Case Study Neuro

University:
The University Of Western Ontario
Course:
Biology 2290F | Scientific Method in Biology
Academic year:

2022
Views:

288

Pages:

3
Author:

Kyuwon J.

Experimental setup ● Objective ○ Effect of Ro15 on dopamine release ■ Induced through d-methamphetamine ■ Ro15 is GABA-A modulator ● Group ○ Vehicle + d-Methamphetamine ○ 1mg/kg Ro15 + d-methamphentamine ○ 1mglkg Ro15 + Vehicle ● Timeline ○ Saline injections in minute 42 (baseline conditions) ○ Treatment injections (Tx Inj) in minutie ) ○ Dopamine measure in minute 112 after injections Group Peak Dopamine (% Baseline) Timing Effect of Ro15-4513 Vehicle + d-Methamphetamine ~1100% ~28–42 min Strong surge in dopamine Ro15-4513 + d-Methamphetamine ~500% ~28–42 min Significantly attenuated Ro15-4513 + Vehicle ~100% N/A No significant dopamine change (control) Interpretation ● d-Methamphenamine increases the extracellular dopamine level ○ 11 times the baselines ● Ro15 reduces the increase done by methamphetamine ○ Inhibitory modulation of GABA-A receptors ● Ro15 alone will not affect baseline dopamine ○ Confirmation of specific interaction onceMA effects Mechanism ● d-Methamphetamine increase dopamine = reversing dopamine transmitter ○ Promotes vesicular release ● Ro15 enhance GABA inhibitory tone ○ Reduction of dopaminergic neurons ○ Dampening drug induced dopamine intake Terminology ● Methamphetamine ○ Psychostimulant drug ■ Synthetic derivative of amphetamine ● Enters presynaptic neuron through DAT dopamine transporter ● VMAT2 enters => displacing dopamine to cytosol ● Reverse transport happens through DAT ○ Massive extracellular dopamine releases ● Affect in Norepinephrine and Serotonin for lesser degree in Acute effect ○ Cardiovascular damage ■ Study model hyperdopaminergic states ■ Will mimic drug abuse ■ Dopamine surge linked to reward and addiction pathway ● GABA ○ Primary inhibitory neurotransmitter ○ Forming glutamate in glutamic acid decarboxylase ○ Binding to GABA receptors ■ GABA-A = Ionotropic ● Cl- channel ● Hyperpolarized neurons ■ GABA-B = Metabotropic ● Opening K+ channels ● Closing Ca2+ channels ■ Reduction of neuronal excitability ○ Promoting calmness, Sedation + muscle relaxations ● Agonist / Modulators ○ Benzodiazepines ○ Barbiturates , alcohols ● RO15 inverse agonist + modulators in GABA-A signalling ○ Damage in excitatory dopaminergic response ○ Dampens excitatory dopaminergic activity