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NBME 23 Answers

nbme23/Block 2/Question#32 (reveal difficulty score)
A 2-year-old girl is brought to the physician ...
N-methyl-d-aspartate (NMDA) ๐Ÿ” / ๐Ÿ“บ / ๐ŸŒณ / ๐Ÿ“–
tags: pharm neuro repeat

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 +19  upvote downvote
submitted by โˆ—nwinkelmann(366)

So, for some reason, neurotransmitters is something I've ALWAYS struggled with... probably because I wasn't taught it well so never really learned it, just learned enough for whatever exam. I just found this boo through NCBI and its FANTASTIC! It's from 2001 so might be old, but it was great. You can search through the book and find the chapters. I pretty much just went through all of the neurotransmitter chapter.

My main take-aways: Glutamate = major excitatory neurotransmitter. Two types of receptors: 1) metabotropic, most of which are presynaptic Gi which leads to decreased NMDA receptor activity and risk of exocitotixicity, or postsynaptic Gq receptors that lead to increase Na+, K+, and decreased glutamate causes depolarization and increased Mg++ displacement and NMDA receptor activity and risk of exocitotxicity, and 2) ionotropic channels including NMDA and AMPA/kainate channels, which all allow nonspecific cation influx, but only NMDA allows Ca++ influx (and only in a voltage dependent manner after sufficient depolarization has displaced the inhibitor Mg++ ion in the channel).

GABA and glycine = inhibitory neurotransmitters. 1) GABA-A and GABA-C = ionotropic channels that lead to eflux of Cl-, and despite this causing depolarization, the neuron still stays below resting potential. GABA-A binding site for barbiturates, steroids, GABA, and picrotoxin = inside pore of channel. GABA-A binding site of benzodiazepines = outside of pore of channel. 2) Glycine channel is a very similar Cl- eflux channel. 3) GABA-B is a metabotropic channel that activates Gi leading to decreased cAMP which activates efflux K+ channels and inhibits Ca++ influx channels leading to hyperpolarization.

Biogenic amines = catecholamines dopamine (coordination of body movement, reward, motivation, reinforcement), norepinephrine (sleep, wakefulness, attention, feeding behavior, epinephrine (lowest concentration in CNS), plus serotonin (sleep, wakefulness, depression, anxiety, nausea) and histamine (arousal, attention, allergy, tissue damage, and may influence blood brain flow). Obviously, all of this is in addition to adrenergic neurotransmission and flight, fright, and fight response.

ATP and other purines = excitatory transmission, co-released with other small-molecule neurotransmitters. Adenosine isn't classically considered a neurotransmitter because it isn't stored/released in Ca++ dependent manner, but derived from ATP before having an excitatory potential.

Acetylcholine = major neurotransmitter involved in neurotransmission via muscarin and nicotinic receptors.

Peptide neurotransmitters = commonly released as propeptide larger precursors that are cleaved by specific enzymes that were in the same neurotransmitter vesicle upon release. Five types = brain/gut peptides, opioid peptides, pituitary peptids, hypothalamic releasing hormones, and those not classified. Examples = precursor that gives rise to substance P (hippocampus, neocortex, and GIT and released from small diameter PNS C fibers that transmit pain and temperature information, powerful hypotensive, inhibited by opioid peptides), neurokinin A, neuropeptide K, and neuropeptide gamma, and opioid peptides including plant alkaloids (like morphine), synthetic opioid derivatives, and endorphins, dynorphins, and enkephalins. In general opioid peptides are depressants (i.e. analgesia mechanism), involved in complex behaviors (sexual attraction, aggressive/submissive behaviors), and implicated (though not definitive) in psychiatric disorders.

Overall, neurotransmitters = type types: small-molecule transmitters and neuropeptides, where small-molecules transmitters are faster and mediate rapid synaptic transmission (i.e. androgen SNS fight/flight/fright quick response), where as neuropeptides (along with biologic amines and some small molecule transmitters) are slower and mediate gradual, prolonged neurotransmission.

Some pictures:,, and

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sweetmed  This is amazing. thank you +
sweetmed  This is amazing. thank you +
paulkarr  Woah... +
brotherimodu  Short video someone posted from NBME-21 answers: +6
dorischang  Didn't finish reading this, but it looks awesome +3
kcyanide101  If you wanna write a text book just say :) +

  • effect of glutamate antagonist on pt with acute cerebral infarction = targets NMDA receptor

  • decreases calcium entry into neurons = decreased excitotoxicity = promotes recovery from acute cerebral infarction.

 +19  upvote downvote
submitted by โˆ—sympathetikey(1599)

Tough question.

Recall that Memantine (alzheimer's drug) is a NMDA Receptor Antagonist that helps prevent excitotoxcity by Blocking Ca2+ entry. That's how I remember this.

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veryhungrycaterpillar Great little read, and this is the paper they pretty much based this question on. +
veryhungrycaterpillar  Linked the wrong paper. Meant to link this one: +

a picture for better understanding

^ link is dead :( (they published a 3/e) but here is the re-route to the new site if anyone wants to dig in

+/- drdoom(1203)

 +4  upvote downvote
submitted by โˆ—spow(50)
  • A) GABA-A receptors let Cl- in
  • B) Glycine is used in the spinal cord as an inhibitory neurotransmitter; also lets Cl- in
  • C and E) Metabotropic glutamate receptors are G-protein coupled
  • Therefore, the only thing that could let Ca2+ in is NMDA receptors
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thotcandy  according to this, 5HT3 is an ion channel (mainly Na and K, but some Ca) so that was kinda effy imo +

 +3  upvote downvote
submitted by โˆ—lfsuarez(160)

NMDA receptors in this case are being used for long term potentiation within the brain and out of all of there choices only this receptor uses Ca+

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 +1  upvote downvote
submitted by chasingdreams101(4)

I picked NMDA because itโ€™s stimulatory, but is there any deeper reason for this?

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tea-cats-biscuits  The Q is actually asking which of the receptors use Ca+ ions, and of the choices given only NMDA receptors do so. +32

 +1  upvote downvote
submitted by โˆ—adong(144)

You can answer by process of elimination. "Competitive interactions" makes you think stimulatory NT. Cross out GABA and glycine. In the cortex so glutamate. Metabotropic would mean there's second messengers involved and the receptor would not transmit calcium. Hence NMDA.

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 +1  upvote downvote
submitted by โˆ—an1(114)

used in long term potentiation (language, memory), May also play a role in gene transcription in neurons

1) NMDA is a Glutamate receptor subtype 2) AMPA is a subtype of NMDA that is initially activated by glutamate release 3) NMDA receptors are found near AMPA receptors but are not activated by low levels of glutamate release due to a Mg ion โ€˜blockingโ€™ the channel 4) Frequent Action potential โ€”> stimulation of AMPA โ€”> depolarizes post synaptic neuron โ€”> voltage dependent Mg block of NMDA receptor removed 5) influx of Ca through NMDA โ€”> causes even more AMPA receptors to be inserted into the membrane (NOTE: AMPA is responsive to Ca and glutamate) 6) Because there are more receptors to respond to it, the cell is more responsive to glutamate

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 +0  upvote downvote
submitted by โˆ—zpatel(36)

all the others a noncompetitive since they have specificity(specific ligands), NMDA is the only nonselective(hence competitive receptor), has a ligand site and ca , na and mg...hence competitive

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hello  the question says competitive interactions, i think this is different from competitive binding. +

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