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MSK Week 5 > ICL 3.1: Synaptic Transmission > Flashcards

ICL 3.1: Synaptic Transmission Flashcards

1
Q

how do neurons communicate with each other and other peripheral structures?

A

through the generation of chemical and electricalsignals

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2
Q

what is a synapse?

A

the junction point from one neuron to the next

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3
Q

what are the two types of synapses?

A
  1. chemical
  2. electrical

these can be either excitatory or inhibitory

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4
Q

how do electrical synapses work?

A

gap junction proteins (connexons) aggregate to form an aqueous channel

action potentials are then transmitted through gap junctions –> no synaptic vesicles of significant synaptic cleft

the molecules passing through could be ions like Ca+2 or other small molecules like ATP

signal transmission is bidirectional

electrical synapses are the fasts way neurons communicate with one another!

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5
Q

how do chemical synapses work?

A

this type of synapse is the most abundant in the human CNS

the way it works is that the presynaptic neuron secretes a neurotransmitter which then binds to receptor proteins in the membrane of the postsynaptic neuron

the NTs will either modulate, stimulate or inhibit the postsynaptic neuron

signal transmission is unidirectional

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6
Q

what are the basic components of a chemical synapse?

A
  1. synaptic cleft
  2. transmitter vesicles
  3. post synaptic neuronal membrane
  4. mitochondria
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7
Q

what is the synaptic cleft?

A

it separates the presynaptic terminal from the postsynaptic neuron

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8
Q

what is the function of the presynaptic terminal?

A

the terminal hastransmitter vesicles and themitochondria

transmitter vesicles contain neurotrans­mitters

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9
Q

what is the function of the postsynaptic neuronal membrane?

A

it containsexcitatory or inhibitory receptors

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10
Q

what is the function of mitochondria in a chemical synapse?

A

mitochondria provide ATP to use as an energy source for neurotransmitter synthesis

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11
Q

what are the events that happen at a chemical synapse?

A
  1. an action potential depolarizes the presynaptic membrane
  2. voltage gated Ca2+ channels on the presynaptic membraneopen and a large number of Ca2+ ions enter the presynaptic terminal
  3. Ca2+ entry leads to the exocytosis of synaptic vesicle contents
  4. NTs are released into the synaptic cleft
  5. NTs bind to receptors on post synaptic membrane
  6. brief opening of specific ion channels
  7. NTs are soon released and degraded or recycled
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12
Q

how much neurotransmitters are released at a chemical synapse?

A

Quantity of neurotransmitter released is directly related to the number of Ca2+ ions that enter the presynaptic neuron

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13
Q

after an event at a chemical synapse, how is the synaptic cleft cleared?

A
  1. Its can be returned to axon tmerinals for reuse or transported into glial cells
  2. enzymes can inactivate NTs
  3. NTs can diffuse out of the synaptic clef
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14
Q

what breaks down acetylcholine?

A

acetylcholinesterase

ACh is made from choline and acetyl CoA –> in the synaptic cleft, ACh is broken down by acetylcholinesterase and the choline is transported back into the axon terminal and used to make more ACh

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15
Q

how do synaptic vesicles in the presynaptic neuron exocytose their NTs into the synaptic cleft?

A

the synaptic vesicles dock at defined sites on the target plasma membrane –> the SNARE family of proteins is what mediates the docking of the transport vesicles with the target membrane

Ca2+ influx triggers the fusion leading to the opening of the pore

once the vesicles fuse with the membrane, NTs are related into the synaptic clef

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16
Q

what is the MOA of botulism?

A

Botulinum neurotoxins are synthesized primarily by different strains of the anaerobic bacteriaClostridium botulinum

botulinum toxin, or botox, is used in the therapeutic setting to reduce muscle tension, toreduce muscle spasticity

the botox injection work by weakening or paralyzing certain muscles or by blocking certain nerves

they do this by cleaving SNARE complex proteins which prevents the fusion of vesicles to the plasma membranes

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17
Q

what are the 2 major classes of neurotransmitters?

A
  1. small molecule transmitters

ionotropic receptors and metabotropic receptors

  1. peptide transmitters

metabotropic receptors

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18
Q

what are small molecule transmitters?

A

they’re the most acute and rapid responses

they’re used for the transmission of sensory signals to the brain and of motor signals back to the muscles

class I-IV: examples include ACh, epinephrine, serotonin, histamine, glycine, nitric oxide etc.

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19
Q

where are small molecule transmitters synthesized?

