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dumb brain > 2 - Cells and Signalling > Flashcards

2 - Cells and Signalling Flashcards

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1
Q

what are multi, bi, and unipolar neurons

A

m: one axon has many dendrites
b: one axon has one dendritic tree
u: one stalk from soma

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2
Q

define axoplasmic transport

A

active process (ATP) moving substances from one axon end to the other via microtubules

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3
Q

what directions are antereo and retrograde transport

A

antero: soma to terminal buttons
retro: vice versa

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4
Q

define glia

A

supporting cells of the CNS by surrounding neurons and holding them in place

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5
Q

functions of glia cell

A

destroy/remove dead neurons
insulate neurons from each other so signals don’t mix
nutrient control

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6
Q

what processes do astrocytes (macroglia) control

A

neuron structural support
produce chemicals needed by neurons
provide nutrients

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7
Q

what things do astrocytes regulate

A

oxygen, glucose sypply to neurons, phosphate ions

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8
Q

what cells are involved in phagocytosis

A

astrocytes as form scar tissue when dead tissue removed

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9
Q

roles of oligodendrocytes

A

support CNS axons by forming semi-rigid tissue between neurons, provide myelin sheath and nutrients

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10
Q

what do oligodendrocytes produce

A

processes: they wrap around axon segments to produce myelin

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11
Q

what cells act as macrophages

A

microglia to protect brain from debris and bacteria

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12
Q

what are the roles of microglia

A

primary inflammatory response
remodelling NS during development
secreting chemicals when glia and blood vessels form

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13
Q

roles of ependymal cells

A

form lining for ventricles and central canal of the spinal cord
secrete/circulate CSF

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14
Q

what are satellite glial cells sensitive to and associated with

A

injury-sensitive

assoc w neuropathological states like pain

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15
Q

how do satellite glial cells regulate extracellular chemical environments

A

protect, nourish, maintain neurons

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16
Q

where are satellite glia found

A

PNS’ sensory, sympathetic, and parasympathetic ganglia

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17
Q

how are Schwann cells different to oligodendrocytes when forming the myelin sheath

A

Schwann cell one axon each in PNS and whole cell surrounds axon

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18
Q

define blood-brain barrier

A

selectively permeable barrier between blood and brain produced by brain’s blood capillary wall cells

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19
Q

why can’t some substances pass through the brain-blood barrier

A

capillary fenestrations too small for some to pass through so food chemicals affecting composition can’t pass

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20
Q

what does the brain-blood barrier maintain

A

extracellular fluid composition to prevent message transmission in the brain from being disupted

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21
Q

what types of substances can pass through the barrier

A

small, lipid soluble, not highly charged

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22
Q

define action potential

A

electrical signal carrying message in axon from soma to axon terminals

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23
Q

when the brain is trying to initiate inhibition, to prevent reflexes for example, how does it work

A

IPSPs produced from inhibitory NTs released in synapse

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24
Q

resting potential

A

-70mV

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25
Q

threshold

A

-55mV

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26
Q

where is potassium normally

A

intracellular due to positive extracellular charge

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27
Q

where is chlorine usually

A

higher conc extracellular as intracellular is negatively charged

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28
Q

where is sodium usually

A

higher conc extraceullar so diffuses into the axon

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29
Q

what happens when the threshold is released and voltage-gated sodium ion channels open

A

influx of sodium ions inside the axon leading to depolarisation as +40mV reached

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30
Q

when do the VG K+ channels open

A

after Na+ diffuses in so K+ diffuses out

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31
Q

why do VGK+ ion channels let K+ leave the cell

A

electrostatic pressure is too positive intracellular and membrane potential has decreased

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32
Q

when do VGNa+ channels reset

A

when resting potential reached

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33
Q

why does hyperpolarisation occur

A

too much K+ diffused out so VGK close and NaK pump works

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34
Q

what does the NaK pump do

A

cause resting potential to be reached to remove 3 Na+ and allow in 2 K+

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35
Q

describe the rate law

A

strong stimulus means a high rate of firing and strong muscular contraction

36
Q

define saltatory conduction

A

AP passes over nodes of Ranvier on myelinated axons and is faster as less diffusion

37
Q

what two factors affect speed of action potential transmission

A

temperature and axon diameter (wider = less resistance)

38
Q

define PSP

A

brief hyperpolarisations of depolarisations which increase or decrease a post-synaptic neuron’s rate of firing

39
Q

how do axoaxonic alter the amount of neurotransmitters released by post-synaptic axons

A

presynaptic modulation, inhibition, and facilitation

40
Q

what are ionotropic receptors

A

receptors allowing direct activation through a specific nt binding to the binding side of the nt-dependent ion channel to open it

41
Q

what are metabotropic receptors’ role

A

using metabolic energy, a G protein is activated when the nt binds to the receptor, activating an enzyme producing a secondary messenger to open the ion channel by attaching to it

