Neuronal responses Flashcards

1
Q

where are the synapses located and name some axons

A
  1. Axosecteroy – axon terminal secretes directly into the blood stream
  2. Axoaxonic – axon terminal secretes into another axon
  3. Axodendritive – axon terminal ends on a dendrite spine – most common
  4. Axoextracellular – axon with no connection secretes into extracellular fluid
  5. Axosomatic – axon terminal ends on soma
  6. Axosynaptic – axon terminal ends on another axon terminal
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2
Q

describe basically what happens when the action potential arrives at the axon terminal

A
  1. Action potential arrive at the axon terminal
  2. Causes a change in the membrane charge
  3. This causes voltage gated calcium ion channels to open
  4. Calcium enters the cell
  5. Calcium signals to the vesicles
  6. Vesicles move to the membrane
  7. Docked vesicles release neurotransmitter by exocytosis
  8. Neurotransmitter diffuses across the synaptic cleft and binds to receptors
    - The response depends on what receptor that the neurotransmitter binds to
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3
Q

what does the response to neurotransmitters depend on

A

depends on the receptor type

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4
Q

what does the action potential generated depend on

A
  • depends if the receptor is inhibitor or excitatory

- depends in the neurotransmitter is inhibitor or excitatory

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5
Q

what does the release of ACh at neuromuscular junctions cause

A

it always gives an excitatory response

- all nicotinic acetylcholine responses are excitatory

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6
Q

what happens at most synapses

A

excitatory or inhibitory response

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7
Q

what kind of receptor type is the ligand gated sodium channel

A

nicotinic acetylcholine receptor

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8
Q

what has to happen for the action potential to be trigger

A

• For an action potential to be triggered the sum of all the inputs msut be above the threshold value
- action potential is only produced in the sum of all inputs is enough to depolarise the neurone above the threshold

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9
Q

what is an example of an EPSP

A
  • Increases membrane Na+ permeability causing depolarisation
  • E.g. nicotinic ACh receptor open cation channel leading to influx of sodium ions
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10
Q

what is an example of IPSP

A
  • Increases K+ permeability (moves out making outside more positive) or increase Cl- permeability (moves in so makes inside more negative) causing hyperpolarisation so that more sodium is required for the threshold value to be reached
  • E.g. muscarinic ACh receptor opens K+ channel g protein coupled acting by a 2nd messenger – M2 receptor on the heart
  • E.g. GABAA receptor directly open the Cl- channel this causes hyper polarisation and makes it more difficult get an excitatory post synaptic potential
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11
Q

what does an excitatory post synaptic potential do

A

increase sodium permeability

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12
Q

what does an inhibitor post synaptic potential do

A

increase potassium or chloride permeability

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13
Q

what happens in sub-threshold stimuli

A

• For sub-threshold stimuli no action potential will be generated if they do not overlap

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14
Q

what happens in temporal summation

A
  • rapid firing of a single input
  • second EPSP occurs before the first has died away
  • reaches threshold
  • post-synaptic neurone fires an action potential
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15
Q

what happens in spatial summation

A
  • stimulus activation from two inputs
  • the sum of the two EPSPs reaches threshold
  • post synaptic neurone fires an action potential
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16
Q

ISPSs can…

A

can cancel out ESPSs meaning no change in membrane potential and therefore no action potential is generated

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17
Q

describe the ligand gated ion channel

A
  • opens when ligand(neurotransmitter or drug) binds to it and opens the channel
  • ionotropic meaning it allows the ion directly in
  • response is in milliseconds
18
Q

describe an example of a ligand gated ion channel

A

• E.g. nicotininc ACh (requires 2 ACh molecules - permits na+ movement from synaptic cleft to post synaptic neurone),
- Glutamate NMDA and non-NMDA receptors, GABAA - inhibitory - glutamate binds to these receptors one the channel and allow for sodium and calcium to enter therefore it is excitatory
• Gaba – benzodiazepines for sleep and reducing anxiety cl- moves through channels on binding and hyperpolarises the neurone. Sedative, sleep inducing no action potentials as threshold isnnt reached and shuts off cns = calming effect and prevents overstimulation
the benzodiazepines bind to the GABAa receptor and cause the structural change

