Unit 3: Nervous System Communication, Autonomic Pathways, and Muscle Physiology

Comprehensive review flashcards for General Human Physiology (Biology 206) Unit 3, covering Chapter 9 (Neuron Function and Communication), Chapter 12 (Autonomic and Somatic Motor Pathways), and Chapter 13 (Muscular System Activation and the Sliding Filament Theory).

What are the primary functional regions of a typical neuron, and what role does each play?

Dendrites receive incoming chemical signals; the axon hillock acts as the integrating center and trigger zone to evaluate signals; the axon propagates electrical action potentials; and the axon terminals release neurocrine signal molecules across synapses.

What are the specific functions of the four types of glial cells found in the central nervous system (CNS)?

Astrocytes support the blood-brain barrier, take up $K^+$, water, and neurotransmitters, secrete neurotrophic factors, and provide substrates for ATP production; microglia act as immune scavengers; ependymal cells line ventricles and secrete cerebrospinal fluid (CSF); and oligodendrocytes form myelin sheaths around CNS axons.

What are the two types of glial cells in the peripheral nervous system (PNS), and what do they do?

Schwann cells (neurolemmocytes) form myelin sheaths around PNS axons and provide metabolic support; satellite cells surround and protect neuron cell bodies located within autonomic ganglia.

What is the typical resting membrane potential of a neuron, and how is it established?

It is typically approximately $-70\text{ mV}$, established by the normal concentration disequilibrium and differential membrane permeability of $K^+$, $Na^+$, $Ca^{2+}$, and $Cl^-$.

How do excitatory post-synaptic potentials (EPSPs) differ from inhibitory post-synaptic potentials (IPSPs)?

An EPSP is a graded depolarization of the dendrites or cell body (typically caused by $Na^+$ influx) that moves the neuron toward threshold, whereas an IPSP is a graded hyperpolarization (typically caused by $K^+$ efflux or $Cl^-$ influx) that moves it away from threshold.

What threshold voltage must graded potentials achieve at the axon hillock trigger zone to initiate an action potential?

The integrated membrane potential must reach approximately $-55\text{ mV}$.

What is the difference between spatial summation and temporal summation in postsynaptic neurons?

Spatial summation occurs when graded potentials originating simultaneously from multiple physical locations across the cell body and dendrites combine; temporal summation occurs when multiple graded potentials arrive from the same presynaptic input in rapid succession before previous potentials have dissipated.

Based on the action potential diagram shown, what occurs at step 4 and step 5?

At step 4, rapid $Na^+$ entry through open voltage-gated $Na^+$ channels depolarizes the cell; at step 5, voltage-gated $Na^+$ channels close (inactivate) and slower voltage-gated $K^+$ channels fully open, halting depolarization near $+30\text{ mV}$.

How do the absolute and relative refractory periods differ during an action potential?

During the absolute refractory period, voltage-gated $Na^+$ channels are inactivated and cannot be reopened, preventing any second action potential; during the relative refractory period, $Na^+$ channels have reset to their closed resting state, but an action potential requires a stronger-than-normal stimulus (greater than $+15\text{ mV}$) because the cell is hyperpolarized by lingering open $K^+$ channels.

What allows saltatory conduction along myelinated axons to be faster and more energy-efficient than continuous propagation along unmyelinated axons?

Myelin provides electrical insulation that prevents current leakage through the axolemma, allowing depolarization to spread rapidly under insulated internodes and regenerate action potentials exclusively at the Nodes of Ranvier where voltage-gated channels are concentrated.

What sequence of events triggers neurotransmitter exocytosis when an action potential reaches the presynaptic axon terminal?

Depolarization arrives at the axon terminal, opening voltage-gated $Ca^{2+}$ channels; the resulting influx of $Ca^{2+}$ binds regulatory proteins to trigger exocytosis of synaptic vesicles containing neurotransmitter into the synaptic cleft.

What three mechanisms terminate neurotransmitter activity at a chemical synapse?

(1) Reuptake into the presynaptic terminal or uptake by surrounding glial cells; (2) enzymatic inactivation/destruction within the synaptic cleft; and (3) passive diffusion away from the synaptic cleft into the extracellular fluid or bloodstream.

How do nicotinic and muscarinic cholinergic receptors differ in their molecular structure and action?

Nicotinic receptors ($N_M$ and $N_N$) are chemically-gated monovalent cation channels permeable to $Na^+$ and $K^+$ that always cause net depolarization (excitatory); muscarinic receptors ($M_1$ through $M_5$) are G-protein coupled receptors (GPCRs) that can be either excitatory or inhibitory depending on their intracellular signaling cascade.

Which three major catecholamines are synthesized from the amino acid tyrosine?

Dopamine, norepinephrine, and epinephrine.

According to the autonomic reflex integrating centers diagram, what are the primary regulatory functions of the hypothalamus, medulla oblongata, and pons?

The hypothalamus controls temperature, water balance (osmolarity), hunger/appetite, and sex drive; the medulla oblongata controls cardiovascular function (heart rate and vessel diameter), baseline ventilation, swallowing, and vomiting; and the pons modulates ventilation rate and regulates urinary bladder control (the micturition reflex).

What is the structural two-neuron arrangement of autonomic efferent pathways?

A preganglionic neuron originates in the CNS and synapses inside an autonomic ganglion onto a postganglionic neuron, which extends to innervate target effectors.

What neurotransmitters and receptors are used at the autonomic ganglia versus target tissues in sympathetic and parasympathetic pathways?

