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Chika- SF2 > Neurotransmitters and Neuromodulators-Polston > Flashcards

Neurotransmitters and Neuromodulators-Polston Flashcards

1
Q

Most Nts are small molecules.

A

True

which comprises the AA: glutamate, GABA, glycine

the brainstem NTs: most of the cell bodies live in the brainstem: ACh

brainstem monoamines with two classes: catecholamines and indoleamines

neuropeptides
steroid hormones

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2
Q

Presynaptic terminal

A
  • voltage gated channels

- docking of vesicle containing NTs

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3
Q

Receptors on Post-synaptic cells

A

two kinds:

ionotropic: ion channels; they are usually multi unit that form a core that can be open or closed (default); when NT binds you get opening of channel, you get influx or efflux of ions (either depolarization or hyperpolarization of postsynaptic membrane
metabotropic: SLOWER; require secondary messengers; G-protein coupled receptors; you phosphorylate a channel or dephosphorylate and you’ll make the channel leaky or less leaky; no NTs binding, you’re affecting the receptors

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4
Q

What is a NT?

A

-it has to be synthesized in the neurons: that’s why steroid hormones are not NTs

  • it has to be present in presynaptic terminal
  • its release will cause an action in the post-synaptic cell
  • should have the same affect in lab and in natural biology

ALL NTs have some kind of mechanism that will remove it from the synaptic cleft: typically we release more than we need; we want them to have discrete actions and thus you have to get this stuff out of the synaptic cleft if you don’t use it

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5
Q

Small molecule NTs

A

AA:

glycine is EXCITATORY; it is an agonist of glutamate( primary excitatory NT)

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6
Q

AA NTs

A
  • derived from a single AA (glutamine or glutamic acid and then we do different things to it)
  • glutamate is EXCITATORY NT ALWAYS; predominate NT in the CNS ; it has COOH at each end
  • most synapses will release glutamate; widespread throughout the brain
  • a very small molecule and most of it diffuses out of the synapse (when discussing getting it out of the synaptic cleft)
  • there are glial cell that can get glutamate out and buffer the interstitial environment and make sure neurons are happy
  • glutamate is a critical player in learning and memory; involved in synaptic plasticity (use or lose it)
  • synapse potentiation: long term potentiation which means (EPSPs): is a persistent strengthening of synapses based on recent patterns of activity
  • b/c glutamate is excitatory can be pathological when it is in excess: epileptic sz (neurons over-excite and fire too much you get cytotoxicity = you kill neurons in the brain)
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7
Q

Glutamate has both ionotropic and metabotropic receptors.

A

3 types: if you put these in you get the same response as glutamate

NMDA receptors: binding sites for glu and gly (augments excitatory transmissions); permeable to sodium and calcium; one of the big players in cytotoxicity which is not good for the cell; the major type

At resting membrane potentiation NMDA channel is blocked by a magnesium channel. It takes a little bit of depolarization to get the ion out.

Glutamate has to interact first with the below receptors to get the magnesium out to get depolarization.

AMPA receptors
KAINATE receptors

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8
Q

metabotropic receptors-glutamate

A

on the presynaptic neurons , post-synaptic neuron, and glial cells

hear very little about these receptors

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9
Q

GABA

A

every cell has the gene for glutamic decarboxylase (GAD) but not every cell expresses this gene

  • if you are a neuron that expresses GAD you have the enzyme required to convert glutamate to GABA (pay attention to the COOH)
  • GABA is INHIBITORY; causes chlorine influx which hyperpolarizes; dominant inhibitory NTs
  • lots of INTERNEURONS are GABA
  • removal from cleft is through diffusion as it’s very small molecule
  • it is a neuron quieter (keeps the brain quiet)
  • benzodiazepine (anxiety drugs) act through the gaba system; sedative/ anesthesia/ alcohol; they are highly addictive; drugs to counteract over-excitation of seizures
  • also has ionotropic (bigger one) and metabotropic
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10
Q

Ionotropic: GABA

A

GABAa receptor: binding sites for GABA, benzodiazepines, barbiturates.

