Craviso: CNS Neurotransmission Flashcards by Megan Foggia

T/F: Average neuron forms ~ 1000 synaptic connections and receives even more

True

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What is the activity of a neuron dependent on?

the ratio of excitatory to inhibitory inputs to that neuron

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What are the small molecules involved in CNS functioning?

serotonin
norepi
dopamine
ACh
histamine

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neurotransmitter; sleep, arousal, mood, appetite

serotonin

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neurotransmitter; mood, arousal, appetite

norepi

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neurotransmitter; movement (motor control), behavior, mood, perception

dopamine

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neurotransmitter; arousal, cognition (memory and learning)

ACh

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neurotransmitter; wakefulness, equilibrium

histamine

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Excitatory amino acid neurotransmitter

glutamate (glutamic acid)

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Inhibitory amino acid neurotransmitters

GABA

glycine

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Neuropeptides involved in pain transmission

methionine
leucine enkephalin
substance P

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Endocannabinoids involved in memory, cognition, and pain perception

anandamide
2-arachidonylglycerol

**post-synaptic neurons make endocannabinoids and they are retrograde NTs

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Pattern of neuronal connectivity: Transmission is highly sequential and interconnected neurons are related to each other in a hierarchical fashion - e.g., primary sensory and motor pathways
Pain transmission!

long-hierarchical (relay)

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Pattern of neuronal connectivity:
Neurons from a single anatomical location extend multiple, divergent connections to target cells outside the region in which the neurons originate

non-hierarchical, projecting

ex: serotonin, norepi, dopamine, ACh, 5HT

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Where do serotonin neurons project from?

raphe nucleus

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Functions of 5HT (serotonin)

sleep, arousal, mood
behavioral changes
hallucinations
feeding behavior
vomiting

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Where do norepinephrine neurons project from?

locus coeruleus

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Functions of norepinephrine

arousal and mood (frontal cortex)
appetite (hypothalamus)
cardiovascular control

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Where do dopamine neurons project from?

midbrain
striatum
hypothalamus

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Functions of dopamine

mood
behavioral changes
motor control (nigrostriatal pathway)
neuroendocrine function
vomiting

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Where do ACh neurons project from?

forebrain and brainstem

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Functions of ACh

arousal
learning and memory (think of Alzheimer’s disease)
motor control (nigrostriatal pathway)

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The effects of cholinergic neurons can be via (blank) (GPCR) receptors or (blank) (ionotropic) receptors located presynaptically

muscarinic; nicotinic

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Where do histamine neurons project from?

hypothalamus

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Functions of histamine

arousal and wakefulness | equilibrium

effects on synthesis, storage, release, reuptake and/or degradation of neurotransmitters; agonist or antagonist activity at nerve terminal autoreceptors

pre-synaptic mechanisms by which neurotransmitters are modulated

receptor agonist, antagonist or modulatory activity; degradation of neurotransmitters

post-synaptic mechanisms by which neurotransmitters are modulated **ACh is inactivated by degradation

With these receptors, responses occur within several hundreds of milliseconds and last for seconds and even minutes

GPCRs (metabotropic receptors)

Some metabotropic receptors (GPCRs)

all alpha and beta adrenergic receptors (norepi receptors) dopamine muscarinic ACh histamine neuropeptide and endocannabinoid receptors most 5HT receptors (except those involved in vomiting) metabotropic glutamate and GABA receptors

How to GPCRs work?

1. neurotransmitter binds 2. activates G-protein 3. G-protein intracellular messengers modulate ion channels 4. ion channels open 5. ions flow across membrane

Ionotropic receptors are also called (blank)

ligand-gated ion channels

Where are most ionotropic receptors found?

at neuromuscular junctions

With these receptors, responses occur within a few milliseconds and last for only MILLISECONDS

