9.2 Flashcards

(44 cards)

1
Q

peripheral nervous system

A

afferent
-sensory
efferent
-motor

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2
Q

central nervous system

A

central -brain and spinal chord
peripheral - pairs of nerves which originate from the brain or spinal chord

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3
Q

efferent nervous sytem

A

somatic
-under voluntary control
autonomic
-involuntary

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4
Q

autonomic nervous system

A

sympathetic
-positive stimulation
-speed up
-fight or flight
parasympathetic
-inhibitory
-slows down activity
-resting and digesting

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5
Q

compare and contrast sym and para

A

sim -
NS fibres leave the CNS in a ganglion (collection of nerve fibres)
dis-
sym, ganglia close to the CNS
para, ganglia close to the effector organ y

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6
Q

compare and contrast sym and para funtions

A

sym
-produces noradrenaline
-fight or flight response
-activated in times of stress or active
-adrenergic synapses

para
-slower, inhibitory effect
-acetychloine neurotransmitter produced
-maintains normal functioning of the body
-chloinergic synapses

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7
Q

resting potential

A

inside of the axon is negatively charged compared to the outside of the axon
outside ions more concentrated
axon is polarised
-70mV

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8
Q

sodium pottasium pump

A

requires energy
3 Na+ ions moved out of the membrane for every 2 K+ ions in
ATPase in pump uses ATP to move cations

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9
Q

how is resting potential maintained

A

sodium pottasium pump
Na+ out K+ in
K+ move through pottasium chanells
NA chanells close
outside more positive than inside

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10
Q

action potential

A

stimulus is recieved
causes a tempary reversal of the charge on the axon membrane - inside less negative
moves to about +40mv
membrane depolarised

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11
Q

depolarisation

A

-resting potential some k voltage-gated channels are open but Na channels are closed
-the stimulus causes some Na gates in the axon membrane to open and therefore some sodium ions move into the axon via facilitated diffusion
as they are +vly charged they trigger a reversal in the pd
-as it is more +ve more voltage-gated sodium channels open - +ve feedback
-once the action potential is around +40mv the voltage-gated sodium ion channels close
-excess sodium ions are pumped out by Na-K pump

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12
Q

repolarisation

A

-voltage-gated potassium channels open so K ions move out the axon by facilitated diffusion down the conc grad
-cell is repolarised and becomes more negative

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13
Q

hyperpolarisation

A

-more potassium flows out
- the inside is more negative than the outside so more negative than the resting potential

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14
Q

after hyperpolarisation

A

gates on K+ channels now close and Na-K pumps Na to be out and K in
-70 mv is reestablished

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15
Q

action potential simplified

A

Na+ voltage gated channels open
Na+ diffuse rapidly into axon
potential difference reversed
Na+ voltage gates close
K+ voltage gated chanells open
K+ diffuse out of axon
inside axon returns to negative
resting potential restored

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16
Q

absolute refractory period

A

sodium chanells are completly blocked and the resting potential hasnt been restored
milisecond
second stimulus will not trigger a second action potential

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17
Q

relative refractory period

A

pottasium chanells are able to repolarise the membrane and pottasium ions difuse out of axon
Normal resting potential can not be restored until these K channels are closed.
Last several milliseconds.
During this time, a greater than normal stimulus is required to initiate an action potential.

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18
Q

refractory period

A

time taken for an area of the axon membrane to recover after an action potential
depends on
-Na/K pump
-membrane permeability to potassium ions

19
Q

purpose of a refractory period

A

enure action potentials are only in one direction
produce discrete impulses - action potentials are separated
limits the number of action potentials

20
Q

events at synapse

A

Action potential depolarises the presynaptic neuron.( increases the permeability )
Calcium channels open and calcium diffuses in down conc grad
Synaptic vesicles move to and fuse with the pre-synaptic membrane.
The neurotransmitter is released into the synaptic cleft.
Neurotransmitter moves across cleft by diffusion.
Neurotransmitter binds to specific protein receptors on the sodium channel on the post synaptic membrane..
Sodium channels open and sodium diffuses in.
This causes a change in the potential difference of the membrane and an excitatory post-synaptic potential (EPSP) to be set up.
if there are enough epsp the +ve charge exceeds the threshold level and an action potential is set up

21
Q

types of synapse

A

cholinergic
adrenergic
-use noradrenaline

22
Q

Inhibitory post-synaptic potential (IPSP)

A

is a kind of synaptic potential that makes a postsynaptic neuron less likely to generate an action potential.
Here, different ion channels open in the membrane, allowing inward movement of negative ions.
This makes the post-synaptic cell more negative than normal resting potential.
This means an action potential is less likely to occur.