-Permeable to chloride ions, hyperpolarization

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11
Q

MEtabotropic- GABA

A

GABAb:

b1 binds the GABA and activates b2

b2: G-protein coupled part that will ultimately hyperpolarize the neuron

Dimerization, “allosteric modulation”.
Actions through G-protein mechanisms
Increased K+ conduction, hyperpolarization

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12
Q

ACh

A
  • ACh primarily produces in the nucleus basalis and pedunculopontine nucleus
  • is synthesized by a choline and an acetyl group
  • ACh is an Ester
  • plays a role in learning and cognition
  • nicotinic (always excitatory) is ionotropic
  • muscarinic (could excitatory or inhibitory) is metabotropic; depends on what signaling pathway they’ll activate
  • WE DO NOT SYNTHESIZE CHOLINE; need to get them from diet or supplements
  • degraded by AChesterase in the synaptic cleft which will give us back our ester molecules (We keep) and choline which we excrete
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13
Q

Brainstem NTs

A

-have a single amine group (3 types)

Catecholamines are TYROSINE based:
-dopamine
-Norepinephrine
uses tyrosine hydroxylase

AND Indoleamines (tryptophan based)

from this point will no longer discuss ionotropic

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14
Q

Dopamine

A
  • only acts through metabotropic receptors
  • primarily D1 and D2
  • tyr–> L-DOPA–> (decarboxylase) dopamine
  • basal ganglia motor function pathways depend on dopamine
  • dopamine population in the substantia nigra: pigmented neurons (black) in the midbrain; important in Parkinson’s dz as these neurons are the one dying and thus motor loss; causes hypokinesis; one of the symptoms is cogwheel rigidity

-second dopamine pathway (population): mesolimbic pathway (midbrain to limbic area); involved in motivation and reward; dopamine binding in these pleasure centers is a big part of ADDICTION

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15
Q

Norepinephrine (adrenaline)

A

-goes through dopamine synthesis before it becomes a norepinephrine

-need a third enzyme called DA-beta-hydrolase
-made in the pons!! in a pair of bilateral nuclei: locus coeruleus
; these are also pigmented neurons that look blue

  • primarily involved in stress and arousal
  • can be inhibitory or excitatory depending on how they are hooked up to their secondary messenger pathways
  • presynaptic uptake mechanisms removes extra NTs
  • Norepinephrine are synthesized in the nerve terminals, where they have everything they need
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16
Q

Indoleamines (tryptophan based)

A
  • serotonin is produced in the raphe nuclei that spread along the brainstem along the midline
  • trp–>5-hydroxytryptophan–>5-hydroxytryptamine (Serotonin)
  • serotonin is a great interest in the psychiatry; plays a role in good mood
  • to remove excess from the cleft we have reuptake mechanism
  • mood disorders involved in inadequate serotonin transmission; treat these disorders with reuptake inhibitors; leaving serotonin in the cleft; leave it there; SSRI; much better than the benzodiazepine
17
Q

neuropeptides

A
  • are peptides
  • are very very SLOW
  • SLOW to produce (you don’t have everything you need like in the nerve terminal)
  • has dense core vesicles
  • released from secretory vesicles which are slower
  • always act through metabotropic
  • slow to act, slow to replenish, slow to get more of
  • DCV: look like a dense core and have lots of neuropeptides
18
Q

Types of neuropeptides:

A

endorphins: pain inhibitors
tachykinins: pain transmitters
somatostatin: hypothalamic peptide

CCK: a brain peptide; that were originally isolated in gut (aids with digestion) and we found out it’s in the brain (appetite) too

19
Q

steroid hormones

A
  • not true NTs but act on the brain
  • are lipophilic, can diffuse across the membrane
  • acts as a transcription factor
  • in the blood and cross the BBB as they are very small
  • diffuse across membrane
  • every neuron will get steroid hormones
  • limiting factor is do you express the receptor or not
  • mechanism of action is genomic
  • VERY SLOW acting
  • have global extended action (not discrete like NTs)
20
Q

Steroid actions in brain (organizational)

A

2 types:

  • organizational effects (in early years) as they permanently organize how the brain will be; important in development exposure to gonadal steroids
  • male song birds: testes produce the hormones to do so; but not in female (could give them the hormones and they get the same results they just don’t have the testes to do so)

-male brain shuts down ovulation center; female will ovulate

  • female are good at identifying subtle difference
  • males are good at rotating 3D objects
21
Q

steroid hormones (Acitivational)

A
  • limited to brain areas where you see the receptors
  • very global slow background effects
  • hippocampus is a major site for learning (damaged in Alzheimer’s); has receptors for cortisol
  • chronic levels of cortisol is neurotoxic (killing the neurons which are your learning neurons)
  • exercising; talking on the phone; TV break
  • limbic system is a big center of emotion; sex steroids can affect our mood (mood swings at menopause or periods)
  • steroid rage in men can cause anger issues
22
Q

Sex differences in brain will gives us differences in disorders

A
  • Men are less likely to target PTSD than women.
  • Men are more likely to get autism (1/4) than women.

MEN are more likely:

  • autism
  • early onset schizophrenia
  • alcoholism
  • antisocial personality
  • ADHD
WOMEN more likely:
-depression
anxiety disorder 
somatic complaints 
-PTSD
-Alzheimer's dz

Chika- SF2 (63 decks)

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