Functional Neuroanatomy & The Exam Flashcards
(92 cards)
What is the resting membrane potential for a large nerve fiber?
-90 millivolts
What happens when you have a calcium deficit?
Causes Na+ channels to become activated with little increases in membrane potential, leading to a very excitable nerve (ie. Tetany)
What is the threshold for stimulation of an action potential?
-65 mV
What 3 things result in the inhibition of excitability?
High extracellular Ca (decr membrane permeability to Na), local anesthetics (Na channel blockers), when AP strength to excitability threshold = <1
What are the different cells that form myelin for the CNS and PNS, and what is the clinical significance of this?
CNS: oligodendroglial cell processes; PNS: rolled up Schwann cell membrane; different populations of cells > get different cancer manifestations
The amount of Ca inflow from voltage-gated Ca channels on the presynaptic membrane after an AP depolarizes it is directly related to what?
Transmitter release
What are the two types of ion channels located on the postsynaptic neuron?
- Cation channels (allow Na ions to enter, excitatory)
- anion channels (allow Cl ions to enter, inhibitory)
What is occurring during excitation of a postsynaptic receptor?
- Opening Na channels
- decr conduction thru Cl/K channels (both raise intracellular membrane potential towards zero)
- internal metabolic changes to excite cell activity
What is occurring during inhibition of a postsynaptic receptor?
Opening of Cl channels, incr K out of neuron (both make the intracellular membrane potential more negative), activation of receptor enzymes to inhibit cellular activity
How do small-molecule neurotransmitters differ from neuropeptides and what are some examples of each?
Small molecule NTs are rapidly acting, while neuropeptides are slow acting or they are growth factors that have central and long-acting effects
- Small: ACh, NE, Epi, GABA, Glycine, Glutamate
- Neuropeptides: ACTH, GH, Insulin, Glucagon, Angiotensin
Describe acetylcholine
- Acetyl coenzyme A + choline
- transported into vesicles
- released into cleft
- rapidly split into acetate/choline by cholinesterase in cleft
- choline actively recycled
- usually excitatory (inhibitory in some PS nerve endings ie. Vagus)
What is a condition in which the patient has adequate ACh, but doesn’t have enough receptors for it to bind to?
Myasthenia gravis
Describe norepinephrine
Synthesized in the adrenergic nerve terminal (tyrosine>dopa>dopamine), transported into vesicles> dopamine to NE
Removal: active reuptake into adrenergic endings, diffusion away, enzymatic destruction (ie. monoamine oxidase)
An excitatory postsynaptic potential does what to elicit an action potential?
Incr Na permeability, neutralizing the RMP, and requires a discharge of many terminal at once or in sequence (spatial vs. temporal summation)
Inhibitory postsynaptic potentials do what to prevent the generation of an action potential?
Open Cl channels > Cl in and/or K out, incr negativity in the cells (hyperpolarization)
What occurs with presynaptic inhibition?
Release of inhibitory substance (GABA) onto presynaptic fibrils > cancels effect of sodium influx; occurs in many sensory pathways to minimize sideways spread
What is the effect of fatigue on synaptic transmission?
Decrease in discharge of postsynaptic neuron
What is the effect of pH on synaptic transmission?
Alkalosis increases excitability, acidosis depresses it
What are the effects of caffeine, theophylline and theobromine on synaptic transmission?
Reduce threshold for excitation
What are the effects of strychnine on synaptic transmission?
Inhibits glycine (inhibitory NT) in spinal cord, causing excitation/tetany
What are the effects of anesthetics on synaptic transmission?
Anesthetics increase threshold for excitation, decreasing transmission
Describe the process of skeletal muscle excitation
Mostly Na enters the muscle fiber, creating a local positive potential in the muscle fiber (the end plate potential)
When does fatigue occur at neuromuscular junctions?
Stimulation of the nerve >100x/second for minutes depletes ACh vesicles, so impulses fail to pass, resulting in fatigue
What 3 drugs stimulate the muscle fiber by ACh-like action and are long-lasting because they are not broken down by cholinesterase?
Methacholine, carbachol, nicotine > can result in long-lasting toxicities