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PSYC 475 > Chemical Signaling by neurotransmitters(Chapter 3) > Flashcards

Chemical Signaling by neurotransmitters(Chapter 3) Flashcards

1
Q

how does communication occur between neurons?

A

Communication between neurons occurs at synapses via chemical neurotransmitters that cross the synaptic cleft

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2
Q

which way is transmission between neurons?

A

Transmission is one-way, from presynaptic cell to postsynaptic cell

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3
Q

Synaptic veiscles

A

are in the pre-synaptic neuron contain neurotransmitters

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4
Q

what are the three criteria that must be met to verify if a chemical is a neurotransmitter?

A
  1. The presynaptic cell should contain the proposed
    substance along with a mechanism for manufacturing it.
  2. A mechanism for inactivating the substance
    should also be present.
  3. The substance should be released from the axon
    terminal upon stimulation of the neuron
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5
Q

what are the two major categories of neurotransmitters. what do those categories contain?

A
  1. Classical neurotransmitters - amino acids, monoamines, and acetylcholine
  2. nonclassical neurotransmitters - neuropeptides, lipids, and gasses
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6
Q

where are most of transmitted synthesized?

A

synthesized in the axon terminals

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7
Q

what makes two differences make neuropeptides synthesis different that most neurotransmitter?

A
  1. Neuropeptides are synthesized from precursor proteins that are synthesized in the cell body and shipped to the axon terminals.
  2. Replenishment of neuropeptides is slower than for small-molecule transmitters.
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8
Q

explain the three step process of features for neurotransmission using neuropeptides

A
  1. Neuropeptides are synthesized from larger precursor proteins, which are packaged into large vesicles by the
    Golgi apparatus.
  2. During transport from the cell body to the
    axon terminal, enzymes that have been packaged within the vesicles break down the precursor protein to liberate the neuropeptide.
  3. After it is released at the synapse and stimulates postsynaptic receptors, the neuropeptide is inactivated
    by degradative enzymes.
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9
Q

what are neuromodulators?

A
  1. Chemicals That Do Not ACT Like Typical Neurotransmitters
  2. alter the action of standard neurotransmitters
    (enhancing, reducing, or prolonging the transmitter’s effectiveness)
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10
Q

what is volume transmission?

A

a property that neuromodulators have. such that, They diffuse away from the site of release to influence more distant cells

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11
Q

why is the use of the term neuromodulator vague?

A

because some neurotransmitter act as both neurotransmitter and neuromodulator.

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12
Q

explain the 10 step process involved in neurotransmission at a typical synapse that uses a classical neurotransmitter

A

1.Neurotransmitter is synthesized and then stored in vesicles.

2.An action potential invades the presynaptic terminal

3.Depolarization of presynaptic terminal causes opening of voltage-gated Ca2+ channels

  1. influx of Ca2+ ions come into the presynaptic terminal through channels
  2. Ca2+ causes vesicles to fuse with presynaptic membrane

6.Neurotransmitter is released into synaptic cleft via exocytosis

7.neurotransmitter binds to receptor molecules in postsynaptic membrane…

  1. causing opening or closing of postsynaptic channels

9.postsynaptic current causes excitatory or inhibitory
postsynaptic potential that changes the excitability of
the postsynaptic cell.

  1. Vesicular membrane is retrieved from plasma membrane
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13
Q

what the difference between lipid and gaseous transmitter compared to classical neurotransmitters?? give 3 criteria

A
  1. not stored or released by synaptic vesicles
  2. Synthesized on demand by postsynaptic cell after receptor activation by a classical transmitter
  3. not released by exocytosis but simply diffuse out of the nerve cell through the cell membrane.
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14
Q

why are lipid and gaseous neurotransmitter called retrograde messenger?

A

they are called retrograde messengers because they work backwards. such that, the signal information from the postsynaptic is sent to the presynaptic cell

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15
Q

what are 6 mechanisms that control the rate of a neurotransmitter release by nerve cell?

A
  1. Rate of cell firing.
  2. Probability of transmitter release – synapses vary in the probability that vesicles will undergo exocytosis

3.Presence of autoreceptors (on axon terminals or cell bodies and dendrites). there are two autoreceptors. Terminal autoreceptors and Somatodendritic autoreceptors

  1. Terminal autoreceptors inhibit further transmitter release.
  2. Somatodendritic autoreceptors slow the rate of cell firing.
  3. Heteroreceptors: receive transmitters at axoaxonic synapses; either
    enhance or reduce transmitter release.
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16
Q

where are terminal and somatidendritic autoreceptor located?

A

terminal autoreceptors are located on the axon terminal

somatidentrictic autoreceptors are located on the dendrite or cell body

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17
Q

what are three mechanisms involved in neurotransmitter inactivation?

A
  1. Enzymatic breakdown within or near the synaptic cleft(attached to the postsynaptic cell)
  2. Removal from synaptic cleft by transporter proteins on the axon terminal membrane(presynaptic cell) (reuptake).

3.Uptake by postsynaptic cell or glial cells(with transporter)

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18
Q

what are receptor?

