Neuronal communication II Flashcards

1
Q

receptors in postsynaptic neuron can be:

A
  • ionotropic

- metabotropic

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2
Q

ionotropic receptors: features

A
  • closed state until NT binds to receptor -> change shape
  • allow passage of charged ions
  • rapid opening of channel
  • ligand dissociates from receptor and channel closes
  • postsynaptic potential (PSP, graded potential lasts few ms)
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3
Q

metabotropic receptors: direct coupling

A
  • G protein coupled receptors (GPCRs)
  • membrane proteins coupled to ion channels through messenger molecules (G proteins)
  • direct coupling: activated G protein subunit acts as ligand for ion channel
  • slow acting (secs)
  • longer lasting PSP
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4
Q

metabotropic receptors: indirect coupling

A
  • G protein activates/ inhibits enzyme that causes changes in intracellular conc of secondary messenger molecule (ligand)
  • 2ndary messenger binds to ion channels -> open/ close
  • slower acting (secs)
  • longer lasting PSP
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5
Q

postsynaptic potentials (PSPs):

A
  • each presynaptic neuron generally releases only 1 type of NT
  • depending, postsynaptic neuron membrane potential either polarised or depolarised
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6
Q

excitatory synapses: EPSPs - ionotropic

A
  • fast response mediated by ionotropic receptors
  • binding of NT causes nonspecific ion channels (Na, K) in membrane to open
  • depolarised (Na flowing in more)
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7
Q

excitatory synapses: EPSPs - metabotropic

A
  • slow response
  • NT activates G protein -> activates membrane bound enzyme adenylate cyclase
  • ATP -> cAMP (2ndary messenger)
  • interior of postsynaptic cell depolarised (adds phosphate to K selective ion channels and closes)
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8
Q

inhibitory synapses: IPSPs - ionotropic K channels

A
  • fast
  • ligand/ NT binds to receptor
  • K ion channels open
  • K leaves cell
  • hyperpolarised inside postsynaptic cell
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9
Q

inhibitory synapses: IPSPs - ionotropic Cl channels

A
  • fast
  • ligand binds to receptor (eg. GABA to GABA a)
  • hyperpolarised
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10
Q

inhibitory synapses: IPSPs - metabotropic receptors

A
  • slow
  • ligand binds to metabotropic receptors
  • activation of G protein causes enzymatic cascade= opening K channels
  • hyperpolarisation (K leaves cell)
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11
Q

synaptic circuitry:

A
  • neurons communicate w each other and effector organs

convergence:
- axon terminals converge/ synapse w single neuron

divergence:
- axon from single neuron branches out and synapses w many other neurons

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12
Q

multiple EPSPs required to generate depolarisation that reaches threshold needs:

A
  • temporal summation

- spatial summation

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13
Q

collective potential of summation (both excitatory and inhibitory) at axon hillock

A
  • grand postsynaptic potential (GPSP)
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14
Q

temporal summation:

A

one synapse through time

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15
Q

spatial summation:

A
  • several synapses at same time
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16
Q

neuron receives types of synaptic input:

A
  • axodendritic
  • axosomatic
  • axoaxonic
17
Q

axodendritic and axosomatic synapses:

A
  • postsynaptic facilitation or inhibition

- nonselective effect on postsynaptic neuron through generation of EPSPs or IPSPs

18
Q

axoaxonic synapses:

A
  • presynaptic facilitation or inhibition

- selective effect on NT release by presynaptic cell at 1 particular synapse

19
Q

synaptic modulation/ plasticity:

A
  • efficiency of synaptic transmission is dynamic (esp chemical synapses)
  • synaptic strength can be modified over short/ long time scales
  • strength altered by physiological, molecular and structural changes
  • essential for strengthening functional circuits during development
  • changes in synaptic strength -> basis of learning and memory
20
Q

forms of synaptic plasticity:

A
  • heterosynaptic (extrinsic) plasticity

- homosynaptic (intrinsic) plasticity

21
Q

define extrinsic plasticity:

A
  • changes in strength of synapse due to activity in other pathways:
  • presynaptic facilitation/ inhibition
22
Q

define intrinsic plasticity:

A
  • changes in strength of synapse due to its own activity:
  • synaptic facilitation (short/long term effects)
  • synaptic depression (short/long term effects)
23
Q

heterosynaptic plasticity: axoaxonic synapses function as

A
  • modulatory synapses

- presynaptic facilitation/ inhibition

24
Q

heterosynaptic plasticity: presynaptic facilitation

A
  • activating modulatory neuron causes greater release of NT from normal excitatory neuron is active
25
Q

heterosynaptic plasticity: presynaptic inhibition

A
  • activating modulatory neuron causes reduction of NT released when normal excitatory neuron is active
26
Q

homosynaptic plasticity: short term enchancement

A
  • postsynaptic potentials get larger w subsequent action potentials
  • paired pulse facilitation (PPS) ms
  • augmentation (secs) and post tetanic potentiation (PTP) mins
27
Q

homosynaptic plasticity: short term depression

A
  • postsynaptic potentials get smaller w subsequent APs
  • paired pulse depression (secs)
  • post tetanic depression (mins)
28
Q

homosynaptic plasticity: long term plasticity

A
  • long term potentiation (LTP) long lasting increase in synaptic strength following repeated stimulation
  • long term depression (LTD) long lasting decrease in strength
29
Q

short term enhancement: paired pulse facilitation

A
  • increased amplitude of postsynaptic potential induced by AP that arrives within few ms of previous identical AP
  • residual Ca accumulated in cell following first AP increases no. of NT filled vesicles released by presynaptic terminal -> synaptic cleft
  • larger PSP
  • last ms
30
Q

short term enhancement: augmentation and post tetanic potentiation

A
  • repetitive high frequency (>1 Hz) and long lasting stimulation of presynaptic neuron
  • raised Ca conc activates enzymes -> increase no. and size of NT vesicles
  • larger PSP in post synaptic cell
  • last several secs (augmentation) or minutes (PTP)
31
Q

short term depression: paired pulse depression

A
  • decreased amplitude of PSP induced by AP that arrives within few ms of previous identical AP
  • first AP depolarises cell
  • cause Ca influx
  • subsequent AP will depolarise cell but no. of vesicles readily available for release into synapse are reduced
  • less NT released
  • smaller PSP in postsynaptic cell
32
Q

short term depression: post tetanic depression

A
  • reduction of amplitude of PSP during and after repeated stimulation
  • inactivation of presynaptic voltage gated Ca channels from repeated stimulation
  • reduced influx of Ca during depolarisation
  • less NT released
  • smaller PSPs
33
Q

autoreceptors:

A
  • feedback mechanism to modulate release of NT
  • receptors on axon terminals of presynaptic neuron that bind ligands (NTs) released by same presynaptic cell (autocrine signalling)
  • eg. dopaminergic neurons use NT dopamine
34
Q

dopamine autoreceptors:

A
  • dopamine release stimulates postsynaptic cell but also metabotropic dopamine autoreceptors on presynaptic axon terminal
35
Q

dopamine autoreceptors: short term effects

A
  • G protein mediate increase K+ and decrease Ca reduce ability of terminal to depolarise in response to further AP
  • increased uptake of dopamine from synaptic cleft = reduced stimulation of postsynaptic cell
36
Q

dopamine autoreceptors: long term effects

A
  • decreased synthesis/ packaging of dopamine into vesicles cause reduction in release of dopamine in response to AP and reduced stimulation of postsynaptic cell
  • negative feedback to reduce dopamine release