A

they’re synthesized in the cytosol of the presynaptic terminal and absorbed by active transport into transmitter vesicles

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20
Q

what are the 8 important small molecule neurotransmitters?

A
  1. acetylcholine
  2. norepinephrine
  3. dopamine
  4. serotonin
  5. glutamate
  6. nitric oxide
  7. glycine
  8. GABA
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21
Q

what is the function of acetylcholine?

A

a small molecule neurotransmitter

it’s a majorexcitatory neurotransmitter of somatic motor neurons

it has some inhibitor effects like the inhibition of the heart by the vagus nerves

it also has a modulatory role in cognitive functions like paying attention

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22
Q

what is the function of norepinephrine?

A

a small molecule neurotransmitter

it’s mostly excitatory and is secreted in the brain stem and hypothalamus

it controls overall activity and mood of the mind – so your sense of feeling good or being alert

it also increases heart rate and BP

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23
Q

what is the function of dopamine?

A

a small molecule neurotransmitter
it’s released from the brain and it mediates various aspects of cognition

so it facilitates your sense of feeling good and your reward pathway

in Parkinson’s, there’s a loss of dopamine neurons in the midbrain-substantial nigra

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24
Q

what is Parkinson’s MOA?

A

in Parkinson’s, there’s a loss of dopamine neurons in the midbrain-substantial nigra

as the substantia nigra degenerates in Parkinson’s disease, the nigrostriatal pathway is disrupted, reducing striatal dopamine and producing PD symptoms

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25
Q

what is the function of serotonin?

A

a small molecule neurotransmitter
that’s released from the brain and it mediates various aspects of cognition

it’s an inhibitor of pain pathways in the spinal card

it also regulates endocrine activity aka hormonal controls!

its also involved in the mood of a person and controls sleep/wake cycles; it causes sleepiness

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26
Q

what happens if someone has inadequate serotonin levels?

A
  1. severe depression
  2. obsessive/compulsive disorders
  3. anger issues
  4. eating disorders
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27
Q

what is the function of glutamate?

A

a small molecule neurotransmitter that is secretes and concentrated in the brain

it’s the major excitatory neurotransmitter in the CNS

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28
Q

what is the function of nitric oxide?

A

a small molecule neurotransmitter that’s secreted by nerve terminals in areas of the brain responsible for long-term behavior and memory

it’s synthesized instantly as needed and diffuses out of the presynaptic terminals and then into postsynaptic neurons

it changes intracellular metabolic functions that modify neuronal excitability in the postsynaptic neuron

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29
Q

what is the function of glycine?

A

a small molecule neurotransmitter that is secreted mainly in the spinal cord

it is inhibitory*

it’s also a co-transmitter for some glutamate receptor (binding is important for the activity)

30
Q

what is GABA?

A

a small molecule neurotransmitter secreted in the spinal cord and CNS

it’s the most important inhibitory transmitter int he brain!!!

it’s what inhibits NTs that cause anxiety

31
Q

what are benzodiazepines? give examples

A

benzodiazepines are tranquilizers that are used for anxiety and insomnia

they work with GABA to limit anxiety

ex. valium (diazepam) and xanax (alprazolam)

32
Q

what are peptide transmitters?

A

neuropeptides have slower but longer lasting effects (days, months or years)

they’re present in smaller quantities but are more potent

33
Q

where are peptide transmitters synthesized?

A

they’re synthesized by ribosomes in the neuronal cell body

they undergo packaging in the ER and subsequently the golgi

then, vesicles are transported to the tips of the nerve fibers byaxonal streaming (slow process)

34
Q

what are the two types of receptor proteins of a synapse?

A

the membrane of the postsynaptic neuron contains a large numbers ofreceptor proteins

  1. ionotropic receptors
  2. metabotropic receptors

each receptor has an extracellular components that protrudes into the synaptic cleft and binds the neurotransmitter

there’s also an intracellular component extending into the interior of the postsynaptic neuron

35
Q

what are ionotropic receptors?

A

a type of receptor in a synapse that gates ion channels directlyand allows for passage of specific ions

so they’re membrane-bound receptor proteins that respond to ligand binding by opening an ion channel and allowing ions to flow into the cell, either increasing or decreasing the likelihood that an action potential will fire

there are both cation channels and anion channels

they’re fast and precise

36
Q

what are metabotropic receptors?

