate fewer slow-twitch fibers, and produce smaller forces. o Large motor units have large neurons, innervate more fast-twitch fibers, and produce greater forces. 2. Force Regulation: o Muscles increase strength by: § Multiple-fiber summation (spatial summation): Increasing the number of motor units activated. § Frequency summation (temporal summation): Increasing the frequency of motor unit activation, leading to smooth contraction. o Motor units are recruited in an orderly manner, starting with smaller units for precise control and increasing to larger units for greater force.  3. Tetanization: o High-frequency stimulation can fuse individual twitches into a smooth, sustained contraction (complete tetany). o Tetany is normal for skeletal muscle but would be fatal for cardiac muscle due to the need for relaxation for heart filling. 4. Electromyogram (EMG): o EMG measures the electrical activity of muscles during contraction using electrodes. o It helps diagnose muscle or nerve-related disorders by analyzing electrical signals, similar to how an ECG assesses heart function. 4o You said: more detail plz ChatGPT said: ChatGPT Here’s a more detailed summary of the information: 1. Motor Units and Their Role in Muscle Contraction Definition: A motor unit consists of one alpha (α) motor neuron and all the extrafusal (force-generating) muscle fibers it innervates. Muscle Fiber Types: o All fibers within a motor unit are of the same type (e.g., either fast-twitch or slow- twitch). o When an action potential is triggered in the motor neuron, all the muscle fibers within that motor unit contract simultaneously. Motor Unit Size and Function: o Small motor units have small neurons with narrow, slower-conducting axons and innervate fewer, slow-twitch muscle fibers. These produce smaller, less fatigable contractions. o Large motor units consist of larger neurons with faster-conducting, wider axons that innervate many fast-twitch muscle fibers. These produce stronger contractions but fatigue more quickly. 2. Mechanisms for Varying Muscle Contraction Strength Spatial Summation (Multiple-Fiber Summation): o The force of muscle contraction can be increased by activating more motor units at the same time.  o The CNS recruits additional motor units as needed, beginning with small motor units for fine, precise movements and progressively activating larger motor units for more forceful movements. Temporal Summation (Frequency Summation): o Muscle contraction force is also regulated by increasing the rate of activation of a motor unit. o If a second action potential occurs before the muscle has relaxed from the first, the two contractions summate, resulting in increased force. o At higher frequencies, individual twitches fuse into a smooth, sustained contraction (tetany), producing maximal force. 3. Orderly Recruitment of Motor Units The size principle governs motor unit recruitment, where smaller motor units (with slow- twitch fibers) are activated first for fine control, followed by larger motor units (with fast- twitch fibers) as greater force is needed. This orderly recruitment ensures smooth increases in muscle force, starting with small increments for fine motor tasks and leading to large increments when higher tension is required. 4. Tetanization and Its Importance Complete Tetany: o As the stimulation frequency increases, individual twitches merge into a smooth, continuous contraction without relaxation between twitches. This is known as complete tetany. o This is a normal and necessary mechanism for generating maximum force in skeletal muscle. Cardiac Muscle Exception: o Tetany in cardiac muscle would be fatal because the heart requires relaxation between contractions to allow blood to fill the chambers. Therefore, cardiac muscle has mechanisms to prevent tetany, which is discussed in greater detail in cardiac physiology. 5. Electromyogram (EMG) and Its Use What It Measures: o EMG records the electrical activity in a muscle as it contracts by detecting the electrical signals generated by action potentials in muscle fibers. o The electrical potential is measured either with electrodes placed on the skin or inserted into the muscle. Clinical Relevance: o The EMG is used clinically to assess muscle function and diagnose conditions that affect muscles or the nerves controlling them, similar to how an electrocardiogram (ECG) monitors heart function.  