The neurobiology of slow synaptic transmission.
Nerve cells communicate with each other through two mechanisms, referred to as fast and slow synaptic transmission. Fast-acting neurotransmitters, e.g., glutamate (excitatory) and gamma-aminobutyric acid (GABA) (inhibitory), achieve effects on their target cells within one millisecond by virtue of opening ligand-operated ion channels. In contrast, all of the effects of the biogenic amine and peptide neurotransmitters, as well as many of the effects of glutamate and GABA, are achieved over hundreds of milliseconds to minutes by slow synaptic transmission. This latter process is mediated through an enormously more complicated sequence of biochemical steps, involving second messengers, protein kinases, and protein phosphatases. Slow-acting neurotransmitters control the efficacy of fast synaptic transmission by regulating the efficiency of neurotransmitter release from presynaptic terminals and by regulating the efficiency with which fast-acting neurotransmitters produce their effects on postsynaptic receptors.
Pubmed ID: 11691979 RIS Download
Adenylate Cyclase | Animals | Brain | Dopamine | Dopamine and cAMP-Regulated Phosphoprotein 32 | Glutamic Acid | Humans | Nerve Tissue Proteins | Neurons | Neurotransmitter Agents | Phosphoprotein Phosphatases | Phosphoproteins | Phosphorylation | Presynaptic Terminals | Protein Kinases | Receptors, Neurotransmitter | Second Messenger Systems | Signal Transduction | Synaptic Transmission