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neuroscience psychology > lecture 3- neurotransmitters 1 > Flashcards

lecture 3- neurotransmitters 1 Flashcards

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1
Q

what is the action potential in action

A

-the signal that is sent within the cell
- a resting cell has a negative charge and when an action potential is sensed it depolarises because positive ions come flooding into the cell causing its charge to get positive very quick and thats the signal that sends along the length of the axon

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2
Q

the synaptic cleft including presynaptic and postsynaptic

A
  • the gap between neurons (20-30nm)
  • presynaptic neuron: sends out the signal
  • postsynaptic neuron: the one of the other side of the cleft that will receive the signal
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3
Q

what are the two types of signalling?

A
  • electrical communication and chemical transmitters
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4
Q

electrical signalling

A
  • electrical synapses: pre and post-synapse are linked at a gap junction
  • direct, passive flow from one neuron to another
  • ions diffuse through channels, continuing the action potential
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5
Q

electrical signalling cont.

A
  • electrical signalling is very fast
  • the post synaptic neuron can start to signal within ms of receiving input from pre synaptic neuron.
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6
Q

electrical signalling cont…

A

-allows for synchronisation of signals
- brainstem neurons regulating breathing
- secretion of hormones
-action potentials fire at practically the same time

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7
Q

chemical signalling

A

-chemical synapses: no link between neurons
- neurotransmitters are released from presynaptic cell
- they diffuse across the gap and bind to receptors on the post-synaptic cell membrane
- neurotransmitter either excites or inhibits the neuron that receives it
- increase/decrease the likelihood of the receiving neuron producing its own action potential

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8
Q

stages of chemical signalling

A
  • 1-6: synthesis, storage and release of neurotransmitters (NTs)
  • 7: binding of NTs to post-synaptic receptors
    -8-9: changes in post synaptic cell
  • 10-11: deactivation of NTs to end the signalling

NTs= neurotransmitters

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9
Q

synthesis and storage of NTs

A
  • a substance is a NT if:
    • its present in the pre-synaptic terminal, stored in a vesicle
    • its released in response to an action potential arriving at the terminal
    • there are receptors on the post-synaptic cell it can bind to
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10
Q

what are the two categories of neurotransmitters?

A
  • small molecule neurotransmitters
  • neuropeptides

differences
- the way they look are different
- the way they function is different

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11
Q

post synaptic influence

A
  • the two categories also differ in their response to low or high frequency stimulation of the pre synaptic neuron
  • if the stimuli is low frequency, there will only be a localised increase in Ca2+
  • only the small molecule neurotransmitters will be released
  • high frequency stimuli will cause a more distributed release of Ca2+
  • both types of transmitter will be released
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12
Q

release of NTs

A
  • triggered by the arrival of the action potential at the presynaptic terminal
    • influx of Ca2+
  • vesicle packages merge with the synapse membrane
  • contents released into cleft (exocytosis)
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13
Q

binding to receptors- ionotropic receptors

A
  • the transmitter binds to the ion-channel opens
  • the channel opens
  • ions flow across and into the post-synaptic cell
  • the action potential is triggered in the post synaptic cell
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14
Q

binding to receptors- metabotropic receptors

A
  • the neurotransmitter binds to a receptor protein
  • the receptor activates the attached G-proteins
  • the G-proteins detaches and can dock onto an effector protein
  • the effector protein triggers the opening of an ion channel
  • alternatively, the G-protein docks on the ion channel directly
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15
Q

changes in post-synaptic cell: summation

A
  • cells receive multiple inputs from neighbouring neurons
  • excitatory or inhibitory
  • influences are summed to determine if signals are sent
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15
Q

NT deactivation

A
  • NT detaches from the receptor and is then:
  • transported back into the pre-synaptic neuron (reuptake)
    or
    -broken down by enzymes in the synaptic cleft
  • by products of this breakdown may be recycled
15
Q

how drugs work

A
  • psychoactive drugs interact with neurotransmitter systems
  • drugs can influence all the stages of NT production
16
Q

what are the two types of drugs?