Both branches release acetylcholine (ACh) onto $N_N$ nicotinic receptors at the autonomic ganglia; at target tissues, parasympathetic postganglionic neurons release ACh onto muscarinic receptors, while sympathetic postganglionic neurons release norepinephrine (NE) onto adrenergic ($\alpha$ or $\beta$) receptors.

What specialized cells in the adrenal medulla act as modified postganglionic sympathetic neurons to release epinephrine directly into the blood?

Chromaffin cells, which are axonless modified postganglionic sympathetic neurons that secrete epinephrine directly into the bloodstream as a neurohormone upon stimulation by preganglionic sympathetic neurons.

How do autonomic varicosities differ functionally from traditional axon terminals?

Varicosities are a series of swollen swellings along postganglionic autonomic axons that release neurotransmitters diffusely over large areas of smooth muscle or glandular effector cells, rather than across a single, discrete synapse.

How does sympathetic stimulation affect heart rate, airway diameter, pupil diameter, and digestion?

Sympathetic activity increases heart rate and contraction force, dilates bronchioles (airways), dilates pupils, and inhibits gastrointestinal motility, enzyme secretion, and insulin release.

What enzyme inactivates norepinephrine inside sympathetic varicosities following reuptake?

Monoamine oxidase (MAO), which breaks down cytosolic norepinephrine inside mitochondria.

How does the somatic motor efferent pathway differ anatomically and functionally from autonomic pathways?

The somatic motor pathway consists of a single myelinated motor neuron originating in the CNS that directly innervates skeletal muscle cells; it releases acetylcholine onto $N_M$ nicotinic receptors at the neuromuscular junction and is always excitatory.

In the somatic motor pathway and neuromuscular junction (NMJ) shown, what receptor type is located on the folded motor end plate, and what ion movement results from its activation?

Nicotinic cholinergic receptors ($N_M$), which are chemically-gated monovalent cation channels; binding of two ACh molecules opens the channel, allowing net $Na^+$ influx (greater than $K^+$ efflux), which generates a depolarizing end plate potential that reaches threshold.

What enzyme is responsible for terminating acetylcholine activity at the neuromuscular junction, and what becomes of its products?

Acetylcholinesterase (AChE) rapidly hydrolyzes acetylcholine into acetate and choline; choline is transported back into the presynaptic terminal by active transport to synthesize new acetylcholine via choline acetyltransferase.

In excitation-contraction coupling, how is a sarcolemmal action potential transduced into $Ca^{2+}$ release inside the muscle cell?

The action potential propagates down transverse tubules (T-tubules) and activates voltage-sensitive dihydropyridine (DHP) receptors, which are mechanically coupled to and open ryanodine receptor (RyR) channels in the sarcoplasmic reticulum, releasing $Ca^{2+}$ into the cytosol.

In the sarcomere diagram shown, what giant protein stabilizes thick filaments by anchoring them between the Z disk and M line, and what protein stabilizes thin filaments?

Titin stabilizes the thick filaments (myosin) by anchoring them between the Z disk and M line, while nebulin stabilizes and aligns the thin filaments (actin, troponin, and tropomyosin) anchored to the Z disk.

What are the three main proteins that compose thin filaments in skeletal muscle, and what is the role of each?

(1) Actin (F-actin polymers of G-actin subunits), which contains binding sites for myosin; (2) tropomyosin, which physically blocks myosin-binding sites on actin in relaxed muscle; and (3) troponin, a three-subunit complex that binds $Ca^{2+}$ and shifts tropomyosin away from the active sites.

What event during the crossbridge cycle causes the myosin head to detach from the actin filament?

Binding of a new molecule of ATP to the myosin head causes it to release actin, breaking the rigor state.

What causes the myosin head to execute the 'power stroke' during skeletal muscle contraction?

The release of inorganic phosphate ($P_i$) from the myosin head triggers the head to swivel toward the M line, pulling the attached thin filament along with it.

How is relaxation achieved in skeletal muscle after somatic motor stimulation stops?

Sarcoplasmic/endoplasmic reticulum $Ca^{2+}$-ATPase (SERCA) pumps actively transport cytosolic $Ca^{2+}$ back into the sarcoplasmic reticulum; as free cytosolic $Ca^{2+}$ declines, $Ca^{2+}$ unbinds from troponin, allowing tropomyosin to slide back over the myosin-binding sites on actin.

Based on the provided smooth muscle diagram, what calcium-binding protein activates myosin light chain kinase (MLCK), and what enzyme dephosphorylates myosin to bring about relaxation?

Calmodulin (CaM) binds cytosolic $Ca^{2+}$ to activate myosin light chain kinase (MLCK), which phosphorylates myosin light chains to initiate contraction; relaxation requires myosin phosphatase (MLCP) to dephosphorylate myosin, decreasing myosin ATPase activity.

How does the contraction mechanism of smooth muscle fundamentally differ from that of skeletal muscle?

Smooth muscle lacks sarcomeres, troponin, and motor end plates; it utilizes calcium from both the ECF and sarcoplasmic reticulum (via calcium-induced calcium release); contraction is regulated by calmodulin and phosphorylation of myosin light chains via MLCK; and contractions are graded rather than all-or-none.

How do slow-twitch oxidative (Type I) and fast-twitch glycolytic (Type IIb/IIx) skeletal muscle fibers differ in metabolism and fatigue resistance?

Slow-twitch oxidative fibers contract slowly, are rich in myoglobin, mitochondria, and capillaries, utilize aerobic cellular respiration, and are fatigue resistant; fast-twitch glycolytic fibers contract rapidly and forcefully, have low myoglobin and mitochondrial content, store abundant glycogen, rely on anaerobic glycolysis, and fatigue rapidly with lactic acid production.