ionotropic receptors

Which receptors DEPOLARIZE cells? What ion is involved?

``` AMPA *Na ion channel kainate *Na ion channel NMDA *Ca++ and Na nicotinic ACh receptors 5HT3 receptors (vomiting) *Na ``` **Na+ or Ca++ are involved

Which receptors HYPERPOLARIZE cells? What ion is involved?

GABA-A and glycine receptors **Cl- ion channels

How do ionotropic receptors work?

1. neurotransmitter binds directly to channel 2. channel opens 3. ions flow across membrane

So, which occur more quickly, metabotropic or ionotropic receptor reactions? Which have longer lasting effects?

ionotropic are faster; metabotropic last longer

Amino acid neurotransmitters mediate major excitatory inputs via (blank) and inhibitory inputs via (blank)

glutamate; GABA

Excitatory transmission is balanced by feed-forward and recurrent inhibitory actions of (blank) released from interneurons

GABA

Inputs to neurons are paired to achieve a coordinated balance between excitatory and inhibitory events, but (blank) neuro-transmission predominates

inhibitory

T/F: Interference of the relationship b/w excitatory and inhibitory neuro-transmission is highly disruptive

True **can cause two extremes - comatose or seizures

synthesized from glutamate, by glutamic acid decarboxylase that requires pyridoxal phosphate

GABA

What is GABA metabolized by in the mitochondria of neurons and glial cells?

GABA-amino transferase

What is unique about endocannabinoid transmission?

retrograde transmission - synthesized in post synaptic neuron

What does GABA bind to?

metabotropic receptors in nerve terminal which can modulate GABA release ionotropic GABA receptors postsynaptically, they will enhance the actions of GABA

There is a high conc of these receptors in the spinal cord

GABA-B receptors

an agonist at GABAB receptors, is used for treating spasticity (involuntary and abnormal muscle contractions) in individuals with amyotrophic lateral sclerosis (ALS) and multiple sclerosis (MS)

Baclofen (Lioresal)

When GABA binds, you are conducting (blank)

Cl-

What does GABA do to cells?

hyperpolarizes

The majority of GABAs effects are mediated by (blank) receptors

GABA-A

Contrast phasic and tonic neurotransmission

tonic - continuous activation of extra-synaptic receptors phasic - rapid, synchronous opening of channels in synaptic cleft; resolves in time and space

What is this? GABA gets released, and diffuses outside the synaptic cleft - binds to high affinity receptors and causes continuous activation of extra-synaptic receptors

tonic inhibition

Glycine are (blank) conducting ion channels

Cl-

occurs in nature in certain seeds; an ingredient in rat poison; an antagonist of glycine neurotransmission and a powerful convulsant!

strychnine **causes seizures when you block inhibitory neurotransmitters

What happens to glutamate after its release?

reuptake occurs via transporters present on nerve terminals and astrocytes (mostly astrocytes) - glutamate is converted to glutamine

These cells are responsible for much of the uptake and regulation of glutamate

glial cells

2 types of non-NMDA glutamate receptors

AMPA receptors | Kainate receptors

primarily Na+ - conducting ion channels; some receptors also permeable to Ca2+ mediate the majority of excitatory synapses play a major role in neural plasticity

AMPA receptors

primarily Na+ - conducting ion channels; some receptors also permeable to Ca2+ Located both pre- and post-synaptically physiologic role not known but play a role in neural plasticity

Kainate receptors

Ionophores that conduct primarily Ca2+; also conduct Na+ Are essential mediators of neural plasticity and are capable of converting specific patterns of neuronal activity into long-term changes in synapse structure and function (e.g., play a role in learning and memory)

NMDA glutamate receptors

What is an essential co-agonist necessary for NMDA receptors to be activated by glutamate?

glycine!!!

What blocks the NMDA channels and must be overcome with a strong depolarizing stimulus to activate the NMDA receptors?

magnesium

What two things must happen for NMDA receptors to be activated?

1. simultaneous binding of two agonists (glutamate and glycine) 2. strong enough depolarization to overcome Mg2+ block

What is neural plasticity?

the constant pruning and altering of neuronal dendritic connections; mostly due to the actions of glutamate

Increases sensitivity of post-synaptic neurons to glutamate

long-term potentiation

Decreases sensitivity of post-synaptic neurons to glutamate

long-term depression

How do NMDA receptors mediate neural plasticity?

If NMDA receptors are being activated more frequently, the number of AMPA receptors will increase and will cause a stronger, quicker response. Also, with increasing Ca++ due to activation of NMDA receptors, genes will be turned on that can change the synapse structure and make for stronger synaptic connections If NMDA receptors are not being activated frequently, AMPA receptors will be internalized and there will be weaker synaptic connections

Excessive activation of NMDA glutamate receptors causes (blank)

excitotoxicity

What is excitotoxicity?

too much activation of NMDA --> too much Ca++ coming in --> activates a lot of cellular processes --> NO and other free radicals build up --> leads to death of neurons