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NERVE MUSCLE PHYSIOLOGY
1. THE NEURON : STIMULUS AND EXCITIBILTY
1.Neuron Structure and Function Neurons are the functional units of the nervous system. They are specialized cells responsible for transmitting electrical signals throughout the body. Basic Structure: A neuron consists of three main parts: Cell Body (Soma): Contains the nucleus and organelles. Dendrites: Short, branching processes that receive signals from other neurons. Axon: A long, thin process that transmits electrical impulses (action potentials) away from the cell body to other neurons, muscles, or glands. The axon may be myelinated (covered with myelin sheath) or unmyelinated. Myelination increases the speed of signal transmission.
2. Resting Membrane Potential Neurons, like all cells, have a resting membrane potential (RMP) due to the distribution of ions across the cell membrane. The RMP of a neuron is typically around -70 mV. This is mainly due to the differential concentrations of ions like sodium (Na⁺), potassium (K⁺), chloride (Cl⁻), and other ions, maintained by active transport mechanisms like the Na⁺/K⁺ pump.
The cell membrane is more permeable to potassium ions, leading to a negative interior relative to the exterior.
3. Action Potential An action potential (AP) is a rapid, temporary reversal of the membrane potential, which is essential for nerve impulse transmission. The AP is initiated when the neuron receives a sufficiently strong stimulus that causes depolarization (a reduction in the negative charge inside the cell). Phases of Action Potential: Resting State: The neuron is at rest with a membrane potential of -70 mV. Voltage-gated Na⁺ and K⁺ channels are closed. Depolarization: When the neuron receives a stimulus that reaches the threshold potential (usually around -55 mV), voltage-gated Na⁺ channels open, allowing Na⁺ ions to rush into the cell. This makes the inside of the cell more positive. Repolarization: After a brief period, Na⁺ channels close, and voltage-gated K⁺ channels open. K⁺ ions flow out of the cell, restoring the negative charge inside the cell. Hyperpolarization: The K⁺ channels may remain open longer than needed, causing the membrane potential to drop below the resting potential. Return to Resting State: The Na⁺/K⁺ pump restores the ion concentrations to their resting levels, and the neuron returns to its resting membrane potential. 4. Refractory Period The refractory period is the time following an action potential when the neuron is less excitable or unable to fire another action potential.
to greater synaptic transmission and muscle contraction (in the case of motor neurons).
7. Synaptic Transmission Neurons communicate with each other at synapses, which are junctions between the axon terminal of one neuron and the dendrites (or cell body) of another. Chemical Synapses: When an action potential reaches the presynaptic terminal, it triggers the release of neurotransmitters into the synaptic cleft. These neurotransmitters bind to receptors on the postsynaptic membrane, which can either depolarize (excitatory) or hyperpolarize (inhibitory) the postsynaptic neuron. Electrical Synapses: Less common, but they involve direct electrical communication between neurons through gap junctions, allowing for faster transmission. 8. Factors Affecting Excitability Several factors influence the excitability of neurons: Ion concentrations: Changes in the concentration of extracellular ions, such as Na⁺, K⁺, or Ca²⁺, can alter the resting membrane potential and the ability of the neuron to generate action potentials. Temperature: Higher temperatures generally increase the rate of ion channel opening, speeding up the action potential. Drugs and toxins: Some substances can enhance or block the function of ion channels, affecting neuronal excitability. 9. Role of Neurons in the Nervous System Neurons are involved in numerous functions including sensation, movement, cognition, and autonomic regulation.
The ability of neurons to respond to stimuli and transmit signals is essential for all higher-order processes, including sensory perception, motor control, and cognition. Summary The chapter focuses on the properties of neurons related to their ability to respond to stimuli, including the mechanisms of action potentials, their propagation along axons, and synaptic transmission. It also discusses the factors that influence neuronal excitability, such as ion gradients, ion channel function, and external factors like drugs or temperature. The neuron’s excitability is fundamental to the nervous system’s role in communication, processing information, and initiating physiological responses.
