Lect 2 - neuro excitation/inhibition/modulation Flashcards

what makes thing ex or in Glu GABA ACh ionotropic metatropic

1
Q

differentiate between excitatory, inhibitory, and modulatory

A

excitatory - increase excitability of the cell

inhibitory - makes resting membrane less likely to depolarise

modulatory - indirectly change excitability of the pre or postsynaptic membrane without having direct effects

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2
Q

what is reversal potential, what’s its relationship to the quilibrium potential, does it differ between excite and inhib reps

A

reversal potential is the membrane potential at which there is no net movement of ions across the membrane

it is the same as the equilibrium potential

lower Erev mean that the membrane is capped at that voltage therefore if threshold is higher than it, the postsynaptic response is more likely to be an IPSP

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3
Q

which one is bigger, ESPS or EPP? what consequences does this have on ESPS

A

EPSP is much smaller, so EPSP must always be summed for it to have an effect. EPP are much larger and is fail-safe in that it will always have an excitory postsynpatic response

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4
Q

what is an example of excitatory NT

A

gluatmatergic, e.g. glutamate or aspartate

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5
Q

what is an example of modulatory NT

A

norepinephrine

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6
Q

how is modulatory synapse different to the other two

A

modulatory synapse doesn’t have direct effect on synapse, but makes them more or less sensitive

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7
Q

describe the typical characteristic of modualtory synapse, why do we need them

A

generally mediated by slower metatropic receptors (G-protein coupled receptors)

hence they are slower and last longer, they will undergo signal amplification.

there is also more potential and flexibility to vary excitability

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8
Q

what happens when K channels are closed

A

cells harder to depolarise, leading to greater excitablity

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9
Q

compare what happen in excitation vs inhibition in terms of ion channels openning

A

excitation: we dont want K to go, we dont want Cl to come in

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10
Q

what is the presynaptic effect

A

reduced NT release or production

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11
Q

list some types of NTs, what are some differences between them

A

gases, amino acids, monamines, catcholamines, purines, lipid metabolites, peptides

amino acids and biogenic amines are small and fast acting

peptides are slower acting but have long term change

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12
Q

what are the 3 ways by which NT signals achieve its effect

A
  1. ligand-gated (fastest, 1 bound receptor = 1 open channel)
  2. amplification by membrane pathway aka G-protein
  3. amplification by signally cascade, longer term change
    (e. g. bound receptor -> alpha-subunits -> make many cAMPs -> protein -> protein kinase opens heaps of channels)
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13
Q

what are examples of inotropic receptors

A

a

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14
Q

differentiate between ionotropic and metatropic

A

a

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15
Q

describe the glutamate cycle

A

a

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16
Q

what are the 3 main ionotropic glutamate receptors

A

a

17
Q

why is there a delay in repolarization with NMDA receptors

A

a

18
Q

what are the types of metabotropic glutamate receptors

A

a

19
Q

describe the typical exitatory synpase

A

most of them use glutamatergic

opens non-selective Na/K ion channels (fast)

increase excitabiliyt of membrane

20
Q

describe the typical inhibitory synpase

A

most use GABAergic or glycinergic, e.g. GABA or glycine

also mediated by fast ionotropic receptors

IPSP by opening Cl channels - negative keeps the cell polarised, they keep membrane voltage away from potential threshold

in reality, the excitability of most neurons is determined by the balance of excitory and inhibitory

21
Q

what are the two types of excitatory synapses?

A

glutamatergic - glutamate

cholinergic - ACh

22
Q

why is glutamate controlled, and how is it controlled

A

highly toxic, controlled via uptake, using e.g. astrocytes

EAAT transports glutamate to either glial cells, where it is made into glutamine, or back into the presynaptic terminal for reuse

23
Q

what are the 3 ionotropic glutamate receptors, and what are their characteristics

A
  1. AMPA - for fast stuff
  2. NMDA - synaptic plasticity (therefore need to be slow)
  3. Kainate - regulates release of GABA
24
Q

compare AMPA with NMDA

A

AMPA - nice and fast, open even with negative membrane potential

NMDA - slower acting, opens when Vm is more positive (because of Mg plug). this brings in Ca which signals long term change

NMDA is like a coincidence detector, important for plasticity and developent

25
Q

how are metabotropic glutamate receptors different

A

metatropic means signal requires second messenger.

Glu meta receptors function in the perisynaptic membrane

there are different subtypes, one of which is autoreceptor

26
Q

difference between nicotinic and muscarinic, where are they found

A

nicotinic - ionotropic ACh receptor
found in NMJ CNS

muscarinic - metabotropic ACh receptor
efferents innervating the heart

27
Q

what are the 2 types of inhibitory synapses

A

GABA

Glycine

28
Q

what are interneurons

A

neurons that are within the same nuclei

29
Q

how is GABAa and GABAb different, where are they located

A

GABAa is ionotropic
GABAb is metabotropic

GABAa is fast in CNS
GABAb is slow in CNS

30
Q

what are the 5 type of modulatory synapses

A
  1. gasses
  2. biogenic amines
  3. purines
  4. peptides
  5. lipid
31
Q

what are some examples of biogenic amines

A

dopamine
noradrenaline
serotonin
histamine

32
Q

what are the roles of these basic amines

A

setting global states such as arousal, attention, mood

33
Q

what is an example of modulatory purine

A

ATP, which is coreleased with NT

ATP modifies the action of other transmitters such as NA, DA, Glu, GABA

34
Q

how does cannibis affect the brain

A

through G-protein coupled receptors

reduce the opening of Ca channels, this leading to reduce in Glu or GABA