Flashcards in Neurophysiology Deck (40)
The basic element of all rapid signal processing within the body. A neuron consists of a cell body (soma), dendrites, and the axon (nerve fiber).
Transmit impulses from peripheral receptors to the CNS
Transmit impulses from the CNS to the periphery
Afferent neuron classifications
A, B, and C by fiber diameter and velocity of conduction of nerve impulses.
Diameter 12-20 (largest of afferent neurons)
Conductions velocity 70-120 (fastest conduction velocity)
Fxn: innervation of skeletal muscles & proprioception
Fxn: touch and pressure
Fxn: skeletal muscle tone
Fxn: Fast pain, touch, temperature
Conduction Velocity: 3-15
Fxn: preganglionic autonomic fibers
Diameter: 0.4-1.2 (SMALL!)
Velocity: 0.5-2 (slow due to a small diameter and lack of myelin)
Fxn: chronic, slow pain; postganglionic sympathetic fibers; touch and temp
Surrounds A and B fibers
Acts as an insulator to prevent the flow of ions across nerve membranes.
Type C fibers are unmyelinated.
Nodes of Ranvier
Allow for saltatory conduction (jumping of conduction). This allows for a 10-fold increase in the velocity of nerve transmission.
Resting membrane potential
The resulting voltage differences across the cell membrane. The cytoplasm is electrically negative (-60 to -80mV) relative to the extracellular fluid.
A rapid change in transmembrane potential due to the opening of Na+ channels (depolarization) and rapid influx of Na+ ions down the concentration gradient, reversing the net negative charge within the cell. The membrane resting potential is restored by the closing of Na+ channels and the opening of K+ channels (repolarization) after the action potential has passed.
A deficiency of calcium ions in the extracellular fluid (hypocalcemia) prevents the Na+ channels from closing between action potentials (tetany).
Low K+ effects on action potentials
Low K+ concentration in extracellular fluid increase the negativity of the resting membrane potential, resulting in hyperpolarization, and decrease cell membrane excitability.
Local anesthetics effect on action potentials
Local anesthetics decrease the permeability of nerve cell membranes to sodium ions, preventing achievement of a threshold potential that is necessary for the generation of an action potential.
Chemical mediators that are released in the synaptic cleft in response to the arrival of an action potential at the nerve ending. Neurotransmitter release is voltage dependent and requires the influx of Ca++ ions into the presynaptic terminal. Mg2+ counteract this.
NTs may be excitatory or inhibitory.
Glutamate vs. GABA
Glutamate is the major excitatory NT in the CNS vs. GABA is the major inhibitory NT.
NTs that play a role in the sleep pathway
ACh, Dopamine, histamine, and NE are widely distributed in the CNS and play an important role in the sleep pathways that are impacted by GA
Can either by stimulatory, promoting a specific enzymatic reaction within the cell, or inhibitory, depressing a specific enzymatic reaction.
Gas proteins vs. Gai proteins
B-adrenergic receptors couple with stimulatory Gas proteins and increase the activity of adenylyl cyclase. Opioid receptors are associated with inhibitory Gai proteins that decrease the activity of adenylyl cyclase. By regulating the level of activity of AC, the B-adrenergic and opioid receptors modulate the internal level of cAMP, which functions as an intracellular second messenger.
High concentrations in basal ganglia. Can either be stimulatory or inhibitory, depending on the specific dopaminergic receptor it activates. It plays an essential role in the reward center of the brain and addiction.
Norepinephrine is present in large amounts in the RAS and hypothalamus and plays an essential role in natural sleep and analgesia. It is released the lowest during sleep, rises during wakefulness, and reaches much higher levels during situations of stress or danger, in the so-called fight-or-flight response.
In the brain, norepinephrine increases arousal and alertness, promotes vigilance, enhances the formation and retrieval of memory, and focuses attention; it also increases restlessness and anxiety. In the rest of the body, norepinephrine increases heart rate and blood pressure, triggers the release of glucose from energy stores, increases blood flow to skeletal muscle, reduces blood flow to the gastrointestinal system, and inhibits voiding of the bladder and gastrointestinal motility.
Co-released by terminals of pain fibers that synapse on the substantial gelatinosa of the spinal cord.
Endogenous opioid peptide agonists (act through the mu receptor, the same receptor responsible for the effects of administered opioids.
Ion channel types
1. Ligand-gated ion channel (excitatory and inhibitory)
2. Voltage-gated ion channels
3. Ion channels that respond to other types of gating
Excitatory ligand-gated ion channels
Cause the inside of the cell to become less negative typically by facilitating the influx of cations into the cell (ACh, glutamate, 5HT)
Inhibitory ligand-gated ion channels
Cause the inside of the cell to become more negative, typically by facilitating the flux of Cl- (GABA and glycine)