Which among the following is a feature of denervation of smooth muscle?
In excitable cells, repolarization is closely associated with one of the following events:
What is the primary reason for the unidirectional nature of neuronal synaptic conduction?
Post-tetanic potentiation is due to what?
Which of the following parameters decreases from its peak after the overshoot of an action potential?
Single-unit smooth muscles are seen in which of the following?
Golgi tendon organs are innervated by which type of nerve fibre?
Holstein-Lewis fracture is associated with injury to which nerve?
Which of the following statements is true regarding type 2b muscle fibers?
What is the physiological condition in which the ratio of potassium permeability to sodium permeability (PK/PNa) is maximized?
Explanation: ***Increased sensitivity to chemical mediators*** - Denervation of smooth muscle leads to **denervation supersensitivity**, meaning the muscle becomes more reactive to agonists due to an increase in receptor numbers or changes in post-receptor signaling pathways. - This increased sensitivity specifically applies to circulating or locally released chemical mediators, even at low concentrations. *Atrophy of the muscle.* - While denervation of **skeletal muscle** often leads to significant atrophy, **smooth muscle cells** are less prone to severe atrophy following denervation. - Smooth muscle tone is significantly influenced by both nervous and intrinsic myogenic activity, so loss of innervation alone does not typically cause complete incapacitation or severe atrophy. *No change in the number of receptors for neurotransmitters.* - Denervation often leads to an **increase in the number of receptors** on the smooth muscle cell surface, a phenomenon known as **upregulation**, contributing to denervation supersensitivity. - This adaptive change helps the muscle respond more strongly to any available neurotransmitters or circulating hormones. *Decreased neurotransmitter release At NMJ* - This option describes a potential cause of denervation (e.g., nerve damage leading to reduced release) rather than a feature of the denervated smooth muscle itself. - Denervation refers to the state where the nerve supply to the muscle is lost, not a change in neurotransmitter release from the now-absent nerve endings.
Explanation: ***K+ efflux*** - Repolarization in excitable cells is primarily caused by the **outward movement of potassium ions (K+)** through voltage-gated potassium channels. - This **efflux of positive charge** makes the inside of the cell more negative, returning the membrane potential to its resting state. *Na+ efflux* - **Na+ efflux** is primarily mediated by the **Na+/K+ ATPase pump**, which is crucial for maintaining the resting membrane potential but does not directly cause repolarization during an action potential. - The pump expels 3 Na+ ions for every 2 K+ ions taken in, slowly contributing to the negative resting membrane potential. *Na+ influx* - **Na+ influx** is responsible for the **depolarization phase** of an action potential, where the membrane potential becomes more positive. - This occurs when voltage-gated sodium channels open rapidly, allowing sodium ions to rush into the cell. *K+ influx* - **K+ influx** occurs during the **resting membrane potential** and is maintained by the Na+/K+ ATPase pump, which brings K+ ions back into the cell. - This influx helps to establish the potassium concentration gradient, which is critical for K+ efflux during repolarization.
Explanation: ***Chemical mediators are released from the presynaptic terminal.*** - **Neurotransmitters** are stored in vesicles within the **presynaptic terminal** and are released into the synaptic cleft only from this side. - The **postsynaptic membrane** contains specific receptors for these neurotransmitters, ensuring that the signal transmission occurs exclusively in one direction. *Dendrites can be depolarized and repolarized.* - While dendrites do undergo changes in potential, their primary role is to **receive signals**, not to initiate chemical transmission across a synapse in a backward direction. - This property alone does not explain the **unidirectional chemical synapse**, as it pertains to electrical excitability, not the chemical release mechanism. *An area can be depolarized again after repolarization.* - This statement describes the **refractory period** and the ability of a neuron to fire subsequent action potentials, which is crucial for signal propagation along an axon, but not the unidirectional nature of a **synapse**. - It does not explain why a signal cannot cross the synapse from the postsynaptic to the presynaptic neuron. *Antidromic impulses are less effective than orthodromic impulses.* - An **antidromic impulse** is one traveling in the "wrong" direction along an axon, opposite to the normal physiological direction. - While they are indeed less effective or non-physiological, this refers to **axon conduction**, not the reason for unidirectional transmission at the **synaptic cleft**.
