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BIOL 203 – Anatomy & Physiology > Lecture 19 – NS V -- Synapses > Flashcards

Lecture 19 – NS V -- Synapses Flashcards

1
Q

LO1: how are messages transmitted form one neuron to another?

A

electrical synapse and chemical synapse

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2
Q

LO1: how are messages transmitted form one neuron to another?

electrical synapse (explain, advantages, disadvantages):

A

adjacent cells joined by gap junctions

ions diffuse directly from 1 cell to next

advantage: much faster

disadvantage: can’t integrate info

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3
Q

LO1: how are messages transmitted form one neuron to another?

chemical synapse (explain, advantages, disadvantages):

A

gap b/n 2 neurons

info passes chemically in form of neurotransmitters

advantage:
NTs can be both excitatory and inhibitory
quantity can vary –> allows integration of info

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4
Q

LO2: what kind of molecules are neurotransmitters?

“classical” neurotransmitters are ___

A

small molecules

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5
Q

LO2: what kind of molecules are neurotransmitters?

___ neurotransmitters are small molecules

A

“classical”

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6
Q

LO2: what kind of molecules are neurotransmitters?

list out different types of “classical” NTs:

A

amino acids

monoamines

acetylcholine

ATP and its derivatives (adenosine)

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7
Q

LO2: what kind of molecules are neurotransmitters?

A

“classical” NTs:
(amino acids, monoamines, acetylcholine, ATP & derivatives)

peptides

some “unconventional” NTs (modulators)

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8
Q

LO2: what kind of molecules are neurotransmitters?

examples of amino acid NTs:

A

glutamate – excitatory

GABA – inhibitory

glycine – inhibitory

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9
Q

LO2: what kind of molecules are neurotransmitters?

examples of monoamine NTs:

A

catecholamines:
(dopamine
norepinephrine
epinephrine)

serotonin
histamine

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10
Q

LO2: what kind of molecules are neurotransmitters?

what are peptides?

A

short protein chains of 2-40 amino acids

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11
Q

LO2: what kind of molecules are neurotransmitters?

examples of peptide NTs:

A

B-endorphin
substance P

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12
Q

LO2: what kind of molecules are neurotransmitters?

examples of “unconventional” NTs (modulators):

A

gases like nitric (NO) and carbon monoxide (CO)

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13
Q

LO3: which steps are involved in the synthesis and release of “classical” NTs?

A

1) enzymes that synthesize the NTs are made in rough ER

2) enzymes sent to Golgi apparatus

3) enzymes are modified in Golgi apparatus

4) enzymes are transported along axon to nerve terminal by anterograde axonal transport

5) precursor needed for synthesis of NTs is taken up into the presynaptic nerve terminal mb –> NT is synthesized in presynaptic nerve terminal

6) NT is taken out of cytoplasm and into small vesicles by Vesicular MonoAmine Transporter (VMAT)

7) NT is released by exocytosis when appropriate stimulus comes

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14
Q

LO4: Describe the steps (including enzymes) in the biosynthesis of catecholamines. Which are the 2 major enzymes responsible for their catabolism.

what are all catecholamines derived from?

A

tyrosine

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15
Q

LO4: Describe the steps (including enzymes) in the biosynthesis of catecholamines. Which are the 2 major enzymes responsible for their catabolism.

what is the rate-limiting step in the biosynthesis of catecholamines?

A

tyrosine hydroxylase

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16
Q

LO4: Describe the steps (including enzymes) in the biosynthesis of catecholamines. Which are the 2 major enzymes responsible for their catabolism.

describe the steps:

A

tyrosine –> DOPA –> dopamine –> norepinephrine –> adrenaline

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17
Q

LO4: Describe the steps (including enzymes) in the biosynthesis of catecholamines. Which are the 2 major enzymes responsible for their catabolism.

what are the 2 major enzymes responsible for catecholamine catabolism in the brain:

A

catechol-O-methyltransferase (COMT)

monoamine oxidase A (MAOa)

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18
Q

LO4: Describe the steps (including enzymes) in the biosynthesis of catecholamines. Which are the 2 major enzymes responsible for their catabolism.

how is epinephrine (adrenaline) synthesized?

