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Medical Neuroscience Block 1 > 6 - Neurotransmitters > Flashcards

6 - Neurotransmitters Flashcards

1
Q

What is chemical communication used to transmit signals of the nervous system differentiated by?

A

Distance between transmitting and receiving cells

Types of signaling evoked

Stability of the transmitting molecule

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2
Q

Neurotransmitters do what type of signaling?

What about neuromodulators?

Hormones?

A

Nts: synaptic signaling

Neuromodulators: paracrine signaling

Hormones: endocrine signaling

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3
Q

What are the four types of signaling?

A
  1. Fast and short-term change in synaptic membrane potential
  2. Slower/longer change in syn. membrane potential
  3. Retrograde regulation of release/synthesis
  4. Long term changes in gene expression
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4
Q

What are fast and short changes in synaptic membrane potential mediated by?

A

Ligand-gated ionotrophic receptors.

Changes in ionic conductance result in changes of membrane potential.

Summation of these potentials regulate probability of AP generation.

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5
Q

What are slower and more lasting changes in membrane potential mediated by? How does the signaling compare to ionotrophic signaling?

A

G-protein coupled receptors; the signal is indirect as a result of changes in phosphorylation triggered by 2nd messengers.

Capable of hyperpolarization or depolarization.

Take longer to develop, but last longer than ionotrophic receptor signaling.

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6
Q

What type of change in conductance will produce an ipsp (inhibitory postsynaptic potential) in a normal CNS neuron?

A

An increase in potassium conductance, which would cause K+ to move down its gradient out of the cell and make the membrane potential more negative (hyperpolarization).

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7
Q

What 6 nts are involved in producing epsp’s and ipsp’s through activation of ionotrophic receptors?

A

Acetylcholine

Amino acids: Glutamate, Aspartate, GABA, Glycine

Purines: ATP

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8
Q

How is Ach made? What is it metabolized by?

A

Choline and acetylcoA via acetyltransferare (ChAT).

Metabolized by acetylcholine esterase (AChE) an efficient enzyme at the neuromuscular junction.

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9
Q

What is the rate limiting step of in acetylcholine?

A

Choline being taken back into the synthesizing neuron.

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10
Q

What would be the most efficienct way to increase the amount of acetylcholine available in the synapse?

A

Inhibiting acetylcholine esterase

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11
Q

What are the characteristics of nicotinic receptors?

A

They are fast, ligand gated sodium channels at the neuromuscular junction.

Involved in reward and arousal circuits - can result in dependence via CNS receptors.

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12
Q

What are the characteristics of muscarinic receptors? What can they be blocked to treat?

A

Slow; member of the G protein coupled receptor family.

Located at parasympathetic ganglia, basal forebrain, and striatum.

Used to treat parksinson’s disease.

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13
Q

Synthesis and degradation of glutamate are linked through what? Where are the membrane carriers found?

A

The glutamine/glutamate shuttle.

Membrane carriers are on both astrocytes and neurons and also carry aspartate.

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14
Q

How is glutamate transporterd?

A

It’s packaged into vesicles via the Vglut family.

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15
Q

What are the two types of ionotrophic receptors for glutamate in the CNS?

A

AMPA and Kainate receptors

NMDA receptors

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16
Q

What are the characteristics of AMPA and kainate receptors? What ions do they use? What is their function?

A

Sodium is the primary ion, activation results in epsp, primary mechanism for excitatory info flow from point to point in the brain.

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17
Q

What do NMDA receptors require to open? What ions are use and what is the function? What do they allow into the cell when open?

A

Require both glutamate to bind and membrane depolarization to open.

Calcium as well as sodium is conducted into the cell.

Required for long-term learning potentiation and memory.

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18
Q

What special ion is found in NMDA receptors and what is its function?

A

MG plug in the channel that sticks there unless the membrane in the region has been depolarized

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19
Q

What are the negative effects of glutamate?

A

It can activate too many proteases and also puts an energetic burden on the cell because ATP is needed to pump Ca back out.

Ca will activate proteases which will injure the cell more.

20
Q

How is glutamate related to stroke? How is it related to neurodegenerative disorders?

A

In stroke, anoxia is through to trigger the release of excessive amounts of glutamate.

Glutamate reuptake is reduced in parkinsons, ALS, Alzheimers.