- **ACTION POTENTIAL OF NERVE
- Basic Properties of Neurons** Neurons, as the primary cells of the nervous system, transmit electrical impulses that facilitate communication throughout the body. The action potential is a key concept in neuronal function and is responsible for the rapid transmission of signals along nerve fibers. The chapter explains how neurons are capable of generating electrical impulses due to their excitability—a property that allows them to respond to stimuli. 2. Resting Membrane Potential Neurons maintain a resting membrane potential (RMP), typically around -70 mV in humans, which is the difference in electrical charge across the cell membrane at rest. The RMP is created by the unequal distribution of ions, especially sodium (Na⁺), potassium (K⁺),
potential will be initiated, and its magnitude will always be the same regardless of the strength of the stimulus (as long as the stimulus reaches threshold). The action potential does not vary in amplitude based on the strength of the stimulus; however, the frequency of action potentials can convey information about the intensity of a stimulus (e.g., more intense stimuli produce higher frequencies of action potentials).
5. Refractory Period The refractory period is the time during and immediately after an action potential when the neuron is less excitable and cannot generate another action potential. It is divided into: Absolute Refractory Period: During this phase, no new action potential can be generated, regardless of the strength of the stimulus. This is due to the inactivation of sodium channels. Relative Refractory Period: A new action potential can only be generated if a stronger-than- normal stimulus is applied. This occurs because the membrane potential is still in the process of returning to its resting state. 6. Conduction of Action Potentials The action potential propagates along the length of the axon from the axon hillock to the axon terminal. In myelinated fibers, the action potential travels faster through saltatory conduction, where the electrical impulse "jumps" from one node of Ranvier (gaps in the myelin sheath) to the next, dramatically speeding up the conduction velocity. In unmyelinated fibers, the action potential travels more slowly in a continuous wave along the membrane.
The axon diameter also affects conduction velocity: larger axons conduct impulses faster because they offer less resistance to ion flow.
7. Factors Affecting Nerve Conduction Myelination: The presence of myelin speeds up nerve conduction by preventing ion leakage and allowing the action potential to jump between nodes. Axon Diameter: Larger-diameter axons conduct signals faster due to reduced internal resistance to current flow. Temperature : Higher temperatures increase the rate of ion channel opening and increase conduction velocity. Conversely, lower temperatures slow down nerve conduction. Ion Concentrations: Changes in the concentrations of extracellular ions, especially Na⁺, K⁺, and Ca²⁺, can affect the resting membrane potential and the ability of the neuron to generate action potentials. Drugs and Toxins: Certain substances, like local anesthetics, can block sodium channels, inhibiting the initiation or propagation of action potentials. Other substances, such as tetrodotoxin, can block sodium channels as well, leading to paralysis or death. 8. Propagation of Nerve Impulses When a depolarizing current spreads along the axon, it causes adjacent areas of the membrane to reach threshold and initiate their own action potentials. Bidirectional Propagation: In myelinated fibers, the action potential propagates in one direction from the axon hillock to the axon terminal, where neurotransmitter release occurs. This unidirectional propagation is ensured by the refractory period that prevents backward propagation.
efflux. The propagation of the nerve impulse refers to the movement of the action potential along the length of the axon, away from its point of initiation, and toward the axon terminal where it can trigger neurotransmitter release. The propagation process relies on the local currents that spread depolarization from one segment of the axon to the next, triggering the opening of sodium channels along the way.
2. Mechanisms of Action Potential Propagation Depolarization of the Membrane : The initial depolarization (when the membrane potential reaches threshold) causes sodium channels to open, allowing Na⁺ to flood into the axon. This depolarizes the local area. Local Current Flow : Once a region of the axon depolarizes, it creates a local current that spreads the depolarization to adjacent areas. This current causes the opening of sodium channels in the neighboring segments of the axon, thus propagating the action potential in a wave-like fashion. Sequential Depolarization and Repolarization: As one segment of the axon depolarizes and the next segment reaches its threshold, it generates a new action potential. Simultaneously, the previous segment is undergoing repolarization (where potassium ions move out of the cell), which restores the resting membrane potential and prepares that segment for the next impulse. 3. Direction of Propagation The action potential typically propagates in one direction, from the axon hillock to the axon terminals. This is because the segment of the axon behind the depolarizing front is in the refractory period (specifically the absolute refractory period), preventing the action potential
from moving backward. The unidirectional flow of the nerve impulse ensures that the signal moves toward its target, whether that be another neuron, muscle cell, or gland.
