Neuropharmacology 2: Transmision and Transduction

Terms in this set (13)

which neurotransmitters are released together?***imp
Dopamine and Enkephalin
Glutamate and Substance P (for pain)
where can anti-epileptic drugs act?
GABA ion channel, or/both Na, K, Ca
Give an example of retrograde communication?**Imp
EC (endo cannabionoid - Anandamide) binding to CB1 receptors on presynaptic; Marihuana - THC also works on CB1 receptors
What drug blocks Na-gated ion channels during synaptic communication?**Imp
Lidocaine; also used as anti-arrhythmic drug
Carbamezepine; also used as anti-epileptic, trigeminal neuralgia, and neuropathic pain
What drug blocks Ca ion channels during synaptic communication?**Imp
Gabapentin and Pregabalin; they block the release od neurotransmitter, glutamate which would have caused seizures
what is the effect/action of caffeine on adenosine in post-synaptic site?**imp
Caffeine blocks adenosine from it's receptors. It makes the NEURONS INCREASE IN NUMBER
Having Adenosine in the brain would cause what? And what type of receptor does it use in the heart, and blood vessels?***IMP
Adenosine in the brain is sedative
Heart - A1 receptor and DECREASE HR
BV - A2 receptor and DiLATE BV and DECREASE BP
How does caffeine induces Insomnia(inability to sleep)?**Imp
It BLOCKS A2a receptors
Which people are sensitive to caffeine?**Imp
People with gene variation ADORA2a; so ask people about caffeine use
A patient complained of throbbing headache, drowsiness, depression, lethargy (lack of energy). what is likely cause?**Imp
Caffeine withdrawal symptoms
What can cause the level of Norepinephrine and serotonin level in synaptic cleft to Increase?***IMp
Duloxetine; it binds to presynaptic receptor and prevents reupate.
What do increase level of serotonin and norepinephrine do in synaptic cleft?***Imp
They bind to G-protein linked receptor and cause BDNF level to increase which would stimulate and control SYNAPTOGENESIS, NEUROGENESIS and SYNAPTIC PLASTICITY
What happened in stroke?**Imp
There is loss of GABA input, which allows Glutamate to react and cause damage.

DRUG is most effective to block glutamate during ATAXIC phase while it would be better to enhance glutamate during CHRONIC PHASE
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