21
Q

NMDA receptor inhibitors are used to treat what?

A

Alzheimer’s and ALS.

22
Q

Our goal is to pharmacologically reduce glutamate-induced excitotoxicity, how would we do this?

A

Inhibit the NMDA channel.

You couldn’t inhibit glu synthesis or block AMPA receptors because those are important for communication between neurons.

23
Q

What is gaba? What is it’s function?

A

Major inhibitory nt in the CNS that plays a role in point to point info flow in the striatum and cerebellum and in interneurons in the CNS.

24
Q

How is GABA made? What is an essential cofactor? What happened when it was left out of baby formula?

A

GABA is synthesized from glutamate by GAD.

Vitamin B6 is an essential cofactor; when left out of formula is causes seizure because of the loss of GABA.

25
Q

What is responsible for reuptake of GABA?

A

Glia and neurons.

26
Q

Describe GABA a receptors?These receptors are the site of action for which drugs?

A

Ionotrophic, conduct chloride to produce ipsp.

Many allosteric binding sites sites in the receptor complex.

Ethanol, general anesthetic, valium, and barbituates.

27
Q

Describe the GABA b receptors?

A

GPCRs that result in hyperpolarization via potassium channel opening.

28
Q

What are three functions of GPCRs?

A
  1. Alpha subunit and beta-gamma subunits can both signal.
  2. Regulation includes receptor-triggered exchange of GDP for GTP bound to the alpha subunit.
  3. Regulation involves hydrolysis of GTP to GDP by GTPase of the alpha subunit.
29
Q

Describe the onset of biogenic amines? What are the biogenic amines?

A

Slower onset and offset changes in synaptic potential.

Dopamin, norepi, epi -catecholamines

serotonin, and histamine.

30
Q

What do biogenic amines signal through? Where are the cell bodies located?

A

GPCR

Cell bodies are in the brainstem and hypothalamus and project widely to cortical and subcortical regions.

31
Q

All biogenic amines start from what? What is dopamine and norepi made from? What about serotonin? Histamine?

A

Amino acids.

Dopamine and norepi: tyrosine
Serotonin: trp
Histamine: histidine

32
Q

How are biogenic amine nts regulated?

A

product feedback.

33
Q

What drugs target serotonin reuptake transporters (SERT)?What do they treat?

A

SSRI’s, used for the treatment of depression.

34
Q

What drugs target dopamine reuptake transporters (DAT)?

A

Cocaine and amphetamine.

35
Q

What drugs target norepi reuptake transporters (NET)?

A

Tricyclic antidepressants.

36
Q

What is the biological role os norepi?

A

Autonomic outflow in brainstem; sympathetic ganglia; arousal.

Roles in blood pressure regulation and attention.

37
Q

What is the function of dopamine?

A

Regulates reward through the estrapyramidal system.

Roles of addiction and parkinson’s disease.

38
Q

What is the function of serotonin?

A

Regulates sleep/wake and mood.

Role in depression.

39
Q

What is the function of histamine?

A

Regulates sleep/wake and vestibular function.

Sleepiness is a side effect of antihistamines.

40
Q

What are things that can result from administering a drug that inhibits SERT chronically?

A
  1. Serotonin concentrations increase in the synapse

2. Serotonergic receptors down-regulate as a result of increased agonist stimulation.

41
Q

How are neuropeptidases used as signaling molecules? How are they inactivated?

A

They are energetically expensive and low amts are released.

Affinity for receptors is higher than other transmitters.

Inactivated via peptidases or by diffusing away from teh site of action.

42
Q

What is the function of neuropeptides?

A
  1. Transcription and translation of precursor peptides.
  2. Packaging into secretory vesicles at golgi.
  3. Fast axonal transport; processing
  4. Release
  5. Recovery of the membranes
43
Q

Release of neuropeptides from dense core vesicles requires more _____?

A

Calcium in the terminal.

44
Q

Co-release of neuropeptides and amino neurotransmitters allows for what?

A

Increase information content.

45
Q

What are the three types of inhibition of transmitter release? Describe each.

A
  1. Axon-axonal synapses: input selective
  2. Autoreceptors: receptors on preynaptic terminal feedback mechanism that can be inhibitory of facilatory
  3. Retrograde signaling: begins with postsynaptic depolarization triggering Ca influx.

Medical Neuroscience Block 1 (10 decks)

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