4. Conduction Velocity The speed at which an action potential travels down an axon is known as conduction velocity, and it varies depending on several factors: Axon Diameter: Larger-diameter axons have faster conduction speeds because they have less internal resistance to the flow of ions. Myelination: Myelinated axons conduct impulses much faster than unmyelinated axons. Myelin acts as an insulator, preventing ion leakage and allowing the action potential to jump between nodes of Ranvier (the small gaps in the myelin sheath). This process is known as saltatory conduction. Temperature: Higher temperatures generally increase conduction velocity by speeding up the opening and closing of ion channels. 5. Myelination and Saltatory Conduction Myelinated Axons: In myelinated neurons, the myelin sheath prevents depolarization of the axonal membrane in the internodal regions (the areas between nodes). Instead, action potentials "jump" from one node to the next, a process called saltatory conduction. This significantly increases conduction velocity. The nodes of Ranvier contain a high density of voltage-gated sodium and potassium channels that allow for the rapid depolarization and repolarization of the membrane at these specific points.
difficult or impossible to generate another action potential. There are two phases: Absolute Refractory Period: This occurs during depolarization and repolarization, when the sodium channels are either open or inactivated, and no new action potential can be initiated, regardless of the strength of the stimulus. Relative Refractory Period: This occurs during the later stages of repolarization. During this phase, a stronger-than-normal stimulus can potentially trigger a new action potential because some sodium channels have returned to a resting state.
8. Synaptic Transmission and Nerve Impulse The propagation of nerve impulses is critical for communication between neurons at synapses. When an action potential reaches the axon terminal, it triggers the release of neurotransmitters into the synaptic cleft, allowing for communication with a neighboring neuron or effector cell (e.g., muscle). The speed of synaptic transmission also depends on the properties of the neuron, such as whether it is myelinated and the overall conduction velocity of the action potential. 9. Nerve Impulse in Disease States Multiple Sclerosis (MS): In MS, the immune system attacks the myelin sheath, impairing saltatory conduction. This leads to slowed or blocked nerve impulse transmission, resulting in neurological deficits such as weakness, numbness, and vision problems. Guillain-Barré Syndrome: This is a condition where peripheral nerves are affected, leading to demyelination. As a result, nerve conduction velocity decreases, and motor function may be impaired. Hyperkalemia: Elevated levels of potassium in the blood can reduce the membrane potential,
4.PERIPHERAL NERVE DAMAGE making neurons more excitable and potentially leading to arrhythmias or seizures.
1. Overview of Peripheral Nervous System (PNS) The peripheral nervous system consists of all the nerves and ganglia outside the brain and spinal cord, connecting the central nervous system (CNS) to limbs, organs, and tissues. Motor nerves control muscle movements, and sensory nerves transmit sensations like touch, pain, and temperature from the body to the CNS. 2. Types of Nerve Damage Axonotmesis: Injury to the axon (nerve fiber) while the surrounding connective tissue (like the myelin sheath and endoneurium) remains intact. This often occurs due to crush injuries. Axons can regenerate, but the process is slow. Neurotmesis : Complete severance or disruption of both the axon and the surrounding connective tissues. This results in a permanent loss of function if not surgically repaired. Neuropraxia: A temporary block of nerve conduction with no physical damage to the nerve. This typically happens due to compression (e.g., pressure on a nerve) and can recover fully over time without lasting damage. 3. Causes of Peripheral Nerve Damage Trauma: Physical injuries like cuts, fractures, or crush injuries that disrupt the nerve fibers. Compression: Pressure on nerves, for example, from herniated discs, tumors, or prolonged postures. Diseases: Diseases such as diabetes, multiple sclerosis, or neuropathies can cause nerve degeneration. Inflammatory Conditions: Infections or autoimmune diseases (like Guillain-Barré Syndrome) can
muscle weakness caused by nerve damage. Nerve Conduction Studies: Evaluate the speed of nerve impulses and help to determine the site and extent of nerve damage. Imaging: Techniques like MRI or CT scans can be used to assess structural damage, such as compression or trauma to the nerve.
