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Neuroscience > Synapses > Flashcards

Synapses Flashcards

1
Q

What is the function of synapses

A

Send information to another cell or target

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2
Q

Pre-synaptic part of the synapse

A

Axon

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3
Q

Post-synaptic part of the synapse

A

Dendrite

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4
Q

What are the types of synapses?

A
  1. Axo-somatic
  2. Axo-dendridic
  3. Axo-axonal (right by presynaptic terminal)
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5
Q

Do synapses with different locations have different functions?

A

The axo-somatic and axo-dendridic synapses send information. Axa-axonal synapses modulate how much neurotransmitter is released by the second neuron.

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6
Q

What type of ion channels do APs open in the presynaptic terminal?

A

Voltage-gated calcium ion channels

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7
Q

What happens when calcium enters the presynaptic terminal?

A

Calcium activates a series of proteins and enzymes, which moves the vesicles to the presynaptic terminal and releases neurotransmitters into the synaptic cleft

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8
Q

What determines how much neurotransmitter is released?

A

The amount of calcium that enters the presynaptic terminal (more calcium = more neurotransmitter); determine by how many and how long voltage gated-ion channels are opened

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9
Q

What ion channels are involved in EPSPs?

A

Na and Ca ion channels

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10
Q

What ion channels are involved in IPSPs?

A

K and Cl ion channels

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11
Q

In the nervous system, EPSPs can summate to generate an action potential. What kinds of summation are used to do this?

A

Temporal and Spatial; usually need summation to fire AP

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12
Q

Do you need summation at the NMJ to produce EPSP in the muscle to produce a muscle contraction?

A

No, an AP in the motor neuron is sufficient

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13
Q

What happens when there are both EPSPs and IPSPs at a postsynaptic neuron?

A

Summation is important here - depends on which potential summation is stronger

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14
Q

With presynaptic facilitation, the synapses are axon-______. An [inhibitory/excitatory] synapse neuron (1) makes an action potential in the 2nd neuron last [longer/shorter] and [increases/decreases] the number of calcium ions that enter the presynaptic terminal.

A

Axo-axonal; excitatory; longer; increases

{Depolarization}

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15
Q

With presynaptic inhibition, an action potential in the 2nd neuron last [longer/shorter] and [increases/decreases] the number of calcium ions that enter the presynaptic terminal.

A

shorter; decreases

{Hyperpolarization}

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16
Q

Collection of neuorns in one region that communicate among themselves to process things

A

Local circuits

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17
Q

Generalized information that goes from one point to wide-spread regions of the nervous system; i.e., level of arousal, sympathetic nervous system

A

Diffuse systems

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18
Q

Transmit specific information from one point to another; i.e., making your thumb move

A

Relay systems

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19
Q

What are the two receptors for ACh?

A
  1. Nicotinic

2. Muscarinic

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20
Q

What makes acetylcholine? what breaks it down?

A

Choline acetyltransferase (CAT); Acytlcholineesterase (AChE)

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21
Q

What are the type of receptors at the NMJ that bind ACh? What is its function?

A

Nicotinic; contraction of muscles

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22
Q

What are the type of receptors in the autonomic nervous system that bind ACh? What is its function?

A

Muscarinic (target) and nicotinic (postganglionic neuron); Regulate visceral function

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23
Q

What are the type of receptors in the central nervous system that bind ACh? What is its function?

A

Nicotinic and muscarinic; autonomic regulation and selection of objects of attention

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24
Q

What are the main neurotransmitters of central nervous system?

A

Amino acids (aspartate, glutamate, glycine, GABA)

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25
Q

What are the excitatory amino acids?

A
  1. Aspartate

2. Glutamate

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26
Q

What are the inhibitory amino acids?

A
  1. Glycine

2. Gamma-aminobutyric acid (GABA)

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27
Q

What is the principle fast neurotransmitter? what is its functions?

A

Glutamate; Learning, Development, and Neuronal death after CNS injury

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28
Q

Inhibits postsynaptic membranes, particularly in brainstem and spinal cord; act to prevent excessive neural activity; block the effects of these neurotransmitters can produce seizures

A

Glycine

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29
Q

Major inhibitory neurotransmitter in CNS; Interneurons in spinal cord; act to prevent excessive neural activity; block the effects of these neurotransmitters can produce seizures

A

GABA

30
Q

Where are the cell bodies of monoamines located? what are their overall functions?

A

Brain stem; Diffuse systems: sleep, wake, consciousness, attention, regulation of pain

31
Q

What neurotransmitters are included in monoamines?

A
  1. NE (noradrenaline)
  2. Dopamine
  3. Serotonin
  4. Histamine
32
Q

What are the precursors to catecholamines? What is the immediate precursor to dopamine?

A

Phenylalanine and Tyrosine; Dihydroxyphenyl-alanine (l-DOPA)

33
Q

What are the catecholamine neurotransmitters?

A

Dopamine, NE, and epinephrine

34
Q

What does dopamine do?

A
  1. Motor activity
  2. Cognition
  3. Motivation (can result in addiction)
35
Q

What disorder results from too much dopamine?

A

Schizophrenia

36
Q

What is NE’s functions?

A
  1. Autonomic nervous systems (fight or flight, panic disorders)
  2. Attention and vigilance
37
Q

Functions include:

  1. Open/close ion channel
  2. Activate/inhibit enzymes
  3. Regulate calcium levels in cell
  4. Activate/inactivate genes
A

G-protein mediated receptors

38
Q

What are the steps that occur to activate a G-protein mediated receptor?