A

epinephrine is synthesized from norepinephrine w/in the adrenal medulla, which are small glands associated w/ the kidneys

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19
Q

LO5: how does norepinephrine (NE) work in the synapse?

A

1) tyrosine is transported into the noradrenergic nerve terminal

2) dopamine (DA) is transported from cytoplasm into vesicle by vesicular mono amine transporter (VMAT)

3) DA is converted to NE in vesicle

4) AP causes influx of Ca2+ ions –> causes vesicles to fuse to mb surface and expel NE

involves SNAPS and VAMPS

5) NE released into nerve terminal can act on G protein-couple receptors (adrenoceptors)

6) NE can diffuse out of cleft or go back into nerve terminal by NE transporter (NET)

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20
Q

LO6: what type of receptors do NTs bind to?

2 types of receptors:

A

ionotropic receptors

metabotropic receptors

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21
Q

LO6: what type of receptors do NTs bind to?

ionotropic receptors are…

A

ligand-gated ion channel receptors

22
Q

LO6: what type of receptors do NTs bind to?

metabotropic receptors are…

A

G-protein coupled receptors

require intermediate molecules called G-proteins to activate second messenger molecules

23
Q

LO7: how does synaptic transmission finish?

3 ways:

A

diffusion and absorption

degradation

reuptake

24
Q

LO8: what does the monoamine hypothesis of depression suggest?

depression was associated with a deficiency of ___, such as ___ and ___

A

monoamines

serotonin

noradrenaline

25
Q

LO9: how does serotonin work in the synapse?

A

1) synthesis – serotonin is synthesized

2) storage – VMAT2 transports serotonin into storage vesicles

3) release – vesicles release serotonin into synaptic cleft

4) activation – serotonin binds to receptor and initiates a signal to cell body of postsynaptic neuron

5) clearing – receptor clears

6) some leftover serotonin is taken up by SERT (serotonin transporter) back into the presynaptic membrane

7) metabolism – monoamine oxidase (MAO) breaks down serotonin

26
Q

L10: which NT is associated w/ Parkinson’s disease (PD) and how?

A

neurons of substantia nigra and basal ganglia produce nigrostriatal dopamine pathway –> voluntary motor coordination

when neurons of substantia nigra degenerate –> less dopamine –> leads to Parkinson’s

27
Q

LO11: what does the dopamine theory of schizophrenia state?

positive symptoms

A

examples: hallucinations, delusions

receptor: D2

activity: hyper-

brain region: nucleus accumbens in limbic system

28
Q

LO11: what does the dopamine theory of schizophrenia state?

negative cognitive symptoms

A

examples: lack of motivation, cognitive impairment

receptor: D1

activity: hypo-

brain region: prefrontal cortex

29
Q

LO12: describe the 4 dopaminergic pathways in the brain and indicate their associated disorders:

1)

A

D1 –> Schizophrenia –> mesocortical –> prefrontal cortex

cognition and executive function (planning)

emotions and affect

decrease D1 == negative cognitive symptoms (e.g. apathy)

30
Q

LO12: describe the 4 dopaminergic pathways in the brain and indicate their associated disorders:

2)

A

D1 –> Schizophrenia –> nucleus accumbens in limbic system

motivation and reward

increase D2 == positive symptoms in schizophrenia (e.g. hallucinations)

31
Q

LO12: describe the 4 dopaminergic pathways in the brain and indicate their associated disorders:

3)

A

nigrostriatal –> dopamine in substantia nigra and basal ganglia –> Parkinson’s

motor movement

disorders: hypokinetic (e.g. Parkinson’s symptoms) and hyperkinetic movement disorders

32
Q

LO12: describe the 4 dopaminergic pathways in the brain and indicate their associated disorders:

4)

A

tuberoinfundibular –> dopamine in arcuate nucleus –> tuberal region of hypothalamus

inhibition prolactin release

decrease dopamine == hyperprolactinemia

affects motor movement

33
Q

LO13: which inhibitory NT is associated w/ epilepsy?

