Nervous tissue Flashcards
(37 cards)
1
Q
Resting membrane potential
A
- inside membrane negatively charged relative to outside
- exists bc ions unequally distributed between ECF and ICF
- cell membrane more permeable to K than other ions, K leak channels always open
- continuous work that requires ATP and takes up 70% of the energy requirement of the NS
- restored when all voltage-gated channels go back to closed states
2
Q
when is equilibrium reached
A
when there is no net movement of K (potassium)
3
Q
How much more is K concentrated in ICF
A
40x more concentrated and has greatest influence on RMP
4
Q
how much more concentrated is Na in ECF
A
12x more concentrated. Leakage makes RMP slightly less negative than if RMP was only determined by K
5
Q
depolarization
A
shift in voltage across membrane, less negative
excitatory, more likely to fire AP
6
Q
hyperpolarization
A
shift in voltage across membrane, more negative
inhibitory, less likely to fire AP
7
Q
local potentials
A
- temporary, short-range change in voltage
- stimulation triggers
- chemical
- ex. pain signal from damaged tissue, stimulant binds to receptor on neuron
8
Q
properties of local potentials
A
- graded (vary in magnitude)
- decremental (weaker farther from stimulation point)
- reversible (if stimulation stops voltage returns to normal)
9
Q
Action potentials
A
- occur where high density of voltage-gated ion channels
- generated at trigger zone of axon
-excitatory local potential reaches trigger zone and if strong enough it opens a voltage-gated Na channels to generate AP - 1 in a million ions cross membrane during AP, thin layer of ions close to membrane affected
- if threshold reached, neuron fires to maximum voltage, if not reached, simply doesnt fire
10
Q
Action potential process
A
- depolarization
- threshold reached
- voltage peaks at +35
- repolarizes membrane
- hyperpolarization
- voltage returns to RMP, -70 mV, back to pos outside neg inside
11
Q
refractory period
A
period of resistance to stimulation
- absolute: no stimulus of any strength will trigger AP
- relative: stronger stimulus needed to trigger new AP
12
Q
unmyelinated axon fibers
A
- continuous conduction
- voltage-gated channels along length
- depolarization
13
Q
myelinated axons
A
- saltatory conduction
- electrical signal jumps from node to node
- APs generated at nodes ONLY
- voltage-gated ion channels concentrated at nodes
- signal reaches next node, strong enough to depolarize membrane to threshold, Na voltage-gate opens and new full-strength AP occurs
14
Q
Synapses
A
- electrical signal
- triggers release of chem neurotransmitter
15
Q
synapse between two neurons
A
- presynaptic neruon, releases neurotransmitter
- may synapse w/ dendrite, neurosoma, or axon of post synaptic neuron to form axodentric, axosomatic or axoaxonic synapses
- responds to neurotransmitter
16
Q
chem synapse structure
A
- presynaptic has vesicles containing neurotransmitter
- postsynaptic has neuron membrane containing neurotransmitter receptors
17
Q
neurotransmitters
A
- amino acids: aminobutyric acid GABA
- monoamines: epinephrine, norepinephrine
- neuropeptides: cholecystokinin
- NO and CO
- synthesized as needed
- diffuse out of axon terminal
- diffuse into postsynaptic neuron
18
Q
excitatory cholinergic synapse
A
- Ca enters and triggers ACh exocytosis
- ACh receptors open and allow Na and K across membrane
- strong depolarization causes AP to be triggered in postsynaptic cell
19
Q
GABA-ergic synapse
A
- aminobutyric acid as neurotransmitter
- chlorine current hyperpolarizes postsynaptic membrane
20
Q
excitatory adrenergic synapse
A
- monoamine neurotransmitter norepinephrine/ noradrenaline
- fight or flight
21
Q
to end signal
A
- presynaptic cell stops neurotransmitter release
- neurotransmitter in synapse is cleared
22
Q
cessation of signal
A
clear neurotransmitter
- degradation
- reuptake
- diffusion
23
Q
Neuromodulators
A
- alter rate of neurotransmitter synthesis, release, reuptake, or breakdown
- adjust sensitivity of postsynaptic membrane
ex. NO relax smooth muscle
ex. neuropeptides and endorphins inhibit pain signals in CNS
24
Q
neural integration
A
- brain cells are connected allow for complex integration
- trade-off: chem transmission involves synaptic delay and makes info travel slower if no synapse
25
postsynaptic potentials
- neural integration based on postsynaptic potentials in cell recieving chemical signals
- glutamate and aspartate produce APSPs in brain cells
- glycine and GABA produce IPSPs
- ex. ACh which excites skeletal but inhibits cardiac muscles
26
inhibitory postsynaptic potential
cell voltage becomes more negative than at rest, less likely to fire and can result from Cl entry or K exit from cell
27
Parkinsons
-degeneration of dopamine-releasing neurons (normally prevents excessive activity in motor centers)
- pill- rolling motion
28
Alzheimers
- atrophy of folds in cerebral cortex
- neurofibrillary tangles and senile plaques
- formation of amyloid protein from breakdown product of plasma membranes
29
immediate memory
sense of present
30
short term memory
working memory for taking action
31
explicit/ declarative LTM
memory you can put into words
32
implicit LTM
reflexive/unconscious memory, procedural (motor skills) and emotional memories
33
synaptic plasticity
ability of synapses to change
34
synaptic potentiation
process of making transmission easier
35
presynaptic facilitation
increase necessary synaptic transmission
36
presynaptic inhibition
reduce/ halts unwanted synaptic transmission
37
temporal summation
EPSPs add up to voltage threshold and triggers AP
