Neurophysiology - Cells AQ Flashcards

Comprehensive practice flashcards reviewing cellular neurophysiology concepts including neuron anatomy, membrane potentials, action potential propagation, synaptic transmission, and neuropharmacology.

What are the primary divisions of the central nervous system (CNS) and peripheral nervous system (PNS), and how are sensory receptors categorized?

The CNS is divided into the brain and spinal cord, while the PNS consists of the cranial nerves and spinal nerves. Sensory receptors belong to the PNS because sensory organs are the most peripheral extensions of sensory neurons.

Why is brain cancer relatively common even though neurons do not undergo mitotic division?

Brain cancer typically originates from glial cells rather than neurons. Glial cells divide rapidly within the brain, whereas neurons are largely quiescent.

Which PNS glial cell shares a similar function with CNS astrocytes, and how do oligodendrocytes differ from Schwann cells?

Satellite cells in the PNS perform functions similar to astrocytes in the CNS. Oligodendrocytes operate in the CNS and can myelinate multiple axons, whereas Schwann cells reside in the PNS and myelinate only one segment of a single axon at a time.

What is a node of Ranvier, and what is the biological function of the myelin sheath?

A node of Ranvier is an unmyelinated region of an axon located between myelinated internodes, found in both the CNS and PNS. The surrounding myelin sheath insulates the neuron and increases action potential velocity.

How are the three structural classes of neurons categorized by function, and what proportion of CNS neurons are interneurons?

Special sensory neurons are bipolar, somatic sensory neurons are unipolar, and motor neurons are multipolar. Interneurons account for $99\%$ of all CNS neurons and are located exclusively within the brain and spinal cord.

What are the major structural components of a typical motor neuron?

A typical motor neuron consists of dendrites with dendritic spines (elevations where presynaptic synapses form), a cell body (soma) containing the nucleus, an axon wrapped in a myelin sheath formed by Schwann's cells separated by nodes of Ranvier, and terminal axon branches terminating in synaptic knobs.

What are the three structural components of a synapse, and what comprises the synaptic cleft?

A synapse consists of the presynaptic cell, the synaptic cleft, and the postsynaptic cell. The synaptic cleft is filled with interstitial fluid (ISF), through which neurotransmitters transmit signals.

Which microtubule-associated proteins (MAPs) handle axonal transport, and in which directions do they travel?

Dynein transports recycled vesicles from the terminal knob to the soma in the negative direction. Kinesin transports secretory vesicles from the soma to the terminal knob in the positive direction. Both walk along the microtubule cytoskeleton.

What are the equilibrium potential values for $\text{Na}^+$ and $\text{K}^+$, and how do they relate to the resting membrane potential (RMP)?

The equilibrium potential for $\text{Na}^+$ is $+60\,mV$ and for $\text{K}^+$ is $-90\,mV$. Because the actual RMP of a neuron ($-70\,mV$) is close to $-90\,mV$, selective permeability to $\text{K}^+$ via leak channels is the primary determinant of RMP.

Where do graded potentials (GPs) and action potentials (APs) occur in a neuron, and which channels mediate them?

GPs occur in dendrites, the soma, and the axon hillock through ligand-gated and mechanically-gated channels. APs occur at the axon initial segment and nodes of Ranvier through voltage-gated channels.

What are the most abundant intracellular and extracellular cations, and which cation exhibits the steepest concentration gradient?

Potassium ($\text{K}^+$) is the most abundant intracellular cation, while sodium ($\text{Na}^+$) is the most abundant extracellular cation. Calcium ($\text{Ca}^{2+}$) has the steepest concentration gradient across the plasma membrane.

How do ion movements across the plasma membrane cause depolarization or hyperpolarization?

Depolarization (a decrease in potential, becoming less negative) occurs when cations (like $\text{Na}^+$) enter the cell. Hyperpolarization (an increase in potential, becoming more negative) occurs when cations (like $\text{K}^+$) exit or anions (like $\text{Cl}^-$) enter the cell.

Why are graded potentials described as 'graded', 'local', and 'distance-limited'?

They are 'graded' because potential changes are directly proportional to stimulus strength, 'local' because they affect small membrane regions, and 'distance-limited' because current decays as it leaks through membrane channels and capacitance.

What are the specific membrane voltage values for RMP, threshold potential (TP), and peak amplitude in a typical neuron?

The resting membrane potential (RMP) is $-70\,mV$, the threshold potential (TP) in the axon hillock is $-60\,mV$, and the peak amplitude reached during an action potential is $+30\,mV$.

How do absolute and relative refractory periods differ in a neuron?

During the absolute refractory period, a second AP cannot fire because voltage-gated $\text{Na}^+$ channels are open or inactivated. During the relative refractory period, a second AP can fire only if triggered by a larger-than-normal GP stimulus because the cell is hyperpolarized.