A

GABA

gamma-aminobutyric acid –> inhibitory –> amino acid NT –> ionotropic NT

GABA (inhibition) needs to offset glutamate (excitatory)

34
Q

LO14: describe how GABA exerts its inhibitory effects thru the GABAa receptor:

A

GABA binds to ion channel subunits –> causes conformational changes that open chloride ion channels –> lead to neuronal membrane hyperpolarization

35
Q

LO15: what does the cholinergic hypothesis of Alzheimer’s postulate?

A

ACh acts on target neurons in the hippocampus and the cerebral cortex, strengthening the neural circuits that are involved in memory formation

ACh disorder == loss of limbic and neocortical cholinergic innervation

36
Q

LO16: define synaptic plasticity:

neuroplsticity (define)

A

the ability of the brain to change, or rewire, throughout a person’s life

37
Q

LO16: define synaptic plasticity:

synaptic plasticity (define)

A

process of neuroplasticity occurring at the single-cell level (individual synapse)

basis of learning and brain repair after injuries

38
Q

LO17: differentiate the types of neuroplastic changes (temporary vs. long-lasting)

temporary (short-term memory)

A

sec to hrs

neurons can temporarily enhance their connections by:

chemical/synaptic changes

  • release more NT
  • activate a new receptor
  • modify an existing receptor
39
Q

LO17: differentiate the types of neuroplastic changes (temporary vs. long-lasting)

long-lasting (long-term memory)

A

lifetime

requires strong or sustained actives

structural and functional changes
- structural changes in dendrite and synapses
- changes in cortical area
- functional changes

40
Q

LO18: what are the 2 forms of long-term memory?

what are the 2 places important for long-term memory and what do they do?

A

hippocampus – forms memories

cerebral cortex – stores memories

41
Q

LO18: what are the 2 forms of long-term memory?

2 forms of long-term memory

A

explicit/declarative – conscious recollection of facts

implicit – procedural or unconscious (ex. riding a bike)

42
Q

LO18: what are the 2 forms of long-term memory?

what are the 2 forms of explicit/declarative long-term memory?

A

semantic – facts and general knowledge (ex. capital of Spain)

episodic – personally experienced events (ex. what you did on 10th birthday)

43
Q

LO19: differentiate long-term potentiation and depression:

A

depression – weakening of synaptic connection – lose memory

potentiation – strengthening of synaptic connection – improve memory

44
Q

LO19: differentiate long-term potentiation and depression:

how is long term potentiation caused?

A

high frequency (strong experience)

repeated stimulation (studying, revising)

45
Q

LO19: differentiate long-term potentiation and depression:

how is the strength of a synapse measured?

A

measured by the excitability or responsiveness of the post-synaptic neuron in response to a stimulus

46
Q

L20: what is the role of glutamate in memory and Alzheimer’s disease?

A

glutamate is main excitatory NT in CNS

main glutamate receptors are AMPA and NMDA receptors –> ligand-gated ion channels
–> major role in synaptic plasticity

47
Q

L20: what is the role of glutamate in memory and Alzheimer’s disease?

what happens when Ca2+ passes thru postsynaptic NMDA channels?

A

can have 2 different forms of synaptic plasticity – LTP or LTD

too much Ca2+ results in excitotoxicity

48
Q

LO20: what is the role of glutamate in memory and Alzheimer’s disease?

what is a result of too much NMDA activity?

A

too much Ca2+ flows thru NMDA channels –> causes excitotoxicity and promotes cell death –> leads to neurodegeneration and Alzheimer’s

49
Q

LO21: how do AMPA and NMDA receptors induce LTP?

4 steps:

A

1) glutamate release activates AMPA

2) AP allows Ca2+ to flow thru NMDA

3) more AMPA receptors gets inserted in plasma mb

4) postsynaptic cell is now more sensitive to glutamate – has more AMPA receptors, dendritic spines grow, more membrane is depolarized more efficiently

50
Q

LO22: what is the proposed mechanism of LTD at the glutamatergic synapse?

A

1) low firing rate of presynaptic neuron

2) few glutamate molecules

3) calcium that flows thru NMDA does different cellular cascade (phosphatase)

4) endocytosis of AMPA receptors

5) postsynaptic neurons are now less responsive to glutamate bc there are less receptors available

BIOL 203 – Anatomy & Physiology (58 decks)

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