Nervous 1 Flashcards
has a charge, i.e. negatively charged, positively charged.
Polar
Membrane potential:
Can it reach -94mV?
Ion concentration DIFFERENCES, i.e. K+ high inside, but low outside.
Yes
Diffusion potential:
Can it reach -94mV?
The potential difference between the inside and the outside.
No, there is enough repulsion to prevent movement of K+ to the outside
K+ will never reach it’s diffusion equilibrium
Resting membrane potential:
Neuron mV:
Average of all the ions’ diffusion potentials
Neurons: -90mV
calculates potential INSIDE of the membrane for that specific ion
Nernst Equation
Nernst equations combined for all the ions.
Goldman Equation
Membrane is most permeable to…
K+
Na-K ATPase Pump:
3 Na out, 2 K in
Leaky channels are leaky to
K+
Neurons vs Skeletal muscle. Which of these is more excitable?
Neurons
Action Potential Step 1:
Resting (aka polarized)
-90 mV
Action Potential Step 2:
Depolarization (aka going from neg to pos)
+35 mV
0.1ms to occur
PERMEABLE TO SODIUM
Action Potential Step 3:
Repolarization (aka going back to being negatively charged)
-90 mV
0.2ms to occur
Inactivation gate Closed to Na
K channels open wider and K diffuses out
Resets the membrane potential.
Voltage Gated Channels
Inactivation gates are found
Activation gates are found
INACTIVATION gates are found INSIDE.
Activation outside
Voltage Gated Channels
At rest: the activation gate is:
Does Na Enter?
At rest: the activation gate is CLOSED, inactivation open, so no Na enters.
Voltage Gated Channels
At -55mV or between -50 and -70mV:
Activation gate opens, Na pours in, depolarizing cell to like +35mV
Voltage Gated Channels
At +35 mV:
At +35 mV: Inactivation gate closes. Na can’t enter.
Avg nerve fiber has more unmyelinated or myelinated?
Avg nerve fiber has 2x more unmyelinated than myelinated.
Nerve Fibers and Transmission:
Ca2+ is a
membrane stabilizer
Nerve Fibers and Transmission:
Anesthetics disable
Anesthetics (Procaine/Tetracaine) disable Na channels, so nerves impulses fail to pass along the anesthetized nerves
All or none principle
All or none principle = Either the AP goes over the whole fiber or stops completely
Neurotransmitters 1:
Signal enters neuron via the
Signal enters neuron via the dendrites
Neurotransmitters 2:
Signal goes through
Signal goes through neuron
Neurotransmitters 3:
Signal exits via the
Signal exits via the axon terminal
Neurotransmitters 4:
Signal exits via the axon terminal. Axon then
Axon then synapses with some second order neurons and so forth.
Neurotransmitters made where?
made in the cytosol of the presynaptic terminal
Neurotransmitters examples
ACh (I, motor cortex, motor neurons preganglionic of sympathetic and parasympathetic NS)
Norepinephrine (preganglionic SYMPATHETIC NS)
Epinephrine
Histamine
GABA (Inhibition)
Dopamine (Inhibition)
Serotonin (Inhibitor of pain)
Glutamate (Excitation)
Glycine (Inhibition)
Neurotransmitter Dopamine
Inhibition
Neurotransmitter Serotonin
Inhibitor of pain
Neurotransmitter Glutamate
Excitation
Neurotransmitter Glycine
Inhibition
process of NT release and binding:
AP depolarizes which synaptic membrane
AP depolarizes PRE-synaptic membrane
process of NT release and binding:
after calcium channel open
Release of Calcium causes NT release from their vesicles.
process of NT release and binding:
after AP depolarizes PRE-synaptic membrane
Calcium Channels open
process of NT release and binding:
after Release of Calcium causes NT release from their vesicles.
NT binds to the outside binding component
process of NT release and binding:
after NT binds to the outside binding component
Inside Ionophore component is made of the G-protein complex.
process of NT release and binding:
after Inside Ionophore component is made of the G-protein complex.
Alpha component leaves and does most of the actions.
Excitation vs inhibition.
Excitation:
Most Common way: Sodium channels opening
Other ways:
Decreased chloride going inside.
Decreased potassium going to the outside.
Increased # of excitatory receptors
Decreased # of inhibitory receptors
METABOLIC ALKALOSIS
Excitation vs inhibition.
Inhibition:
Opening chloride channels
Increased potassium going to the outside.
Increased # of inhibitory receptors
Decreased # of excitatory receptors
METABOLIC ACIDOSIS
NTs vs Neuropeptides
NTs:
Made in cytosol of presynaptic terminal
Rapidly-acting
NTs vs Neuropeptides
Neuropeptides:
Made as proteins by ribosomes in neuronal cell bodies
Slower acting
1000x more potent and long-lasting
Think hormones!
Decrement of Electrical Conduction & Transmission
Excitation:
Greatest at the tips of the dendrites!!!!
However, as they approach the cell body, they leak potassium.
Decrement of Electrical Conduction & Transmission
Inhibition:
Inhibition:
Greatest closest to the soma/cell body
Polarization increases as you approach the soma, so inhibition is greatest at the axon hillock (-75 on image)
Spatial summation:
Spacial Summation: More synapses firing simultaneously = bigger AP.
More fibers stimulated within a field = greater stimulation.
Temporal summation:
Temporal summation: Consecutive synapses firing = buildup to a bigger AP. More impulses in a set amount of time = greater stimulation
Free nerve endings clustered together in a “receptor field” allowing for stimulation of many pain fibers at once, best describes ________ summation.
Spacial
An increase in the frequency of nerve impulses from each fiber to give a stronger sensation, best describes ____________ summation.
Temporal
Drugs Effects on Synaptic Transmission
Caffeine:
increase neuronal excitability
by reducing threshold for excitation of neurons
Drugs Effects on Synaptic Transmission
Strychnine
increase neuronal excitability
by inhibiting actions of inhibitory transmitters
Drugs Effects on Synaptic Transmission
Anesthetics:
increase neuronal THRESHOLD for excitability, DECREASES excitability/synaptic transmission