Why does cardiac muscle have an AP frequency of $1\text{ AP per } 200\,ms$ compared to skeletal muscle's $1\text{ AP per } 5\,ms$?

The lower AP frequency in cardiac muscle prevents the summation of muscle tension, ensuring the heart cannot undergo sustained tetanic contractions.

How do the two sub-regions of the spike initiation zone function during neural integration?

The axon hillock contains ligand-gated channels where graded potentials summate. The initial segment contains voltage-gated channels where the first action potential occurs if electrotonic spread depolarizes the membrane to $-60\,mV$.

If a neuron receives $32$ EPSPs totaling $+42\,mV$ and $1$ IPSP of $-32\,mV$ at an RMP of $-70\,mV$, will an AP fire?

Yes. The net synaptic input provides a $+10\,mV$ depolarization ($42\,mV - 32\,mV$). Adding $+10\,mV$ to $-70\,mV$ reaches $-60\,mV$, which meets the threshold potential needed to fire an AP.

What are the operating voltage thresholds for voltage-gated $\text{Na}^+$ and $\text{K}^+$ channels during an action potential?

Voltage-gated $\text{Na}^+$ channels open at $-60\,mV$, inactivate at $+30\,mV$, and close at $-90\,mV$. Voltage-gated $\text{K}^+$ channels open at $+30\,mV$ and close at $-90\,mV$.

How do local anesthetics like lidocaine prevent the sensation of pain?

Lidocaine inhibits voltage-gated $\text{Na}^+$ channels, preventing them from opening. As a result, action potentials cannot be generated or propagated along sensory neurons to convey pain signals to the brain.

How do continuous and saltatory conduction differ in mechanism and velocity?

Unmyelinated axons conduct signals continuously down the entire length at $1\text{--}2\,m/s$. Myelinated axons undergo saltatory conduction, regenerating APs only at the nodes of Ranvier, reaching speeds up to $100\text{--}120\,m/s$.

How does demyelination in Multiple Sclerosis (MS) impair signal transmission?

Demyelination decreases membrane resistance and increases capacitance. Electrotonic depolarization leaks across the axolemma, causing voltage to decay before reaching downstream nodes of Ranvier, slowing or completely blocking AP propagation.

What sequence of events occurs at the terminal knob to cause neurotransmitter release?

An AP depolarizes the terminal knob (producing a GP), which opens voltage-gated $\text{Ca}^{2+}$ channels. The resulting influx of $\text{Ca}^{2+}$ causes synaptic vesicles to undergo exocytosis.

What are the characteristics and receptor types of a cholinergic synapse?

Cholinergic synapses use acetylcholine (ACh) as their ligand. They feature two receptor types: Nicotinic receptors, which are ionotropic, and Muscarinic receptors, which are metabotropic.

What ligands and receptor subtypes are associated with adrenergic synapses?

Adrenergic synapses utilize catecholamines (norepinephrine and epinephrine) derived from tyrosine. Their receptors include $\alpha_1$, $\alpha_2$, $\beta_1$, and $\beta_2$ adrenergic receptors.

What are the characteristics of GABAergic receptors, and how does diazepam interact with them?

GABAergic synapses use $\gamma$-aminobutyric acid (GABA). $\text{GABA}_A$ is ionotropic and permeable to $\text{Cl}^-$, while $\text{GABA}_B$ is metabotropic. Diazepam (Valium) acts as an agonist for the $\text{GABA}_A$ receptor.

How do AMPA and NMDA glutamatergic receptors work together in postsynaptic signaling?

Both are ionotropic; AMPA is a ligand-gated $\text{Na}^+$ channel and NMDA is a ligand-gated and voltage-gated $\text{Ca}^{2+}$ channel. $\text{Na}^+$ influx through AMPA depolarizes the postsynaptic cell, ejecting a blocking $\text{Mg}^{2+}$ ion from the center of the NMDA channel to allow $\text{Ca}^{2+}$ influx.

How do ketamine/Spravato differ from gabapentin in treating neural conditions?

Ketamine and Spravato (esketamine) directly antagonize NMDA receptors to provide rapid antidepressant effects. Gabapentin blocks voltage-gated $\text{Ca}^{2+}$ channels to reduce glutamate release, calming overactive signaling for seizures and nerve pain.

What mechanisms are responsible for terminating a synaptic signal?

Mechanisms include cessation of presynaptic firing, unbinding of ligands, diffusion of neurotransmitters out of the cleft, enzymatic degradation (e.g., acetylcholinesterase degrading ACh), and presynaptic reuptake via transporters.

How do MAOIs and SSRIs increase neurotransmitter levels in the synaptic cleft?

MAOIs prevent Monoamine Oxidase from degrading catecholamines (dopamine, norepinephrine, epinephrine). SSRIs (e.g., paroxetine) block the reuptake of serotonin into presynaptic terminals, allowing more serotonin to remain available to postsynaptic receptors.