Glutamate and GABA: the brain's accelerator and brake
Introduces the main excitatory and inhibitory transmitters — the balance that sedatives, alcohol and withdrawal all tip.
Where this fitsConnects to 1 · Unlocks 1
- Connects to
- Plasticity and neurogenesis — NMDA receptors are how 'fire together, wire together' happens.
- Unlocks
- Therapeutic window, steady state, washout — and tolerance — Stopping a depressant abruptly can cause rebound excitation — a withdrawal risk.
Walk through
Glutamate's receptors
NMDA, AMPA and kainate are ionotropic and excitatory. mGlu receptors are metabotropic: group 1 excitatory, groups 2–3 inhibitory. Glutamate is cleared by EAAT transporters and processed in glia.
Analogy and worked example
Analogy: The NMDA receptor is a bank vault needing two keys (glutamate and glycine) plus a timer (depolarization) before it opens. GABA is the car's brake; glutamate the accelerator. Sedatives press the brake harder — take them away suddenly and the car lurches forward.
A person who has drunk heavily every day for months stops suddenly and has a seizure. Why?
- Alcohol boosts inhibition (GABA-A); the brain adapts by increasing excitation.
Tip: the ← and → keys move through the lesson.
Full lesson: Glutamate/NMDA and GABA comparisons