Explanation: ***Increased availability of Ca++*** - **Post-tetanic potentiation (PTP)** is a short-term enhancement of synaptic efficacy that occurs after a brief period of high-frequency stimulation (tetanus). - This phenomenon is primarily due to the **accumulation of residual intracellular calcium ions (Ca++)** in the presynaptic terminal, which leads to increased neurotransmitter release upon subsequent action potentials. *Hyperpolarization of muscle fibers* - **Hyperpolarization** makes the muscle fiber less excitable, thereby *reducing* its response to subsequent stimuli rather than enhancing it. - This effect would decrease muscle contractility, which is opposite to what is observed in PTP. *Rapid K+ efflux* - **Rapid K+ efflux** from a cell typically causes repolarization or hyperpolarization, which would decrease neuronal excitability and thus *reduce* neurotransmitter release. - This process is essential for repolarizing the neuron after an action potential but does not directly cause PTP. *Rapid Na+ influx* - **Rapid Na+ influx** is responsible for the depolarization phase of an action potential, triggering nerve impulse propagation. - While essential for neural activity, it doesn't directly explain the *potentiation* or enhanced neurotransmitter release following tetanic stimulation, which is primarily calcium-dependent.
Explanation: ***Membrane conductance for sodium*** - During the **peak and overshoot phase** of an action potential, voltage-gated sodium channels are maximally open, resulting in **peak sodium conductance**. - **After the overshoot**, these sodium channels rapidly undergo **inactivation**, leading to a sharp decrease in **sodium conductance**. - This decrease in sodium conductance is essential for terminating sodium influx and initiating the **repolarization phase** of the action potential. *Membrane conductance for potassium* - **Potassium conductance** actually *increases* after the overshoot as **voltage-gated potassium channels** open in response to depolarization. - This increased **potassium conductance** facilitates potassium efflux, which drives membrane repolarization back toward the resting potential. *Transference for sodium* - **Transference** refers to the fraction of total current carried by a specific ion, a concept more relevant to solutions and ionic equilibria. - While sodium's contribution to membrane current decreases as channels inactivate, the primary physiological parameter is **membrane conductance**, which directly reflects channel activity. *Transference for potassium* - **Potassium transference** (or its contribution to current) would increase as potassium channels open after the overshoot. - The most physiologically precise parameter for describing rapid ion channel dynamics during action potentials is **membrane conductance**, not transference.
Explanation: ***Ureter*** - The ureter contains **single-unit smooth muscle** which exhibits spontaneous electrical activity and contraction, allowing for peristaltic movement of urine. - In single-unit smooth muscle, cells are connected by **gap junctions**, enabling them to contract as a coordinated unit. *Iris* - The iris contains **multi-unit smooth muscle**, which allows for fine, independent control of each muscle cell for precise pupil dilation and constriction. - Multi-unit smooth muscle cells are not connected by gap junctions and require individual neural stimulation. *Ductus deferens* - The ductus deferens primarily consists of **multi-unit smooth muscle**, which is necessary for the strong, rapid contractions required for sperm expulsion during ejaculation. - This type of muscle allows for graded contractions depending on the intensity of nervous stimulation. *Trachea* - The smooth muscle in the trachea (trachealis muscle) is primarily **multi-unit smooth muscle**, facilitating independent regulation of airway diameter. - Contraction of the trachealis muscle can reduce the tracheal lumen, aiding in coughing or regulating airflow.