A

a type of receptor in a synapse that activates “second messengers”

so there are molecules that activate other substances inside the cytoplasm of the postsynaptic neuron

prolonged postsynaptic neuronal excitation or inhibition (such as memory) is achieved by activating a “second messenger” chemical system inside the postsynaptic neuronal cell

ex. G proteins

37
Q

what are cation channels?

A

usually for Na+ ions but can also be for K+ or Ca+2

the channels are lined with negative charges to attract positively charged Na+ ions –> negative chargesrepel Cl- ions and other anions& prevent their passage

ions will enter when the channel diameter > size of the hydrated Na+ ion

38
Q

what are anion channels?

A

they mainly allow Cl- ions to pass but also minute quantities of other anions

Na+, K+ and Ca2+ ions are blocked because of the size of their hydrated ions

39
Q

how do G proteins work?

A

they’re a type of metabotropic receptor system

the inactive G protein complex is free in the cytosol but it undergoes a conformation change when a receptor is activated by a neurotransmitter

this leads to a series of cellular events via secondary messengers including the opening of ion channels

40
Q

what different things can secondary messengers in a metabotropic receptor system do?

A
  1. opening specific ion channels – often stays open for a prolonged time unlike ion channels
  2. activation fo cAMP or cGMP which then in turn activate highly specific neuronal metabolic machinery and initiate any one of many chemical results
  3. activation of one or more intracellular enzymes – the enzymes in turn can cause any one of many specific chemical functions
  4. activation of gene transcription – this can lead to formation of new proteins which in turn changes nruronal metabolic machinery or structure
41
Q

what’s the resting membrane potential of a spinal motor neuron?

A

the soma of a spinal motor neuron has aresting membrane potentialof ~ − 65 mV

synaptic potentials arise when neurotransmitters activate ion channels

42
Q

what 2 synaptic potentials are there?

A
  1. excitatorypostsynaptic potential (EPSP)

opening of Na+ or Ca2+ channels leads to depolarization of the membrane

  1. inhibitorypostsynaptic potential (IPSP)

opening of K+ or Cl- channels leads to hyperpolarization of the membrane

43
Q

what are excitatorypostsynaptic potentials?

A

they arise at synapses where the transmitter depolarizes the synaptic membrane

opening of Na+ or Ca2+ channels leads to depolarization of the membrane

however, a single EPSP cannot induce an action potential – EPSPs added together can reach the threshold and trigger a postsynaptic cell

44
Q

what are inhibitory postynspatic potentials?

A

they at synapses where the transmitter hyperpolarizes the synaptic membrane

opening of K+ or Cl- channels leads to hyperpolarization of the membrane

so the excitatory neurons have to have a higher potential than the inhibitory neuron for an action potential to happen

45
Q

what is summation in neurons?

A

one synapse is not strongenough to reach the threshold potential in the post synapticneuron

instead, multiple inputs summate their post-synaptic potentials inthe same region of the dendrite at the same time to generate an action potential

generation of an action potential depends on the summation of EPSPs and IPSPs

so ultimate, the algebraic sum of all the EPSPs and IPSPs has to raise the membrane potential to the threshold potential for an action potential to occur

however, if the IPSPs prevail, then the post-synaptic cell will be “silent”

46
Q

what is spatial summation?

A

many presynaptic terminals when stimulated at the *same time *can add up to exceed the threshold potential

so it is the effect of triggering an action potential in a neuron from one or more presynaptic neurons

47
Q

what is temporal summation?

A

rapidsuccessive discharges from a single presynaptic terminal can add up to exceed the threshold potential

48
Q

what are modulatory transmitters?

A

modulatory transmitters alter the response of fast ionotropic transmitter actions

they mediate by altering the opening states of K+ or Ca2+ channels by altering membrane potential and the refractive period

so they can keep the membrane depolarized or hyperpolarized even after the initial impulse ends

ex. excitatory synaptic inputs from cerebral cortex to motor neuron are modulated by slow modulatory synaptic inputs from brain stem (degree of motivation) determining the speed of the movement

49
Q

what is the function of inhibitory synapses?

A

they maintain homeostasis!!

they dampen the excitation that could lead to neuronal damages

they’re important for streamlining relevant and precise sensory information

they’re also important for locomotion

note: drugs against epilepsy usually targets inhibitory transmitters and increase their effect

50
Q

what is disinhibition?

A

when 2 inhibitory neurons coupled in series increase the activity of an excitatory neuron

51
Q

what is strychnine?

A

it blocks inhibitory glycinergic synapses and causes life threatening muscle spasms

52
Q

what is synaptic plasticity?