19
Q

describe the G protein coupled receptors

A
  • Metabotropic – needs some sort of energy
  • Activates a second message using the G protein (with or without using an enzyme such as adenylate cyclase for cAMP)
  • 7 transmembrane segments
20
Q

How do G protein coupled receptors respond to neurotransmitters

A
  • Ligand binds to receptor, activatesg protein- enzyme- 2nd messenger – phosphorylation events( protein kinase)
  • 2nd messengers transmit+ amplify signals from receptors to downstream target molecules – one messsenger can therefore lead to phosphorylation of many proteins
  • 3 different types of 2nd messnegers
  • Hydrophillia]ic water soluble – cAMP, cGMP, Ca2+
  • Hydrophobic water soluble – DAG and PIP3
  • Gases – NO, CO, ROS
  • Response in seconds
21
Q

what is an example of G protein receptor

A

Catalytic receptors enzyme linked – tyrosine kinase – ligands activate intrinsic intracellular enzyme activity, minutes for dimerisation, phosphorylation, 2nd messengers to occur

22
Q

Name what the intracellular receptors do

A

o Steriods, thyroid hormones, growth hormones- bind to receptor and form complex
o Bind to dna
o Affect dna transcription rates, changes production of functionally relevant proteins
o Slow responses

23
Q

What does adaptation do

A

prevents signal overload

24
Q

what does X mean

  • no adaption
  • slow adaption
  • rapid adaption
A
  • No adaptation – maintains initial potential – e.g. otoliths detecting head position
  • Slow adaptation – olfactory system (smells), Ruffini endings (stretching of the skin), Merkel cells (pressure texture)
  • Rapid adaptation – Pacician corpuscle (vibration and mechanical pressure), Meissner corpuscles (light touch – e.g. with clothes) notice start and end not in between
25
Q

what are the problems with perception

A

• Compression – only a set number of action potentials per second
• Transmission – all are the same intensity so only frequency can change
• Perception – information from the optic nerve is interpreted as light even if it is caused by pressure as axons go to specific parts of brain for processing
- sensation - information received by sensory receptors gets sent up to the brain

26
Q

the majority of synapses release…

A

2 or more different neurotransmitters, but they are packaged into different vesicles

27
Q

what do small clear core vesicles have in them

A

mall clear core vesicles generally amino acids and the amines (made locally in synapse) – acetylcholine, small neurotransmitters

28
Q

what do large dense core vesicles have in them

A
  • Large dense core vesicles neuropeptides and large neurotransmitters (made in cell body and transported)
29
Q

what type of receptors does glutamate use

A
  • inotropic or metabotropic receptors
30
Q

what are the skin sensory receptors and adaption

A
Messiner corpuscles
-	Light touch 
Merkel cells 
-	Pressure texture 
Pacinian corpuscle 
-	Vibration 
Ruffini endings 
-	Stretching of the skin
31
Q

what is adaption

A

Adaptation is a decrease in the size of the receptor potential with a constant stimulus

32
Q

what do slow adapting or tonic receptor show

A

Slowly adapting or tonic receptors show little adaptation in response to a prolonged stimulus.

Slowly adapting receptors are better at coding the intensity of a stimulus for its entire duration.

33
Q

what do rapidly adapting or phasic receptors do

A

. Rapidly adapting or phasic receptors adapt quickly

Rapidly adapting receptors code changes in stimulus intensity better but not the duration.

34
Q

what are reflexes

A
  • Reflexes are protective relays that do not need the information be sent to the brain for the action to be taken
35
Q

what is the main excitatory neurotransmitter

A

Glutamate

36
Q

what is the main inhibitory neurotransmitter

A

GABA

37
Q

new …

A

synapses can be formed

38
Q

what does sleep do to synapses

A

– strengths synapses after learning, shrinks spines that are not being used to allow for more new spines to form

39
Q

describe the GABA/gluamate relationship

A

– GABA/glutamate are opposing pathways that act to keep excitation and inhibition balanced in the brain by adjusting the location of GABAA receptors.
– Modulate excitatory response by increase GABA receptor
– Modulate the inhibitory receptor by increases glutamate

40
Q

what does metabotrophic glutamate do

A

– Metabotrophic glutamate increases GABA receptor accumulation

41
Q

what does iontrophic glutamate do

A

– Iontrophic glutamate increases GABA receptor dispersion (less localised