Lect 2 - neuro excitation/inhibition/modulation Flashcards

what makes thing ex or in Glu GABA ACh ionotropic metatropic (34 cards)

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

17
Q

why is there a delay in repolarization with NMDA receptors

18
Q

what are the types of metabotropic glutamate receptors

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
how are metabotropic glutamate receptors different
metatropic means signal requires second messenger. Glu meta receptors function in the perisynaptic membrane there are different subtypes, one of which is autoreceptor
26
difference between nicotinic and muscarinic, where are they found
nicotinic - ionotropic ACh receptor found in NMJ CNS muscarinic - metabotropic ACh receptor efferents innervating the heart
27
what are the 2 types of inhibitory synapses
GABA | Glycine
28
what are interneurons
neurons that are within the same nuclei
29
how is GABAa and GABAb different, where are they located
GABAa is ionotropic GABAb is metabotropic GABAa is fast in CNS GABAb is slow in CNS
30
what are the 5 type of modulatory synapses
1. gasses 2. biogenic amines 3. purines 4. peptides 5. lipid
31
what are some examples of biogenic amines
dopamine noradrenaline serotonin histamine
32
what are the roles of these basic amines
setting global states such as arousal, attention, mood
33
what is an example of modulatory purine
ATP, which is coreleased with NT | ATP modifies the action of other transmitters such as NA, DA, Glu, GABA
34
how does cannibis affect the brain
through G-protein coupled receptors reduce the opening of Ca channels, this leading to reduce in Glu or GABA