42
Q

differences between ionotropic and metabotropic receptors

A

iono is fast, metabo is slow but amplifying

43
Q

how do EPSPs cause depolarisation

A

open Na+ channels so Na enters increasing voltage

44
Q

how do IPSPs work

A

K+ channels open so K+ leaves so intracellular is more negative

45
Q

what happens if inhibitory neurotransmitters open Cl- ion channels

A

resting: nothing
depolarisation: Cl- goes in to return it to resting potential and counteract EPSPs

46
Q

define neural integration

A

interaction of effects of exc/inhib neurons of a certain neuron

47
Q

what happens when EPSPs are produced

A

transmit down dendrites across to axon hillock then axon fires if strong enough

48
Q

what do autoreceptors on pre-synaptic neurons do

A

synthesising and releasing neurotransmitters, which can be inhibitory if over-producing or release more if not enough

49
Q

define reuptake

A

axon terminal rapidly removing neurotransmitters from the synaptic cleft

50
Q

3 forms of reuptake

A

enzymes, diffusion then taken up by other cells, pre-synaptic neuron reuptake channels to be reused

51
Q

acetylcholine pathways and health links

A

pons, hippo, basal forebrain

AD, smoking, myasthenia

52
Q

acetylcholine enzymes and receptors

A

ChAT (syn), AChE (bd)
iono (nicotinic)
metabo (muscarinic)

53
Q

glutamate receptors

A

iono (NMDA, AMPA, kainate)

metabo (mGluR)

54
Q

glutamate enzymes

A

glutaminase syn from glutamine

glutamine in astro brkdn to glutamine

55
Q

glutamate health links

A

suicide
treats epilepsy, anxiety
anaesthetics
alcohol mediation

56
Q

how can glutamate be blocked and what reduces it but increases GABA

A

ket blocks

lithium

57
Q

what type of receptors are D1 like and D2 like

A

metabotropic

58
Q

GABA enzymes

A

cyt glutamic acid decarboxylase syn from glutamine

brkdn same as glutamate

59
Q

GABA receptors

A

iono (GABA A)

metabo (GABA B)

60
Q

GABA health links

A

treats epilepsy, anxiety, mediates alcohol
suicide links
anaesthetic

61
Q

dopamine synthesising enzymes

A

tyrosine hydroxase: L-DOPA from tyrosine

DOPA decarboxylase converts L-DOPA to dop

62
Q

dopamine and noradrenaline breakdown enzymes

A

MAO

COMT

63
Q

noradregergic pathways are where

A

locus coeruleus and project fibres around the cortex

64
Q

noradrenaline synthesising enzymes do what after dopamine synthesis occurs

A

dopamine beta hydroxylase converts to it

65
Q

noradrenaline and serotonin receptors

A

metabo
na has alpha and beta
5HT has many

66
Q

serotonin pathways

A

raphe nuclei all over the brain

67
Q

serotonin synthesis enzymes

A

typtophan converted to S-hydroxytryptophan by tryptophan hydroxylase to S-hydroxytryptomine by aromatic amino acid decarb

68
Q

define drug effects

A

physiological changes observed in animals

69
Q

define pharmokinetics

A

process of absorbing, distributing, metabolising, and excreting the drug

70
Q

how can certain steps in the drug pathway be changed

A

give more chemicals needed to synthesise the nt
change enzyme effectiveness
alter metabolism
change amount released and removed

71
Q

describe oral admin

A

tablets and pills absorbed by stomach before being broken down by enzymes and metabolised in the brain

72
Q

describe intravenous

A

faster onset effect and gets to brain in a few seconds

73
Q

describe tolerance

A

drugs no longer effective as body compensates disturbance to optimal levels

74
Q

describe withdrawal symptoms

A

symptoms opposite to ones produced by drugs when taken repeatedly then suddenly stop

75
Q

what may drugs inactivate and bind to

A

transporter molecules reuptaking

enzymes to change shape

76
Q

describe phase I

A

small # of healthy volunteers use to work out tolerance, side effects, safety, determine range of doses for clinical effect and assess pharmacokinetics

77
Q

describe phase II

A

small # with relevant condition to test tolerance, safety, and efficiency in double blind trial

78
Q

describe phase III

A

same as phase II but w more patients to test against standard treatment and apply for human use licence if successful

79
Q

describe phase IV

A

licence granted and large # of patients tested on for side effects, long term evaluation, and safety

80
Q

define electrolyte

A

substance split into one positive and one negative end

81
Q

how do anions and cations exert electrostatic pressure

A

a/c attracting each other
anions repelling
cations repelling

82
Q

what is spina bifida

A

sac forming on the spine due to the neural tube doesn’t close

83
Q

what types of spina bifida are there from least to most severe

A

occulta, meningocele, myelomeningocele

84
Q

risk factors of spina bifida

A

obese mother, white, baby being female

85
Q

where does the sac need to be to cause paralysis

A

top of the spine

if at bottom then incontinence and minor problems

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