Explanation: ***Ib*** - **Golgi tendon organs (GTOs)** are encapsulated sensory receptors located in the musculoskeletal junction that monitor **muscle tension**. - They are innervated by **Ib afferent nerve fibers**, which are large diameter, myelinated nerve fibers with a high conduction velocity that transmit information to the central nervous system. *Ia* - **Ia afferent nerve fibers** innervate **muscle spindles**, which detect changes in **muscle length** and the rate of change of muscle length. - While both Ib and Ia fibers are involved in proprioception, their specific sensory receptors and functions differ. *II* - **Type II afferent nerve fibers** also innervate **muscle spindles**, primarily sensing sustained changes in **muscle length** (static stretch). - They do not innervate Golgi tendon organs; their role is distinct in providing information about muscle position. *III* - **Type III afferent nerve fibers** are smaller, thinly myelinated fibers that respond mainly to **nociceptive (pain)** and **temperature stimuli** in muscles and joints. - They are not involved in sensing muscle tension or length and do not innervate Golgi tendon organs.
Explanation: ***Radial*** - Holstein's Lewis fracture is a specific fracture of the **distal humeral shaft** that characteristically entraps the **radial nerve**. - Injury to the radial nerve in this region typically results in **wrist drop** and sensory loss over the dorsal hand. *Median* - The median nerve is most commonly entrapped in the **carpal tunnel**, leading to carpal tunnel syndrome. - Injury to the median nerve affects the **flexors of the forearm** and sensation in the first 3.5 digits. *Ulnar* - The ulnar nerve is often injured at the **cubital tunnel** (elbow) or Guyon's canal (wrist). - Its injury leads to a characteristic **claw hand deformity** and sensory loss in the little finger and ulnar half of the ring finger. *Axillary* - The axillary nerve is most susceptible to injury during **shoulder dislocations** or fractures of the surgical neck of the humerus. - Damage to this nerve causes weakness in **shoulder abduction** (due to deltoid paralysis) and sensory loss over the lateral shoulder.
Explanation: ***White, glycolytic, fast contracting*** - **Type 2b muscle fibers** (also known as fast glycolytic fibers) are characterized by their **fast contraction speed** and high capacity for **anaerobic glycolysis**. - They appear **white** due to a lower myoglobin content and fewer mitochondria, relying on glycolytic metabolism for quick, powerful bursts of activity. - These are the classic fast-twitch white muscle fibers optimized for explosive power. *White, glycolytic, slow contracting* - While **Type 2b fibers** are indeed **white** and **glycolytic**, this option inaccurately describes them as **slow contracting**. - Their primary characteristic is their **fast contraction speed**, which allows for rapid, forceful movements. *Red, oxidative, fast contracting* - This describes **Type 2a fibers** (fast oxidative-glycolytic), not Type 2b fibers. - **Type 2b fibers** are predominantly **white** and **glycolytic**, not red and oxidative. - Type 2b fibers have lower myoglobin content and fewer mitochondria compared to Type 2a. *Red, glycolytic, slow contracting* - **Red, oxidative, slow contracting** fibers refer to **Type 1 (slow-twitch) fibers**, optimized for endurance. - This option incorrectly combines characteristics from different fiber types. - Type 2b fibers are neither red nor slow contracting.
Explanation: ***Hyperpolarization*** - During **hyperpolarization**, the membrane potential becomes more negative than the **resting membrane potential**, primarily due to the outflow of **potassium (K+)** ions or influx of **chloride (Cl-)** ions. - This increased K+ efflux or Cl- influx signifies a state where potassium permeability is maximal relative to sodium permeability, making the membrane less excitable. *Action Potential* - An **action potential** involves a rapid **depolarization** phase due to a massive influx of **sodium (Na+)** ions, causing the PNa/PK ratio to be high, followed by repolarization where K+ efflux restores the resting potential. - Therefore, during an action potential, the ratio of PK/PNa is at its lowest during the rising phase when sodium channels are open. *Depolarization* - **Depolarization** is characterized by a decrease in the absolute value of the membrane potential, making it less negative or even positive, primarily due to the influx of **sodium (Na+)** ions. - During depolarization, the permeability to sodium is significantly higher than to potassium, thus the PK/PNa ratio is low. *Resting Membrane Potential* - At **resting membrane potential**, potassium permeability is already much higher than sodium permeability due to **leak potassium channels**, but it is not maximized to the extent seen during hyperpolarization. - The resting potential is established by a balance of ion movements, primarily K+ efflux and limited Na+ influx, maintained by the **Na+/K+-ATPase pump**.
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