Neurons

Hyperkalemia reduces the concentration gradient for K⁺. As a result, less K⁺ leaves the cell through leak channels, leaving more positive charge inside and shifting the resting membrane potential toward depolarization.

Irritability (excitability) is the physiological ability of a neuron or muscle cell to respond to a stimulus by generating an electrical signal. Conductivity refers to its ability to transmit that signal.

Ependymal cells are ciliated, cuboidal-to-columnar glial cells that line the fluid-filled cavities of the CNS (ventricles and central canal) and help secrete and circulate cerebrospinal fluid.

Group A fibers (like somatic motor fibers and large sensory fibers for touch and position) are the thickest, most heavily myelinated fibers in the body, providing the fastest nerve conduction velocities.

Unlike acetylcholine which is destroyed by enzymes, monoamine neurotransmitters (like serotonin, dopamine, and norepinephrine) are primarily cleared by active reuptake transporters bringing them back into the presynaptic knob.

The autonomic (visceral) nervous system controls involuntary physiological functions by regulating the activity of smooth muscles, cardiac muscles, and secretory glands.

Microglia act as the resident macrophages of the central nervous system, migrating to sites of injury or infection to clear away dead tissue, plaques, and pathogens.

Axoaxonic synapses occur when one axon terminal synapses onto another axon terminal. They regulate (facilitate or inhibit) the amount of calcium that enters the second terminal, modulating neurotransmitter release.

Endorphins and enkephalins are endogenous opioids that bind to opioid receptors in the brain and spinal cord, powerfully blocking the transmission and perception of pain signals.

In the PNS, a bundle of axons is called a nerve. In contrast, a bundle of axons in the CNS is called a tract. A ganglion is a cluster of cell bodies in the PNS.

Neuromuscular junctions (motor end plates) are the highly specialized synapses where motor neurons release acetylcholine to trigger skeletal muscle contraction.

Electrical synapses do not use neurotransmitters; instead, they utilize gap junctions (connexons) that physically connect the cytoplasm of adjacent cells, allowing instantaneous, bidirectional current flow.

Because a neuron cannot fire another action potential during the absolute refractory period regardless of stimulus strength, this period sets a strict upper limit on how frequently the neuron can fire.

Following peak depolarization, voltage-gated K⁺ channels open and K⁺ rushes out of the cell down its electrochemical gradient, restoring the negative internal charge during repolarization.

The threshold potential (usually around -55 mV) is the tipping point where voltage-gated Na⁺ channels open en masse, triggering the explosive positive feedback loop of an action potential.

Drugs like local anesthetics (e.g., lidocaine) or neurotoxins (e.g., tetrodotoxin) block voltage-gated Na⁺ channels, preventing the massive sodium influx required to generate and propagate an action potential.

GABA is the major inhibitory neurotransmitter in the brain, functioning primarily by opening chloride channels on postsynaptic neurons to induce hyperpolarization. Glutamate is the major excitatory neurotransmitter.

Contralateral reflex arcs (e.g., the crossed extensor reflex) involve interneurons that cross the spinal cord midline to produce a motor response on the side of the body opposite to the stimulus.

Reciprocal inhibition ensures coordinated movement by using inhibitory interneurons to relax antagonistic muscles while excitatory pathways stimulate the agonist muscles.