23
Q

saltatory conduction

A

mylenated neurones ions can only pass in and out of the axon freely at the nodes of ranvier
action potential can only occur at the nodes
so apear to jump
speed up transmition as the ionic movemetns happen less frequently taking less. time

24
Q

transmission in unmylenated axons

A

A current (change in potential difference) occurs in a part of the neuron.
This is detected in the adjacent part of the membrane.
When it detects the current, it causes voltage gated channels to open and an action potential will occur when the threshold is reached.
The nerve impulse is transmitted as a self-propagating wave of depolarisation.

25
mylenated nerves
schwann cell membrane wraps around cell many times to form mylein sheith gaps called nodes of ranvier -speeds up transmittion and protects from damage
26
factors affecting nerve impulses
mylenation axon diamater -speed of transmission temperatures -rate of diffusion increases
27
breakdown of neurotransmitters
Neurotransmitters are broken down by hydrolytic enzymes in the synaptic cleft They then move back across the cleft, back into the synaptic knob, and are recycled.
28
acethycholine
Acetylcholine is the neurotransmitter which is found at the majority of synapses in humans. nerves using acetylcholine are called cholingernic nerves usually results in excitation at the post synaptic membrane After it attaches to the receptors on the sodium channels, it is broken down by an enzyme called acetylcholinesterase. It hydrolyses acetylcholine into separate acetate and choline. The acetyl and choline diffuse back across the cleft into the presynaptic neuron. This allows the neurotransmitter to be recycled.
29
affects of drugs increasing the response
-increases amount of neurotransmitter -increases release of neurotransmitter from vesicles at the presynaptic membrane -binds to post-synaptic receptors and activates them or increases affect of normal neurotransmitter -prevents the degradtion of neurotransmitter by enzymes or prevents reuptake into presynaptic knob
30
affects of drugs decreasing the response
-blocks synthesis of neurotransmitter -causes neurotransmitter to leak from vesicles and be destroyed by enzymes -prevents releases of neurotransmitter from vesicles -blocks receptors and prevents neurotransmitter binding
31
nicotine
-mimics the effect of acetylcholine and binds to specific receptors in post synaptic membranes -triggers action potential -receptor remains unresponsive for some times -raised heart rate and blood pressure -triggers release of neurotransmitter dopamine
32
lidocaine
-anastethic block voltage-gated sodium chanells preventing action potential - no pain -prevent heart arthimias raises depolarisation threshold so prevents early or extra action potentials
33
cobra venom
toxic and fatal -binds reversibly to acetylcholine receptors in post synaptic membranes and neuromuscular junctions -prevents the transmission of impulses across synapses -including neuromuscular junctions between motor neurons and muscles -muscles not stimulated to contact and person becomes gradually paralysed when reaches muscles for breathing causes death - in low doses can relax muscles of trachea and bronchi in asthma attacks
34
transduction in the eye
converts light into nerve impulses occurs in the retina by cones and rods which are attached to receptors
35
rod cells
spread evenly across retina more rod than cone provides images in black and white -cant distinguish between wavelengths detect at low intensity certain threshold must be detected before a generator potential can occur cannot distingush between close together things as only one impulse is generated connected to bipolar neurone - sensory neuron - optic nerve
36
generator potential
generated by the breakdown of the pigment rhodopsin- bleaching (low light intensities) when bleaching occurs Na ion channels close sodium pump still works so sodium ions removed inside rod cells more negative that normal as hyperpolarisation occurs this is a generator potential if meets threshold can cause action potential rhodopsin must be resythesised before can occur again do not follow the all or nothing rule
37
retianal convergence
allows a generator potential to be reached with low levels of stimulus
38
cone cells
tightly packed in fovea 3 different types for dif wavelengths seperqate bipolar neurones high light intensity can distinguish between seperate sources high light intensity breaks down iodopsin different types of iodoposin larger stimulus required to reach generator potential
39
fovea
part where the light is focused on recieves greatest intensity no rod cells
40
bleaching
Rhodopsin is formed from opsin and retinal. Retinal exists as 2 different isomers: cis-retinal & trans-retinal. In the dark all retinal is in the cis form. When a photon of light hits the rhodopsin, it converts from cis to trans form. This changes the shape of the retinal and puts strain on the bonding between opsin and retinal, breaking up the molecule.
41
nervous system structure
neurons transmit impulses from receptor cells to effector cells or groups of them called sense organs 3 types of neurone
42
eye structure
43
brain structure
44
spinal chord