A

life experiences change the nervous system!

the brain can change and adapt to new information and also there is the basis of memory, acquisition of motor and cognitive skills

plasticity is broadly categorized into short and long term plasticity

53
Q

what is the mechanism of synaptic plasticity?

A
  1. presynaptic terminal releases more/less neurotransmitter in response to an action potential

OR

  1. postsynaptic neuron increases/decreases its response to the transmitter
54
Q

what is short term plasticity?

A

changes in synaptic strength that occur on a sub-second time scale and reverts to “normal” soon afterwards

  1. facilitation
  2. potentiation
  3. short term depression
55
Q

what is facilitation?

A

increased transmitter release by presynaptic neuron

56
Q

what is potentiation?

A

increased synaptic efficiency even after the stimulation ends

57
Q

what is short term depression?

A

weaker post-synaptic response

58
Q

what is long term plasticity?

A

it can last anywhere from minutes to hours, days, or years

this is the dominant model for how the brain stores information!

  1. long term potentiation
  2. long term depression
59
Q

what is long term potentiation?

A

persistent strengthening of a synaptic connection

60
Q

what is long term depression?

A

long-term weakening of a synaptic connection

61
Q

what are the steps in long-term potentiation?

A
  1. glutamate is released from the presynaptic neuron and acts on two receptors: AMPA and NMDA
  2. Na+flows into the postsynaptic neuron only through the AMPA receptor (since Mg2+blocks NMDA receptor )
  3. depolarization of the postsynaptic cell removes Mg2+block on NDMA receptor
  4. Na+and Ca2+ flow through NMDA receptor into postsynaptic neuron
  5. [Ca2+] initiates activation of protein kinase-mediated signaling cascades
  6. this increases the number and sensitivity of AMPA receptors
62
Q

what is late phase long-term potentiation?

A

when sustained activation of the early phase kinases initiates signal cascades leading to protein synthesis, morphological changes of the neuron, and gene expression

this includes both postsynaptic changes and presynaptic changes

  1. postsynaptic changes = increased dendritic area and spines which increase postsynaptic sensitivity or increase in AMPA receptors inserted in the postsynaptic membrane
  2. presynaptic changes = increased binding and release of neurotransmitter vesicles from the presynaptic membrane or increase in the total number of presynaptic neurotransmitter vesicles

these are the underlying mechanisms for learning and addiction!

63
Q

what is long term depression?

A

long term depression decreases the efficacy of a synapse

observed in cerebellum (motor learning), hippocampus (memory decay),the visual cortex, and the prefrontal cortex

mechanism proceeds due to low frequency stimuli and a slow rise in postsynaptic [Ca2+]

example:activation of phosphatase-mediated signaling resulting in the internalization of AMPA receptors

64
Q

what is the MOA of lead poisoning?

A

Blocks NMDA receptors limiting synaptic plasticity and memory

lead accumulates around nerves causing them to degenerate and demyelinate. It also inhibits heme synthesis pathway leading to the build up of substrate δ-Aminolevulinic acid (ALA)which is directly toxic to neurons. Thirdly it blocka NMDA receptors. Effects are particularly potent among children since it interferes with normal neurologic development.

this causes acute encephalopathy through multiple mechanisms

65
Q

what is the correct order in a normal flexion reflex?

A
  1. AP in sensory afferent neuron
  2. EPSP in interneuron
  3. AP in interneuron
  4. EPSP in motor neuron
  5. AP in motor neuron
  6. AP in flexor muscle
  7. contraction of flexor muscle
66
Q

at the negative resting membrane potential, the NMDA receptors little ionic current because…..

A

they are blocked with Mg+2

67
Q

what creates the barrier that is the reason for chemical synapse discontinuity?

A

the synaptic cleft

68
Q

what is the most direct cause for the presynaptic vesicles to fuse with the presynaptic membrane and release a neurotransmitter into the synaptic cleft?

A

release of calcium ions into the presynaptic neuron terminal

69
Q

______ receptor has a direct, mechanical response to the binding of a neurotransmitter?

A

ionotropic

70
Q

_____ is the major inhibitory neurotransmitter in the CNS

A

GABA

71
Q

when would you expect to see an increase in Cl- ions in the neurons? during EPSP or IPSP?

A

IPSP

when Cl- enters the neuron, it hyperpolarizes the neuron and it’s inhibitory

72
Q

long term depression involves…..

A

protein phosphatase mediated internalization of the AMPA receptors

MSK Week 5 (7 decks)

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