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Brain and Behavior > Neurotransmission > Flashcards

Neurotransmission Flashcards

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1
Q

Otto Loewi’s Key Experiment (what was it and what did results lead to?)

A
  • the vagus nerve was stimulated in a solution
  • solution was taken and another heart was placed into it. the hear rate slowed (decreased)
  • indicated that electrical transmission was not the only thing. gave hint towards existent of chemical transmission
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2
Q

Neurotransmitter

A

endogenous (produced within the organism) chemical messenger responsible for neural communication

  • chemical synaptic transmission
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3
Q

Where is NT located?

A
  • synthesized in the neuron (present in presynaptic axon terminals)
  • receptors exist on post synaptic cell
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4
Q

What does NT do?

A
  • is released in sufficient amounts when AP reaches presynaptic terminal to produce response in target cell
  • exogenous (originating outside of organism) administration mimics endogenously produced NT action. By blocking the release of NT, it prevents synaptic activity from affecting postsynaptic cell
  • mechanisms for removal of NT from site of activation include autoreceptors, degradation, reuptake
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5
Q

General Effects of NT: excitatory

A
  • excitatory: increase likelihood of firing AP in postsynaptic cell; opens sodium channel (helps depolarize membrane potential bc it is a positively charged ion. gets less negative. could also be another positively charged ion)
  • glutamate can open sodium channels
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6
Q

General Effects of NT: inhibitory

A

decreases likelihood of firing AP in postsynaptic cell

  • chloride ion channel is involved (negatively charged)
  • GABA
  • hyperpolarized instead of depolarization
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7
Q

Example of how the receptor determines IPSP vs EPSP reaction

  • ex: acetylcholine (ACh)
A

ex: acetylcholine (ACh) binds to two different types of postsynaptic receptors

  • ACh can be excitatory
    *opens positive ion channels (Na+ and K+)
  • ex: skeletal muscles
  • ACh can be inhibitory
    *opening negative ion channels like Cl-
  • ex: heart muscles
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8
Q

General Effects of NT: modulatory

A
  • instead of having direct effect, you can regulate the signal across synapse.
  • modulate activity of postsynaptic cell by influencing effects of chemical messengers
  • usually have more widespread effect
  • NT affecting larger number of diff. neurons
    *widespread effect can lead have more complex effects
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9
Q

Classes of Receptors: ionotropic

A

ionotropic receptors (also called ligand-gated ion channels)
- ion channel is right in the receptor
- there is a direct alteration of the ion channel.
->thus it is fast synaptic transmission

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10
Q

Classes of Receptors: metabotropic

A

dont contain ion channel
- often are G protein-coupled receptor
- G-protein can act as a signaling molecule or can affect messengers

  • indirectly alter ion channels/gene expression
  • other alterations can happen in the cell: can be longer lasting and can potentially enhance signal

->generally slower than ionotropic receptors

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11
Q

Acetylcholine (ACh)

A
  • was the first neurotransmitter to be identified
  • made from choline and acetyl CoA
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12
Q

Cholinergic neurons

A

neurons that use ACh

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13
Q

cholinergic neurons projecting through basil forebrain

A

widespread projections from forebrain to many different regions including the cortex, hippocampus, and amygdala (effect on memory/learning)

  • central in PNS
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14
Q

cholinergic neurons projecting through midbrain/pons

A

projections that are going away from the cortex (down spinal cord) may be signaling to skeletal muscles, internal organs

  • central in CNS
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15
Q

two main sources of cholinergic neurons are in

A

the basil forebrain and midbrain/pons

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16
Q

Functions of ach

A
  • attention, learning
  • really important as a signal for onset of sleep, drowsiness, arousal, and sensory processing and intentional focus
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17
Q

Two types of ACh receptors: muscarinic

A
  • G-protein coupled (metabotropic) receptors for ACh
  • slower
  • can be excitatory or inhibitory
18
Q

Two types of ACh receptors: nicotinic (nAch)

A
  • most are ionotropic and excitatory
  • are the main types of receptors in neuromuscular junction
  • are selective for positive ions (K+, Na+, Ca2+)
19
Q

one of the key components of ach synthesis pathway is

A

choline acetyltransferase (chAT): is an enzyme that transfers acetate ion from acetyl-CoA to choline (which is gotten from food) and turns it into acetylcholine (ACh)

20
Q

where is chAT enzyme found

A

ChAT is found in high concentration in cholinergic neurons
- both in (CNS) and (PNS)

ChAT is produced in the body of the neuron and is transported to the nerve terminal, where its concentration is highest.