o It can help determine if muscle weakness or paralysis is caused by issues with skeletal muscle, neuromuscular junctions, motor neurons, or the central nervous system (CNS). Cardiac Muscle Structure and Function Similarities to Skeletal Muscle: o Cardiac muscle is striated and contains sarcoplasmic reticulum, myofibrils, and transverse tubules. o Actin and myosin form the fundamental contractile components. Differences from Skeletal Muscle: o Cardiac muscle cells are shorter and electrically coupled via gap junctions at intercalated disks. These allow direct transmission of action potentials between cells. o Cardiac cells can possess branching extensions and form interconnected networks with neighboring cells. o Action potentials arise spontaneously in specialized cardiac cells and spread across large areas of cardiac muscle, allowing coordinated contraction (as if the cells were a functional syncytium). o Autonomic nervous system influences heart rate and contraction force, but it is not necessary for action potential generation. 2. Smooth Muscle Structure and Function General Structure: o Smooth muscle cells are smaller and shorter than both cardiac and skeletal muscle cells. o Smooth muscle lacks T-tubules, and the sarcoplasmic reticulum is poorly developed. o Ca2+ ions diffuse from the extracellular fluid to trigger actin-myosin interactions, which drive contraction. Contractile Units: o Actin and myosin molecules form contractile units but are not arranged regularly, so smooth muscle lacks the striated appearance of cardiac and skeletal muscle. o Actin filaments are anchored to dense bodies instead of Z-disks, causing the muscle to wrinkle during contraction. 3. Types of Smooth Muscle Visceral (Unitary) Smooth Muscle: o Found in organs like the gastrointestinal tract, this type has gap junctions that allow cell-to-cell action potential transmission, acting like a functional syncytium similar to cardiac muscle. o Provides coordinated contraction of the muscle tissue. Multiunit Smooth Muscle: o Muscle cells are electrically isolated, contracting independently.  o Found in the iris and ciliary body of the eye, where precise control of contraction is necessary. 4. Smooth Muscle Innervation Autonomic Nervous System: o Smooth muscle is innervated by autonomic neurons, where either acetylcholine or norepinephrine can be released depending on the neuron type. o Smooth muscle can be either excited or inhibited by presynaptic input. Visceral Smooth Muscle: o Receives more diffuse innervation, with neurotransmitter release occurring farther from the muscle cells. o Surface cells can transmit activation to deeper layers through gap junctions. Multiunit Smooth Muscle: o Receives more direct synaptic input, with each cell having its own synaptic input and synaptic clefts similar to skeletal neuromuscular junctions. 5. Additional Control Mechanisms for Smooth Muscle Smooth muscle can also contract in response to self-induced electrical activity, hormones, or mechanical stretch. 1. General Role of Ca2+ in Muscle Contraction Contraction in cardiac, smooth, and skeletal muscle involves the sliding of actin and myosin filaments, requiring ATP and Ca2+ ions. The source of Ca2+ differs between muscle types. 2. Skeletal Muscle Excitation-Contraction Coupling Ca2+ is stored in the sarcoplasmic reticulum (SR). An action potential travels along the sarcolemma and T-tubules, triggering Ca2+ release from the SR. Contraction occurs through Ca2+ binding to proteins, enabling the sliding of filaments. Ca2+ is pumped back into the SR for muscle relaxation. Little to no extracellular Ca2+ influx is needed. 3. Cardiac Muscle Excitation-Contraction Coupling The SR is less developed in cardiac muscle compared to skeletal muscle. Extracellular Ca2+ influx through voltage-gated channels in the T-tubules and Ca2+ release from the SR both contribute to contraction. Ca2+-induced Ca2+ release: Extracellular Ca2+ triggers further Ca2+ release from the SR. Calcium channel blockers can reduce contraction force by limiting Ca2+ influx.  Relaxation occurs through Ca2+ being pumped back into the SR and into the extracellular space. 4. Smooth Muscle Excitation-Contraction Coupling Smooth muscle cells have poorly developed SR and no T-tubules. Contraction primarily depends on extracellular Ca2+ influx through voltage-gated channels located in caveolae (shallow membrane depressions). Relaxation occurs through the slow transport of Ca2+ back to the extracellular space. Calcium channel blockers relax smooth muscle by inhibiting Ca2+ influx, useful for lowering blood pressure. 