Velocity of Nerve Signal Conduction, Physiology of Synapses Flashcards
What causes Conduction Velocity to change?
- Resistance of Membrane (Rm)
- Capacitance of Membrane (Cm)
- Resistance of Interior (Ri)
Resistance is …
resistance to flow
Capacitance is
stored electrical charge
capacitance =
1 / resistance
smaller effective resistance =
faster velocity
Effective resistance is proportional to
SQRT(RmRi)(Cm)
membrane capacitance increases when
the membrane area increases
membrane capacitance decreases when
the membrane area decreases
Effective Resistance Equation
ER is proportional to SQRT((2/pirl)(1/pirSQ))(2pirl)
Causes Rm decrease x2, Ri decreases x4, Cm increase x2
doubling the radius of a nerve
larger diameter fibers
faster conduction velocities
Myelin results in
faster velocity
Why does myelin increase conduction velocity?
- Schwann cell membranes (decrease capacitance, increase Rm)
- Saltatory conduction (impulse jumps from one Node of Ranvier to another, less Na+/K+ ATPase and energy required)
Schwann cell wrap of 25
Lowers Capacitance 50 fold, increases Rm 50 fold.
Always doubled
Autoimmune demyelinating diseases
Multiple Sclerosis
ALS (Amyelotropic Lateral Sclerosis)
close (2-3 nm), gap junction, electrical current crosses without chemicals, common in the heart
Electrical Synapses
wider (30-50 nm), begins with arrival of action potential, accounts for most of delay in signal transduction (0.5 msec)
Chemical Synapses
Synapses Steps
- Action potential impulse
- Voltage gated calcium channels open
- Calcium enters the Presynaptic Ending (down the concentration gradient)
- Release of Neurotransmitter (exocytosis)
- Neurotransmitter moves across synapse and binds to a receptor
- Transient change in postsynaptic membrane ion permeability
- breakdown of neurotransmitter by specific enzyme, recycling of products
- Membrane potential altered in Postsynaptic cell
Causes the synapse stimulation to cease
- negative feedback from the Neurotransmitter at Presynapse
- degradation of neurotransmitter at receptor
cell body to axon flow impulse 99.9% of the time
orthodromic
axon to cell body flow of impulse
antidromic
3 causes of synaptic delay
- release of the neurotransmitter
- travel of the neurotransmitter across synapse
- binding of the neurotransmitter to the post synaptic receptor
activates neurons to fire
Excitatory Post-Synaptic Potential (EPSP)
EPSP fast
increase in Na+ conductance
EPSP slow
decrease in K+ conductance
stops neurons from firing
Inhibitory Post-Synaptic Potential (IPSP)
IPSP fast
increase in Cl- conductance, hyperpolarizes cell, harder to depolarize
IPSP slow
increase in K+ conductance
2 impulses at the same time that total threshold
Spatial Summation
2 impulses in rapid succession that total threshold,
second comes before the first degrades
temporal summation
Presynaptic facilitation
simulation of Ca++ channel opening,
more neurotransmitter released
inhibition of Ca++ channel opening, reduces amount of neurotransmitter released
presynaptic inhibition
multiple nerve impulses work toward one result
Convergent neural network
one neural impulse works to make multiple results
Divergent neural network
mediated by acetyltransferase
Choline + acetyl Co A
Acetyl choline (ACh)
General Action of Acetyl Choline
parasympathetic stimulation (low HR, low BP, fast GI)
neurotransmitter for neuromuscular junction (nerve to muscle)
cholinergic receptor that is stimulated by acetylcholine located on smooth muscle, cardiac muscle, glands, and brain and stimulates the parasympathetic nervous system when activated
Muscarinic Cholinergic receptor
stimulated by Muscarine, blocked by atropine
Muscarinic Cholinergic receptor
located at neurons, skeletal muscle, and on the brain
stimulates the sympathetic nervous system when activated
Nicotinic Cholinergic receptor
stimulated by nicotine, blocked by curare
Nicotinic Cholinergic receptor
prevents degradation of ACh message, causes synapses to get stuck