21
Q

ACh metabolism

A
  1. acetylcholine (ACh) made from choline and acetyl CoA
  2. ACh is rapidly broken down in synaptic cleft by acetylcholinesterase
    - occurs quickly (breaks down molecule in 80 microseconds)
  3. choline is transported back into the axon terminal and is used to make more ACh
22
Q

acetylcholinesterase

A

enzyme that breaks down ACh in synaptic cleft

23
Q

Myasthenia Gravis

A
  • autoimmune disorder
  • attacks receptors for nAch (nicotinic)

ex: neuromuscular junction, esp in the face. some of the symptoms would be drooping in the face, a paralyzed-like facial. first symptom would be the weakness of the eye. muscle activation is inhibited

24
Q

Alzheimer’s Dementia (AD); Cholinergic Deficit Hypothesis

A

progressive cognitive decline

proposes that the symptoms of dementia is due to lack of Ach

death of cholinergic neurons in basal forebrain. ex: there are 500k cholinergic neurons in nucleus basilis but goes down to only 100k in advanced AD

increasing Ach levels or inhibiting Ach breakdown may result in improved cognitive function

25
Q

Alzheimer’s Dementia (AD); inhibiting Ach breakdown

A

prob a better option because of the blood brain barrier

26
Q

Popular approach for addressing AD: enhancing cholinergic transmisison

A

AchE inhibitors (donezepil, Aricept) to help treat AD

inhibiting AChE enzyme -> it increases Ach levels in synaptic cleft. signaling increases

help cognitive symptoms but do not alter disease progression (only 1-3 yr effect)

27
Q

Where in the neuronal pathway could be intervened to increase cholinergic transmission?

A

Ach receptor agonists increase Ach levels in synaptic cleft
-> help cognitive symptoms

Drugs that target ChT1 enzyme (by blocking reuptake)

28
Q

Serotonin 5-HT

A

most cells are in raphe nuclei

serotonergic fibers project widely

in implicated in sleep states, mood, sexual behavior, and anxiety

29
Q

Serotonin Synthesis; diet differences

A

tryptophan (from food) regulates synthesis

large amino acids can compete for transport across BBB

high protein diet increases competition -> less 5-HT

high carb diet reduces competition -> more 5-HT

30
Q

Serotonin Synthesis: rate limiting step

A

rate limiting step: availability of tryptophan hydroxylase (TPH) converts tryptophan to 5-HTP ( the chemical precursor/metabolic intermediate in biosynthesis serotonin)

31
Q

Serotonin Synthesis Metabolism (MAO)

A

mitochondrial membrane enzyme: monoamine oxidase (MAO)

32
Q

What might MAO inhibitors do to serotonin level?

A

MAO enzymes are involved in removing the NTs like serotonin from the brain.

MAOIs prevent removal of serotonin, which makes more of these brain chemicals available to effect changes in both cells and circuits

33
Q

What do antidepressants, such as Prozac, do?

A

they can increase 5-HT activity by inhibiting (blocking) reuptake thus increasing serotonin in synaptic cleft which increases activation of serotonin receptors

34
Q

Gastrointestinal, behavioral, and CNS effects of serotonin

A

GI: gastric secretion, gastrointestinal motility, intestinal secretions, colonic tone, pancreatic secretion

behavioral: visceral pain (internal organs), emotion, stress response, appetite, addiction, sexuality

CNS: motor control, circadian rhythm, cerebellum regulation, body temp, cns vascular tone

35
Q

Dopamine (DA) nigrostriatal pathway

A
  • DA found in neurons in nigrostriatal pathway
  • substantia nigra origin (is affected in parkinson’s)
  • targets striatum which targets motor control
  • neuronal loss is a cause of Parkinson’s disease
36
Q

Dopamine (DA) mesolimbocortical pathway

A

mesolimbocortical DA pathway
- in the ventrotechmental area (VTA- where DA is made)
- targets nucleus accumbens, hippocampus, and cortex
- is involved in how we learn reward, reinforcement learning
- abnormalities associated with schizophrenia

37
Q

Dopamine synthesis

A

tyrosine is a precursor found in our diet -> tyrosine hydroxylase (a rate-limiting enzmye) turns tyrosine into L-DOPA -> L-DOPA is converted into dopamine

38
Q

Dopamine metabolism

A

Monoamine oxidase (MAO) and catechol-O-methyl transferase (COMT) seen in synaptic cleft that break down DA

39
Q

Norepinephrine and epinephrine synthesis

A

also synthesized by tyrosine

any neurons that have tyrosine hydroxylase can produce any catecholamine transmitter

40
Q

Norepinephrine

A

released from locus coeruleus in the pons and lateral tegmental system in the midbrain

cells producing it are noradrenergic

NE systems modulate processes including mood, arousal, and sexual behavior

41
Q

Epinephrine (adrenaline)

A

regulate sympathetic nervous system
fight or flight response
increase heart rate, blood flow, and faster breathing

Brain and Behavior (14 decks)

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