A

agonists: mimic or enhance the effects of a naturally occurring neurotransmitter
antagonists: block or reduce the effects of a naturally occurring neurotransmitter

16
Q

agonists

A

synthesis:
- increase the amount of NT made
- destroys enzymes that break down NTs

release:
- increase amount of NTs released
- blocks autoreceptors, which limit NT release

binding:
- bind to receptor site and cause channel to open

deactivation:
- destroys enzymes that break down NTs
- block reuptake ports for taking NTs back into the cell

17
Q

antagonists

A

synthesis:
- decrease the amount of NT made
- breaks open vesicles so NTs are destroyed by enzymes

release:
- blocks the release of NTs from cell
- activates autoreceptors, to limit NT release

binding:
- bind to receptor site blocking the NT

17
Q

acetylcholine receptors- ionotropic

A
  • nicotinic receptors
  • ionotropic
  • excites skeletal muscles (contractions)
  • in the CNS- involved in learning, memory, arousal and motor control and alertness after waking
18
Q

acetylcholine receptors- metabotropic receptors

A
  • muscarinic receptors
  • metabotropic
  • found primarily in the CNS
  • involved in control of physiological functions/parasympathetic nervous system (eg salivation, lacrimation, digestion)
  • slows heart rate, relaxes smooth muscles (ie in the gut)
19
Q

acetylcholine receptor agonists

A
  • nicotine acts as an agonist on ionotropic receptors, enhancing the effect of ACh in the CNS
  • at lower doses, it produces some feelings of euphoria and relaxation
  • at high doses, it produces nausea, vomiting and mental confusion
20
Q

acetylcholine receptor agonists

A
  • muscarine acts as an agonist on the metabotropic muscarine receptors
  • enhances parasympathetic functions
    • nausea, vomiting, increased salivation, slowed heart rate (bradycardia), reduced blood pressure
  • can lead to circulatory collapse, coma and death
21
Q

acetylcholine receptor antagonists

A
  • nicotinic receptors antagonists
  • α-bungarotoxin- the venom of the banded krait
  • irreversible blocking of nicotinic ACh receptors
  • prevents skeletal muscle activation leading to paralysis
22
Q

acetylcholine receptor antagonists cont

A
  • muscarinic receptor antagonists
  • atropine (deadly nightshade) and scopolamine (henbane)
  • reduces parasympathetic functions
  • may be used to increase heart rate (bradycardic treatment)
  • used in surgery to reduce saliva production
23
Q

glutamate

A
  • most important transmitter for normal brain function
  • almost all excitatory neurons in the central nervous system are glutamatergic
  • over half of all brain synapses are thought to release glutamate
  • glutamate does not cross the blood brain barrier, therefore must be synthesised from local precursors
24
Q

agonists of glutamate

A
  • ibotenic acid: prolongs activation of the NMDA receptor (ionotropic)
  • NMDA: linked to long-term changes in the brain (‘synaptic plasticity’) necessary for learning and memory
  • extended function leads to cell damage and death (excitotoxicity)
25
Q

agonists of glutamate cont

A
  • ketamine: antagonist of the NMDA receptor
  • blocks the excitatory effect of glutamate
  • used as a sedative and anaesthetic
  • also recreationally for its hallucinatory properties
26
Q

Glutamate and ecotoxicity (Olney, 1969)

A
  • glutamate agonists can cause excitotoxicity- cell death due to enhanced activation
  • excitotoxicity also occurs following cell damage due to injury or stroke
  • damage: releases glutamate: glutamate activates post-synaptic cells: cells die
27
Q

Glutamate and ecotoxicity

A
  • if an excess of glutamate is causing damage to the cells, it could be possible to use glutamate blockers to treat stroke or brain damage
  • glutamate antagonists would block the receptors, limiting the damage caused by the excess glutamate (neuroprotective therapy)

specificity:
- glutamate receptors are widespread in the brain
- other glutamate receptors blocked
- signalling reduced or lost

timing:
- sharp increase linked to destruction immediately after injury
- sustained, milder increase days/weeks after injury

neuroscience psychology (6 decks)

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