1 mg is lethal
Sarin, VX Nerve Gas (AChe inhibitor, Organophosphate)
breaks down Acetylcholine
Acetylcholinesterase (AChe)
reverses Sarin, VX Nerve Gas effects
Atropine + Pralidoxime autoinjectors
few ACh receptors due to autoimmune degradation
Myasthenia gravis
decreased ACh synthesis in brain
Alzheimer’s disease
anti-smoking drugs
nicotrol - nicotine replacement therapy
chantix - ACh agonist/antagonist
zyban - Dopamine reuptake inhibitor
Catecholamines
Serotonin
Histamine
Biogenic Amines
Norepinephrine
Epinephrine
Dopamine
Catecholamines
Amine synthesis
Dietary Tyrosine + Tyrosine hydroxylase = Dopa
Dopa + Dopa decarboxylase = Dopamine
Dopamine + Dopamine B- Hydroxylase = Norepinephrine
Norepinephrine + N-methyltransferase = Epinephrine
Norepinephrine deactivation methods
Monoamine Oxidase (MAO, in many Anti Depressants)
Catechol-O-Methyltransferase (COMT, peripheral tissues, liver, kidney, etc)
Nerve tracts using Epinephrine, Norepinephrine
Adrenergic Fibers
General Action of Epinephrine and Norepinephrine
sympathetic stimulation (HR up, BP up, GI tact slow)
E and NE have different actions depending on Receptor Types
Alpha Receptor
Beta Receptors
Adrenergic Receptors
Adrenergic Receptor with a greater affinity for NE
Alpha receptors
Adrenergic Receptor with a greater affinity for E
Beta receptors
stimulates contraction of smooth muscle, (vasoconstriction)
in vessels and the sympathetic nerve tract
IP3
Alpha 1 receptor
inhibition of smooth muscle contraction in GI tract
common in GI tract + pancreas
decreases cAMP
Alpha 2 receptor
stimulates heart rate, contractility, Kidney, fat lipolysis, increases cAMP
Beta 1 receptor
inhibits smooth muscle, increases cAMP
in lungs, heart, skeletal muscle blood vessels
Beta 2 receptors
fat exclusively, lipolysis, increases cAMP
Beta 3 receptors
ACh AND nicotinic receptors are present in which nervous system?
Somatic Nervous system
sympathetic pathways distribution
distributed in thoracolumbar area of spinal cord
ventral roots of the spinal nerves, system runs parallel to the spinal cord
short fibers in the ANS, use ACh as their neurotransmitter
sympathetic pathways
Preganglionic fibers
long fibers in the ANS, use NE as a neurotransmitter
sympathetic pathways,
adrenergic receptors on target tissue
Postganglionic fibers
parasympathetic pathways distribution
distribution via cranial nerves and pelvic nerves from the sacral region
cranial nerves, 3, 7, 9, and 10 have 90^ of the body’s parasympathetic fibers
long in length use ACh as their neurotransmitter
parasympathetic pathways
preganglionic fibers
short in length, on target tissue, use ACh as their neurotransmitter, cholinergic muscarinic receptors are on the target tissue
postganglionic fibers
CNS neurotransmitter, pleasure pathways
Dopamine
Methamphetamine and Cocaine affect this neurotransmitter …
Dopamine
Parkinsons disease in caused by a lack of this neurotransmitter …
and is treated with this therapy …
Dopamine
L-Dopa therapy
derived from Tryptophan (milk, turkey)
catabolized by MAO
excitatory for muscle
inhibitory for sensation
seratonin
amino acid neurotransmitters
glutamate, aspartate, glycine, GABA (Gama Amino Butyric Acid)
excitatory in CNS, important for learning and memory
glutamate and aspartate
inhibitory in CNS, anesthetic action
Glycine and GABA
4 modes of action for alcohol
- Activates GABA pathways (inhibitory)
- Activates Adenosine receptors (inhibitory)
- Blocks Glutamate pathways (stimulatory path, inhibited)
- Membrane soluble (inhibits/slows down second messenger pathways)
Neuropeptide Examples
Endogenous Opioids
Morphine (Codeine, Oxycodone, Ketamine)
Substance P
released in the presence of a stressor
stress, defense, repair, survival system
Vasodilator
Substance P
Action of Endogenous Opioids
Analgesic
Reduces Pain
Assists in memory and learning
Possibly protects the brain from neuronal damage in a stroke
Nitric Oxide