7. Treatment and Management Surgical Intervention: In cases of complete nerve severance (neurotmesis), surgical repair may be required to restore continuity of the nerve fibers. Physical Therapy: Essential for promoting muscle function and preventing atrophy after nerve injury. Medications: Pain management with analgesics, and sometimes medications like gabapentin for neuropathic pain. Nerve Growth Factors: Research into therapies that stimulate nerve regeneration (such as neurotrophic factors) is ongoing. 8. Prognosis of Nerve Regeneration The prognosis of peripheral nerve damage depends on the severity and type of injury: Axonotmesis often has a better prognosis than neurotmesis. Wallerian degeneration can be reversed if the nerve is capable of regenerating and the injury is not too extensive. Regeneration is often slower and less complete in older individuals or in cases with significant scarring or disruption of the nerve. 9. Special Considerations
Diabetic Neuropathy: Chronic high blood sugar can lead to damage of peripheral nerves, often affecting the legs and feet, leading to sensory loss and potential ulcers or infections. Guillain-Barré Syndrome: An autoimmune disorder that causes acute inflammatory polyneuropathy, often resulting in rapid motor weakness and sensory loss, but with potential for recovery. Charcot-Marie-Tooth Disease: A hereditary disorder that affects peripheral nerves, often resulting in progressive motor and sensory loss.
10. Summary Peripheral nerve damage can result from trauma, diseases, toxins, or compression. The recovery of function largely depends on the type and extent of nerve injury. Axonal regeneration is possible but typically slow and may not result in complete recovery, especially after more severe injuries. Diagnosis involves a combination of clinical evaluation, electrophysiologic studies, and imaging techniques, and management often requires a multidisciplinary approach including surgery, rehabilitation, and pain management. **5.NEUROMUSCULAR JUNCTION
- Overview of Neuromuscular Transmission** Neuromuscular transmission is the process by which an action potential (electrical signal) in a motor neuron leads to muscle contraction. The motor neuron communicates with the muscle fiber at the neuromuscular junction (NMJ), a specialized synapse.
fiber membrane. This binding opens ion channels, allowing sodium ions (Na⁺) to enter the muscle fiber and potassium ions (K⁺) to exit. The influx of sodium causes depolarization of the muscle membrane, generating an end-plate potential (EPP). 3.4 Generation of Action Potential in the Muscle Fiber If the end-plate potential reaches the threshold, it triggers an action potential in the muscle fiber, which propagates along the sarcolemma (muscle cell membrane). The action potential spreads into the muscle fiber through the T-tubules (transverse tubules), which are extensions of the sarcolemma. 3.5 Excitation-Contraction Coupling The muscle action potential travels into the T-tubules and reaches the sarcoplasmic reticulum (SR), which stores calcium ions. The SR releases calcium into the cytoplasm of the muscle fiber, where it binds to troponin, causing a conformational change that moves tropomyosin, exposing the actin binding sites for myosin. This allows cross-bridge cycling and muscle contraction to occur. 3.6 Termination of the Signal Acetylcholine’s action is terminated by the enzyme acetylcholinesterase, which breaks down acetylcholine into acetate and choline. The breakdown products are taken back into the presynaptic terminal, and acetylcholine is re- synthesized from choline.
Calcium ions are actively pumped back into the SR, causing muscle relaxation.
4. Factors Affecting Neuromuscular Transmission 4.1 Neuromuscular Blockers Drugs that interfere with neuromuscular transmission can cause paralysis. These include: Non-depolarizing blockers (e.g., curare), which prevent acetylcholine from binding to its receptor, thus blocking muscle contraction. Depolarizing blockers (e.g., succinylcholine), which bind to the acetylcholine receptor and depolarize the muscle fiber, causing a prolonged inactivation of the sodium channels, preventing repolarization and further action potential generation. 4.2 Myasthenia Gravis Myasthenia gravis is an autoimmune disease where antibodies attack and block the nicotinic acetylcholine receptors at the neuromuscular junction, reducing the number of functional receptors. This leads to muscle weakness, particularly in skeletal muscles that control voluntary movement. Treatment involves acetylcholinesterase inhibitors (e.g., pyridostigmine) to increase acetylcholine levels at the NMJ. 4.3 Botulinum Toxin Botulinum toxin (produced by Clostridium botulinum) prevents the release of acetylcholine from the presynaptic terminal, leading to paralysis. This toxin is used clinically in small doses to treat conditions like muscle spasms or to reduce wrinkles. 4.4 Toxins and Chemical Exposure
