Term
| Why is understanding how a neurotransmitter is made useful? |
|
Definition
| it can help you create pharmacological treatments that either enhance or slow down the synthesis of that specific transmitter |
|
|
Term
| 2 pathways for glutamate synthesis |
|
Definition
1. alpha-ketoglutarate --> (via glutamate dehydrogenase) --> glutamate
2. glutamine --> (via glutaminase) --> glutamate |
|
|
Term
| Is glutamate a specific identifier for glutamatergic neurons? |
|
Definition
| no! (glutamate is everywhere) |
|
|
Term
| Can glutamate cross the BBB? |
|
Definition
| no! (it is negatively charged) |
|
|
Term
| 2 requirements for glutamate to get packaged into vesicle |
|
Definition
1. VGLUT (vesicular glutamate transporter)
2. vesicular proton pump (ATPase pump that pumps one proton in) |
|
|
Term
| How do you identify the action of glutamate in a neuron? |
|
Definition
1. stimulate presynaptic neuron --> you get an EPSP
2. puff glutamate onto synapse without stimulating presynaptic neuron --> EPSP |
|
|
Term
| Why do you need glutamate reuptake? |
|
Definition
| so synapse can be ready for the next time a signal comes through |
|
|
Term
| What is the goal of glutamate reuptake? |
|
Definition
| termination of action via taking out/degrading neurotransmitter |
|
|
Term
| ______ bring glutamate right back up into the presynaptic terminal |
|
Definition
|
|
Term
| In the CSF (fluid around neurons & in synapse), there is typically ______ of glutamate |
|
Definition
| 1 micromolar (remember it is ubiquitous & everywhere) |
|
|
Term
| What is the role of glial cells in glutamate reuptake? |
|
Definition
| they kind of isolate the synapse (block on either side) |
|
|
Term
| Once glutamate is in the cell, this reaction happens: ? |
|
Definition
| glutamate --> (via glutamine synthetase) --> glutamine |
|
|
Term
| Once glutamate is back in the presynaptic terminal, _____ works to package it back into vesicles for release |
|
Definition
|
|
Term
|
Definition
| conformational change to an inactive state |
|
|
Term
| AMPA receptors desensitize at a rate of ______ |
|
Definition
| 10's of milliseconds (really fast!!) |
|
|
Term
| blocking AMPAR desensitization --> what happens to the current trace? |
|
Definition
| you get a much wider current trace (takes curve longer to inactivate) |
|
|
Term
| Do NMDA receptors take less, longer, or about the same amount of time to inactivate as to AMPA receptors? |
|
Definition
| they have a much longer time it takes them to desensitize |
|
|
Term
| Is glycine associated more with inhibitory or excitatory? |
|
Definition
|
|
Term
| 2 places where glycine is largely found |
|
Definition
|
|
Term
| _____ is a co-agonist for NMDA glutamate receptors (where glutamate binds so sodium & calcium can go in & potassium can go out) |
|
Definition
| glycine (there is a separate glycine binding site) |
|
|
Term
| Glycine binding ______ glutamate binding to its site on an NMDAR |
|
Definition
|
|
Term
| Why don't we know the result of having a lack of glycine at NMDARs? |
|
Definition
|
|
Term
| Why is glycine called a "co-agonist" for NMDARs? |
|
Definition
| it isn't truly an agonist but it helps glutamate binding so much |
|
|
Term
|
Definition
| serine --> (via serine-trans-hydroxymethyl-transferase) --> glycine |
|
|
Term
| glycine uses _____ to be packaged into vesicles |
|
Definition
|
|
Term
| stimulating the presynaptic terminal of a glycinergic neuron OR puffing glycine onto the synapse --> ? |
|
Definition
|
|
Term
| 2 ways for glycine reuptake |
|
Definition
1. GLYT-2 found in presynaptic neurons
2. GLYT-1 found in glial cells |
|
|
Term
| What is the main inhibitory neurotransmitter in the CNS? |
|
Definition
|
|
Term
| Are there many or only a few GABAergic synapses? |
|
Definition
|
|
Term
|
Definition
| glutamate --> (via glutamic acid decarboxylase [GAD]) --> GABA |
|
|
Term
| how do you get GABA into a vesicle? |
|
Definition
|
|
Term
| stimulation & application of GABA to a synapse --> ? |
|
Definition
|
|
Term
|
Definition
1. GABA-T found in presynaptic neurons & glia
2. GAT found in presynaptic neurons & glia |
|
|
Term
| Schizophrenia seems to arise from an issue with _____ connections |
|
Definition
|
|
Term
|
Definition
| a neurological disorder characterized by sudden recurrent episodes of sensory disturbance, loss of consciousness, and/or convulsions, associated with abnormal, excessive neuronal activity in the brain |
|
|
Term
|
Definition
1. disruptions in neuronal connectivity that lead to excessive excitation or insufficient inhibition
2. damage to brain tissue
3. genetic or developmental abnormalities that prevent normal neuronal connectivity |
|
|
Term
|
Definition
1. medications
2. Neurostimulation
3. dietary approach
4. surgery to remove brain tissue that starts seizures |
|
|
Term
| Only _____% of epilepsy patients get sufficient seizure control with current treatment options |
|
Definition
|
|
Term
| Anti-seizure drugs that modify voltage-gated ion channels --> ? |
|
Definition
| inhibit sodium & calcium channels |
|
|
Term
| Anti-seizure drugs that enhance synaptic inhibition --> ? |
|
Definition
|
|
Term
| Anti-seizure drugs that inhibit synaptic excitement --> ? |
|
Definition
| decrease glutamate activity |
|
|
Term
| Gabapentin is a drug that is structurally similar to ______ |
|
Definition
|
|
Term
| Gabapentin binds to a subunit on _____ channels --> regulate channel activity (prevents it from opening as frequently) |
|
Definition
|
|
Term
| Gabapentin modulates the action of GAD --> ? |
|
Definition
|
|
Term
| Gabapentin stimulates noradrenaline mediated descending inhibition --> ? |
|
Definition
| anti-hypersensitivity in neuropathic pain |
|
|
Term
|
Definition
| drug that basically works to either decrease excitability or increase inhibition |
|
|
Term
| topiramate blocking sodium channels --> ? |
|
Definition
| stabilize inactive form of the channel |
|
|
Term
| topiramate GABA receptor facilitator --> ? |
|
Definition
|
|
Term
| What causes the side effects of antiepileptic drugs? |
|
Definition
| non-specific actions of the drugs |
|
|
Term
| 5 unintended effects of antiepileptic drugs |
|
Definition
1. weight gain
2. liver failure
3. loss of hair
4. depression
5. headaches |
|
|
Term
| Why do antiepileptic drugs get abused? |
|
Definition
| users say it gives them a marijuana-like sense of calmness/relaxation |
|
|
