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Glutamate
⚡ Glutamate is the most abundant excitatory neurotransmitter in the vertebrate nervous system. 🧠 It is central to learning, memory, and cognition. 🔬 It also doubles as a key metabolic molecule in the Krebs cycle.
🧬 Structure and Synthesis
- Structure:
- Chemical formula: C5H9NO4.
- Has carboxyl group, amino group, and a side-chain carboxyl.
- Synthesis:
- From α-ketoglutarate (Krebs cycle) via glutamate dehydrogenase.
- From glutamine by glutaminase.
⚡ Role in Neurotransmission
- Excitatory Neurotransmitter: Main driver of fast synaptic transmission in the CNS.
- Receptors:
- 🟠 AMPA: fast excitatory currents.
- 🔵 NMDA: learning & memory (needs glutamate and depolarisation to open → coincidence detector for synaptic plasticity).
- 🟢 Kainate: additional excitatory control.
- 🔗 mGluRs (metabotropic): G-protein coupled, modulate excitability and plasticity.
- Synaptic Plasticity: Glutamate → LTP & LTD → foundation of memory encoding.
🔬 Metabolic Functions
- 🌍 Krebs cycle: intermediate for energy metabolism.
- 🧪 Ammonia detox: converted to glutamine via glutamine synthetase.
🛡 Regulation of Levels
- Reuptake by EAAT transporters into neurons + glial cells.
- Astrocytes recycle glutamate → glutamine (glutamate–glutamine cycle).
⚠️ Clinical Significance
- Excitotoxicity: Excess glutamate → Ca2+ overload via NMDA receptors → neuronal death (seen in stroke & TBI).
- Neurodegeneration: Dysregulation in Alzheimer’s, Parkinson’s, Huntington’s, ALS.
- Psychiatry: Abnormal glutamate implicated in schizophrenia, depression, anxiety. 💊 NMDA modulators and mGluR drugs are under study.
📌 Quick Summary
⚡ Most common excitatory neurotransmitter. 🧠 Critical for memory & learning (LTP, LTD). 🔬 Links neural activity to metabolism (Krebs). 🛡 Controlled by EAATs & astrocytes. ⚠️ Excess = excitotoxicity → stroke, dementia, ALS.
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