5. Non-Depolarization Contraction in Smooth Muscle Some receptor-mediated contractions occur without membrane depolarization. Activation of G protein-coupled receptors can trigger Ca2+ release from the SR via the IP3-DAG pathway. 6. Ca2+-Induced Cross-Bridge Cycling Differences Skeletal and Cardiac Muscle: o Ca2+ binds to troponin, removing the tropomyosin block, allowing actin-myosin interaction for cross-bridge cycling. o Myosin head ATPase activity is naturally high, aiding efficient contraction. Smooth Muscle: o No troponin; contraction relies on Ca2+ increasing the ATPase activity of myosin. o Ca2+ binds to calmodulin, activating myosin light chain kinase, which phosphorylates the myosin head, allowing interaction with actin. o This process is slower compared to skeletal and cardiac muscle. Components of a Reflex Arc: 1. Sensory Receptor: o Transduces environmental energy (light, heat, pressure, etc.) or chemicals into a cellular response, creating action potentials in sensory neurons. o Example: Receptors in the retina transduce light, muscle spindles transduce stretch. 2. Sensory Neuron (Afferent): o Carries action potentials generated by the receptor to the CNS. o Sensory neurons either directly transduce stimuli (primary) or receive signals from non-neural receptors (secondary). 3. CNS Synapse: o Connects sensory input to motor output neurons. o Can be monosynaptic (one synapse, as in the muscle spindle reflex) or polysynaptic (involves interneurons).  4. Motor Neuron (Efferent): o Sends action potentials from the CNS to the target organ or effector, such as muscles or glands. 5. Target Organ (Effector): o Causes the reflex response, usually a muscle or gland. o Example: In the knee jerk reflex, the target is the quadriceps muscle. Additional Key Points: Reflexes often involve polysynaptic circuits, where more neurons are involved. Reflex responses often include inhibition of antagonistic muscles (e.g., inhibiting the hamstrings during the knee jerk reflex). Reflexes are modulated by other regions of the nervous system; damage to CNS input can exaggerate reflexes. 1. Segmental Reflex: o Reflex arc passes through a small portion of the CNS. o Sensory neuron, CNS circuitry, and motor neuron exit occur in the same region. o Examples: Knee jerk reflex, pupillary light reflex. 2. Intersegmental Reflex: o Reflex arc involves several spinal cord segments rostrally or caudally from the sensory input. o Example: Cutaneous trunci reflex (spinal signals travel from L5-L6 to T8-C1). 3. Suprasegmental Reflex: o Reflex arc involves both spinal cord and brain regions. o Example: Vestibulospinal reflexes (postural adjustments based on head movement). 4. Long-Loop Reflex (Suprasegmental Variation): o Reflex where sensory and motor neurons are in a similar location, but CNS circuitry travels to distant brain regions and back. o Example: Proprioceptive positioning reaction (paw placement after being flexed). Key Points: Reflex arcs are widespread and form a major part of neurological exams. Reflex testing (e.g., knee jerk, pupillary light) helps localize lesions. Malfunction in any reflex component alters or prevents the expected response. G-Protein G-Protein Activation: G-protein activation stimulates an enzyme or ion channel, causing changes in ion concentration or enzyme function.  Second Messengers: Second messengers are molecules or ions in the cytoplasm that transmit signals received from outside the cell (the first message). Examples of second messengers: Inositol trisphosphate (IP3), diacylglycerol (DAG), cyclic adenosine monophosphate (cAMP), and Ca2+. Signal Transduction: G-protein-linked signals are mostly transduced into the cytoplasm via second messengers. Limited Second-Messenger Systems: Despite numerous G-protein-coupled receptors (GPCRs), only a few second-messenger systems exist within cells. Cell-Specific Responses: Different cell types (e.g., smooth muscle vs. nerve cells) respond differently to the same second messenger due to their specialized protein makeup. Open Question: The mechanism of how cells sort out different signals from the same second messenger or similar receptors remains an ongoing question in physiology.