Exam 4: Nervous System: Impulse Conduction Flashcards
what type of event is conduction
electrochemical
formation of a charge differential on membrane
- the induction of an action potential through use of ion gradients
electrical conduction
manipulation of ion concentrations
using chemical signals to effect either excitatory or inhibitory potentials in target cells
chemical conduction
membrane potential
voltage difference across membrane
- resting membrane potential = -70mV
- salty banana: more Na out, more K in, Cl on outside
charge differential on membrane
- formed by selective concentration of positive and negative charges
- resting potential results in net pos charge otside, net neg charge inside
electrical gradient
ion concentrations set up by membrane pumps
- sodium is concentrated outside, while K is concentrated inside cell
- strictly concentration
chemical gradient
what are the main ions involved in membrane potentials
K and Na
voltage gated ion channels
need difference in charge on membrane to open
ligand gated ion channel
need something to bind ex: neurotransmitter
mechanically gated ion channel
distort the membrane
- poke it, vibrate it
ungated ion channel
like aquaporins - control if you put them on membrane
action potential
- neuron at resting potential, stimulus is applied, mechanically gated Na channels open, Na rushes into cell
- once threshold reached -55, Na channels open, if not they reset and no action potential
- depolarization causes Na channels to close and K channels to open , K rushes in
- repolarization occurs, charge reset
- hyperpolarization
K channels close
reset to resting potential
absolute refractory period
in repolarization
cannot send another signal no matter how strong stimulus is
relative refractory period
in hyperpolarization
need super strong signal
factors that affect excitability
-blocking gated channels or altering gradients
caine drugs
serum Ca2+ levels
shifting of K levels
caine drugs effects on excitability
block Na channels preventing depolarization of neuron
- cannot send pain signals hence numb feeling - novacaine, cocaine
serum Ca levels effect on excitability
decrease
less channels blocked, neuron may have small Na channels opening, can reach threshold - hyperexcitability
serum Ca levels effect on excitability
increase
more channels blocked
cardiac muscle - needs external Ca, when raised will not contract as rapidly
- initially the inc riases heart rate bc depolarizing to get more contraction, but as it goes up you get inverse effect - problems with nerve impulses, cardiac irregularities
- harder to depolarize
shifting K levels effect on excitability
releasing K can cause problems, screw up the ion balance making it harder to depolarize the cell
- if acidosis - bring in H but releasing K
what dose is fatal for saxitoxin
0.2 mg
what dose is fatal for tetrodotoxin
1 mg
what does the dosage amount indicate regarding binding affinities?
saxitoxin has a higher affinity for saxitoxin bc it is lower dosage to be fatal
presynaptic vs postsynaptic cell
presynaptic cell: sends impulse
postsynaptic cell: target cell, receiving
cells separated by synaptic cleft, do not directly touch
requires release of neurotransmitter to the target
chemical synapse
cells connected by gap junctions, no neurotransmitter required
found in hippocampus, retina, cerebellum (equilibrium)
rapid, NOT modulated
electrical synapse
synaptic vesicles hold the same amount of neurotransmitter, what is this amount called?
quanta
same amount per vesicle, the release is directly proprtional to what?
strength of signal you are sending
- stronger depolarization, the longer it will last
in chemical synapses what are all of the receptors?
ligand gated
what determines if the effect will be excitatory or inhibitory?
the type of ion channel
depolarization of the end terminals opens…
voltage gated Ca channels, lets in Ca to do exocytosis via the SNARE complex
opening Na channels results in…
opening K channels or Cl channels results in…
Na - EPSP stimulates target cell
K/Cl - IPSP
ionotropic receptors
binding to receptor directly opens ion channels
metabotropic receptors
indirect opening of channels via second messengers, G protein
- dissociation of G protein is what causes channel to open
4 possible cascades of second messengers
Gs, Gi, Gq, Gt
Gs cascade
stimulates adenylyl cyclase
inc cAMP
EPSP
Gi cascade
inhibits adenylyl cyclase
dec cAMP
IPSP
Gq
activates phospholipase C
splits PIP2 into IP3 and DAG
EPSP
Gt
transducin to dec cGMP in retina
inhibits dark current - get bleaching of an image onto the eye
how do you make acetylcholine (Ach)
acetyl CoA and choline
- can not make sufficient amount of choline so get from diet
- make Ach and store in synaptic vesicle
when you depolarize cell you release Ach, what happens?
it hits cholinergic receptor - never enters postsynaptic cell
- does its work on the surface
- once bound, acetylcholinesterase snaps it apart the acetyl group is gone and the choline gets recycled
Where is Ach found?
- both pre-ganglionic and post-ganglionic parasympathetic divisions
- pre-ganglionic sympathetic only
- some CNS
- the ONLY neurotransmitter in somatic division!!!!
ONLY neurotransmitter to interact with skeletal muscle!!
Ach role in the functioning of the CNS?
helps memory processing and formation - hippocampus
nicotinic cholinergic receptors
ionotropic
EPSP
somatic
CNS
all preganglionic (both symp and parasymp)
when neurotransmitter hits it opens Na and depolarizes cell
muscarinic cholinergic receptors
post ganglionic (parasympathetic) CNS - reward, memory formation metabotropic M1-5 some muscle movement
which muscarinic cholinergic receptors are excitatory?
M1, M3, M5
which muscarinic cholinergic receptors are inhibitory?
M2 and M4
M1
EPSP
glands
- inc secretions - salvation, digestion, sweating, mucous production
M2
IPSP
cardiac
- lowers HR, you are relaxed so do not need a pounding HR
M3
EPSP
smooth muscle
- inc peristalsis
- lungs : more contracted in resting state, do not need dilated bronchioles when relaxed
M4
IPSP
brain - muscle movement
- more relaxed muscles
M5
EPSP
brain - reward center
- easier to recall memories, learn
Pesticide poisoning: what happens to Ach concentartion in synapse if you are blocking acetylcholinesterase?
will not be able to breakdown Ach so get a build up of Ach, inc binding of Ach to receptors in post synaptic cel, over stimulation!
what is a drug that blocks ACH activity at muscarinic receptors?
atropine
what are catecholamines derived from
3 examples of catecholamines
tyrosine
norepinephrine, epinephrine, dopamine
when NE removed from adrenergic receptor, what 2 enzymes can break it down?
MAO, COMT
usually recycled or in bloodstream and the liver will break it down liver has MAO and COMT
all adrenergic receptors are…
metabotropic
Alpha 1 adrenergic receptors
Gq
cardiovascular, vasconstriction
inc BP - if in fight or flight situation you want BP up
Alpha 2 adrenergic receptor
Gi
self regulatory
lowers NE (negative feedback, modulation), lowers anxiety
helps you think of an action instead of becoming frozen in fear
all beta receptors are…
stimulatory
Beta 1 adrenergic receptors
heart: gives faster, stronger HR
kidneys: inc pressure of blood going into kidneys
increase BP bc heart is pumping faster
Beta 2 adrenergic receptors
opposite effect
inc cAMP in beta 2 cell dec Ca in muscle, so not strong contraction
- in lungs get bronchodilation and vasodilation - better blood flow for oxygenation, opens air ways
Beta 3 adrenergic receptors
adipose fat cells
lipolysis
release lipids from fat cells to have alternate energy source