A

Ligand binds to receptor -> receptor activates G-protein -> G-protein moves through the cell to its effectors
~takes longer to have an effect, but lasts longer once they happen

39
Q

What are 3 second messengers used in G-protein mediated receptor?

A
  1. Cyclic AMP (cAMP)
  2. Arachidonic acid
  3. Inositol triphosphate
40
Q

2nd messenger that modulates ion channels (pain sensation in PNS)

A

cAMP

41
Q

2nd messenger that produces prostaglandins; regulate vasodilation, Enhances inflammation

A

Arachidonic acid

42
Q

2nd messenger that regulates Calcium ion stores

A

inositol triphosphate

43
Q

Nicotinic, ligand-gated ion channel; at neuromuscular junction, autonomic ganglia, and some parts of CNS

A

ACh receptors

44
Q

What are the functions of ACh receptors?

A
  1. Memory and learning (decrease of receptors seen in Alzheimer’s disease)
  2. Neuronal development
45
Q

G-protein linked receptors; Autonomic targets = heart, Selected areas of brain

A

Muscarinic acetylcholine receptors

46
Q

What are the functions of muscarinic aceytlcholine receptors?

A

autonomic function (parasympathetic; i.e., slows heart)

47
Q

Both ion channels and G-protein linked; Ion Channels - AMPA, Kainite, NMDA;
G-protein – metabotropic receptors

A

glutamate receptors

48
Q

Receptors that have normal neurotransmission; long-term changes in the CNS (Long-term potentiation, Learning and memory); Overactivity may cause epileptic seizures

A

NMDA receptors

49
Q

Chloride ion-channel linked [Effect on cell membrane?]; Barbiturates bind to this = Sedation, Decrease anxiety, Anticonvulsants for treating seizures

A

GABA - A receptors

50
Q

G-protein mediated; Linked to ion channels through 2nd messengers; opens chloride-channels

A

GABA - B receptors

51
Q

What dopaminergic receptor types have the same effect?

A 
D1 = same as D3, D5
D2 = same as D4
52
Q

What types of beta receptors are in the heart? what is its effects when NE binds?

A

Beta-1; increase force and rate of contraction

beta blockers given to reduce amount of O2 needed for heart

53
Q

What types of beta receptors are in the lungs? what is its effects when NE binds?

A

Beta-2; bronchodilation

54
Q

What functions are regulated by serotonin receptors?

A
  1. Cognition
  2. Sleep
  3. Perception (including pain)
  4. Motor activity
  5. Mood
55
Q

What are the main types of opioid receptors?

A
  1. Mu (binds morphine)
  2. Delta
  3. Kappa
56
Q

What are opioid peptide receptors’ main function? where are they located?

A

Primary action is inhibition of slow pain information; Location = hypothalamus, spinal cord, and periaqueductal gray

57
Q

What are the ADRs of opioids?

A

Respiratory depression and slows GI (constipation)

58
Q

What drug is used to treat parkinson’s disease?

A

l-DOPA (increases the amount of dopamine that gets made, side effect can be psychosis due to too much dopamine)

59
Q

What drug is an example that prevents catecholamines to be stored into vesicles?

A

Reserpine

60
Q

What is a commonly used drug that blocks neurotransmitter release?

A

Botulinum toxin aka BOTOX (irreversibly binds to vesicles, and prevents them from releasing ACh at NMJ)

61
Q

How does the effect of botox go away?

A

The neural system makes new presynaptic terminals that branch off the old inactive terminal

62
Q

What’s important to remember as a PT when working with pts who get botox?

A

You want to work with them right away so you can raise level of functionality when the botox effect wears off

63
Q

What do drugs that block neurotransmitter degradation do?

A

prevent neurotransmitters from being broken down so their effects last longer (i.e., MAO-I, acetylcholinesterase)

64
Q

What drug is used in Parkinson’s disease that blocks the break down of dopamine (which produces free radicals) and can reduce the progression of the disease?

A

Monoamine oxidase inhibitors (MAO-I)

65
Q

What drug is used a lot in bug sprays and pesticides (also used in nerve gas)?

A

Acetylcholinesterase inhibitors

66
Q

What drugs act to prevent neurotransmitter reuptake?

A

Tricyclic antidepressants (inhibit monamine reuptake, also act at cholinergic receptors) and Selective Serotonin Reuptake Inhibitors (prozac)

67
Q

Antibodies are produced against voltage-gated calcium channel of the neuromuscular junction;Antibodies block calcium entry into presynaptic terminal; Mostly seen in patients with cancer, usually small cell carcinoma of the lung

A

Lambert-Eaton Syndrome

68
Q

What affect does lambert-eaton syndrome have on ACh release and muscle strength?

A

Decrease in ACh release and decrease in strength

69
Q

Disease where antibodies bind to the nicotinic acetylcholine receptor; Antibody blocks the effect of ACh on the muscle = increasing weakness seen with repeated use of a muscle; Initial sign in about 50% of patients is weakness opening eyelids/moving eyes

A

Myasthenia gravis

70
Q

With myasthenia graves, there is weakness opening eyelids or moving eyes. Why?

A

Because we use eyes/eyelids a lot

71
Q

What are common treatments of myasthenia gravis?

A
  1. Acetylcholinesterase inhibitors
  2. Removal of thymus gland (repress production of antibodies)
  3. Immunosuppressive drugs (repress reproduction of antibodies)
  4. Plasmapheresis: removes antibodies

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