A

are proteins on plasma membranes of a neuron, muscle cell, or secretory cell

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19
Q

what is an effect of a receptor?

A

excitatory or inhibitory

20
Q

what is a receptor subtype?

A

different varieties of receptors for the same
neurotransmitter

21
Q

what are the two types of receptors?

A

ionotropic and metabotropic

22
Q

what does ionotropic consist of?

A

Consist of Multiple Subunits That Together Form an
Ion Channel

23
Q

explain 6 features of ionotropic receptors?

A

1.has a Resting state = ion channel closed.

2.Neurotransmitter binding opens the channel.

  1. Channel closes when transmitter dissociates.

4.Act rapidly.

  1. Receptor channels selective for specific ions, such as Na+, Ca2+, and Cl–

6.Can undergo desensitization

24
Q

what does it mean when a receptor undergoes desensitization?

A

the channel remains closed even though there may be
ligand molecules(neurotransmitter) bound to the receptor

25
Q

what does metabotropic receptors consist of?

A

Consist of a Single Subunit That Works by
Activating G Proteins

26
Q

explain 3 features of metabotropic receptors?

A
  1. Act slower but response lasts longer.

2.Activate G proteins when neurotransmitter binds.

  1. G proteins open ion channels, or stimulate or inhibit membrane effector enzymes.
27
Q

what is a second messenger?

A

is an intracellular molecule regulated by the first messenger (i.e., levels of the second messenger are either increased or decreased through the action of the first messenger on its receptor)

28
Q

what is the purpose of an effector enzyme?

A

Effector enzymes are involved in synthesis or breakdown of second messengers for the metabotropic receptor

29
Q

explain the function of metabotropic receptors

A

metabotropic receptors activate G proteins in the membrane, which may EITHER

(A) alter the opening of a G protein–gated
ion channel

OR

(B) stimulate or inhibit an effector enzyme that
either synthesizes OR breaks down a second messenger

30
Q

what is the mechanism of action of second messenger ?

A

Second messengers work by activating protein
kinases to cause phosphorylation of substrate proteins within the postsynaptic cell

The added phosphate groups alter functioning of the protein.

31
Q

what are the four second messenger system?

A
  1. cAMP
    2.cGMP
    3.Ca2+
    4.Phosphoinositides
32
Q

explain the pathway of cAMP

A

cAMP is a second messenger that is activated by the g proteins.

Once its activated, it activates proteins kinase A, which adds phosphates

33
Q

cGMP own kinase protein is?

A

kinase protein G

34
Q

what inactivates cAMP and cGMP?

A

inactivation is by enzymes called phosphodiesterases (PDEs).

35
Q

why might PDEs be useful for?

A

Inhibitors of specific PDEs may be useful in treating various CNS disorders

36
Q

what is the purpose of phosphoinositide’s?

A

breaks down a phospholipid in the cell membrane to form two second messengers: diacylglycerol (DAG) and inositol trisphosphate (IP3).

37
Q

what does IP3 initiate in the second messenger system?

A

triggers release of Ca2+ from the endoplasmic reticulum, and the combination of diacylglycerol(DAG) causes and elevation of Ca2+ ions within the postsynaptic cell and then this activates the enzyme protein kinase C (PKC).

38
Q

How is CaMKII activated? also explain the overarching chemical

A

through the release of Ca2+ ions which are a result of IP3

39
Q

what does ERK activity mean?

A

what the drug is doing

40
Q

how can drugs alter all aspects of synaptic transmission? give five reason how

A

1.Increase or decrease neurotransmitter synthesis.

2.Block transmitter breakdown or inhibit reuptake.

3.Autoreceptor agonists reduce transmitter release, autoreceptor

  1. antagonists enhance release.

5.Mimic or inhibit transmitter’s effect on receptors

41
Q

which numbers show the area is being stimulated. explain how those areas are being stimulated

A
  1. Drug serves as NT precursor
  2. Drug stimulates release of NT
  3. Drug stimulates postsynaptic receptors
  4. Drug blocks autoreceptors; increases release of NT.
    10.Drug inhibits NT degradation.
    11.Drug blocks reuptake
42
Q

which numbers show the area is being inhibited. explain how those areas are being stimulated

A
  1. Drug inhibits NT synthesis
  2. Drug prevents storage of NT in vesicles
  3. Drug inhibits release of NT.
  4. Drug blocks postsynaptic receptors.
  5. Drug stimulates autoreceptors; inhibits release of NT.
43
Q

what are the two main changes of synaptic plasticity?

A

functional changes
structural changes

44
Q

what are functional changes of synaptic plasticity

A

they are the changes in strength of existing synapses

45
Q

what are the structural changes in synaptic plasticity?

A

loss of synapses or growth of new ones, change in
dendritic length, branching, or spine density.

46
Q

what can neurons do?

A

Neurons can rapidly change the size and shape of dendritic spines, grow new spines, and/or lose existing ones

47
Q

what can abused drugs do to a neuron?

A

Many abused drugs produce changes in neuron dendrites

PSYC 475 (12 decks)

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