2 - Cells and Signalling Flashcards

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
threshold
-55mV
26
where is potassium normally
intracellular due to positive extracellular charge
27
where is chlorine usually
higher conc extracellular as intracellular is negatively charged
28
where is sodium usually
higher conc extraceullar so diffuses into the axon
29
what happens when the threshold is released and voltage-gated sodium ion channels open
influx of sodium ions inside the axon leading to depolarisation as +40mV reached
30
when do the VG K+ channels open
after Na+ diffuses in so K+ diffuses out
31
why do VGK+ ion channels let K+ leave the cell
electrostatic pressure is too positive intracellular and membrane potential has decreased
32
when do VGNa+ channels reset
when resting potential reached
33
why does hyperpolarisation occur
too much K+ diffused out so VGK close and NaK pump works
34
what does the NaK pump do
cause resting potential to be reached to remove 3 Na+ and allow in 2 K+
35
describe the rate law
strong stimulus means a high rate of firing and strong muscular contraction
36
define saltatory conduction
AP passes over nodes of Ranvier on myelinated axons and is faster as less diffusion
37
what two factors affect speed of action potential transmission
temperature and axon diameter (wider = less resistance)
38
define PSP
brief hyperpolarisations of depolarisations which increase or decrease a post-synaptic neuron's rate of firing
39
how do axoaxonic alter the amount of neurotransmitters released by post-synaptic axons
presynaptic modulation, inhibition, and facilitation
40
what are ionotropic receptors
receptors allowing direct activation through a specific nt binding to the binding side of the nt-dependent ion channel to open it
41
what are metabotropic receptors' role
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
differences between ionotropic and metabotropic receptors
iono is fast, metabo is slow but amplifying
43
how do EPSPs cause depolarisation
open Na+ channels so Na enters increasing voltage
44
how do IPSPs work
K+ channels open so K+ leaves so intracellular is more negative
45
what happens if inhibitory neurotransmitters open Cl- ion channels
resting: nothing depolarisation: Cl- goes in to return it to resting potential and counteract EPSPs
46
define neural integration
interaction of effects of exc/inhib neurons of a certain neuron
47
what happens when EPSPs are produced
transmit down dendrites across to axon hillock then axon fires if strong enough
48
what do autoreceptors on pre-synaptic neurons do
synthesising and releasing neurotransmitters, which can be inhibitory if over-producing or release more if not enough
49
define reuptake
axon terminal rapidly removing neurotransmitters from the synaptic cleft
50
3 forms of reuptake
enzymes, diffusion then taken up by other cells, pre-synaptic neuron reuptake channels to be reused
51
acetylcholine pathways and health links
pons, hippo, basal forebrain | AD, smoking, myasthenia
52
acetylcholine enzymes and receptors
ChAT (syn), AChE (bd) iono (nicotinic) metabo (muscarinic)
53
glutamate receptors
iono (NMDA, AMPA, kainate) | metabo (mGluR)
54
glutamate enzymes
glutaminase syn from glutamine | glutamine in astro brkdn to glutamine
55
glutamate health links
suicide treats epilepsy, anxiety anaesthetics alcohol mediation
56
how can glutamate be blocked and what reduces it but increases GABA
ket blocks | lithium
57
what type of receptors are D1 like and D2 like
metabotropic
58
GABA enzymes
cyt glutamic acid decarboxylase syn from glutamine | brkdn same as glutamate
59
GABA receptors
iono (GABA A) | metabo (GABA B)
60
GABA health links
treats epilepsy, anxiety, mediates alcohol suicide links anaesthetic
61
dopamine synthesising enzymes
tyrosine hydroxase: L-DOPA from tyrosine | DOPA decarboxylase converts L-DOPA to dop
62
dopamine and noradrenaline breakdown enzymes
MAO | COMT
63
noradregergic pathways are where
locus coeruleus and project fibres around the cortex
64
noradrenaline synthesising enzymes do what after dopamine synthesis occurs
dopamine beta hydroxylase converts to it
65
noradrenaline and serotonin receptors
metabo na has alpha and beta 5HT has many
66
serotonin pathways
raphe nuclei all over the brain
67
serotonin synthesis enzymes
typtophan converted to S-hydroxytryptophan by tryptophan hydroxylase to S-hydroxytryptomine by aromatic amino acid decarb
68
define drug effects
physiological changes observed in animals
69
define pharmokinetics
process of absorbing, distributing, metabolising, and excreting the drug
70
how can certain steps in the drug pathway be changed
give more chemicals needed to synthesise the nt change enzyme effectiveness alter metabolism change amount released and removed
71
describe oral admin
tablets and pills absorbed by stomach before being broken down by enzymes and metabolised in the brain
72
describe intravenous
faster onset effect and gets to brain in a few seconds
73
describe tolerance
drugs no longer effective as body compensates disturbance to optimal levels
74
describe withdrawal symptoms
symptoms opposite to ones produced by drugs when taken repeatedly then suddenly stop
75
what may drugs inactivate and bind to
transporter molecules reuptaking | enzymes to change shape
76
describe phase I
small # of healthy volunteers use to work out tolerance, side effects, safety, determine range of doses for clinical effect and assess pharmacokinetics
77
describe phase II
small # with relevant condition to test tolerance, safety, and efficiency in double blind trial
78
describe phase III
same as phase II but w more patients to test against standard treatment and apply for human use licence if successful
79
describe phase IV
licence granted and large # of patients tested on for side effects, long term evaluation, and safety
80
define electrolyte
substance split into one positive and one negative end
81
how do anions and cations exert electrostatic pressure
a/c attracting each other anions repelling cations repelling
82
what is spina bifida
sac forming on the spine due to the neural tube doesn't close
83
what types of spina bifida are there from least to most severe
occulta, meningocele, myelomeningocele
84
risk factors of spina bifida
obese mother, white, baby being female
85
where does the sac need to be to cause paralysis
top of the spine | if at bottom then incontinence and minor problems