[Lithium-induced norepinephrine release from hippocampal slices in the absence of extracellular Ca2+]
Abstract:
Slices of rat hippocampus, preincubated with [3H] norepinephrine ([3H]NE) were superfused with Ca(2+)-free medium containing desipramine 1 mumol.L-1, Li+ (40-80 mmol.L-1) evoked [3H]NE release in a concentration dependent manner. It was enhanced by 4 beta-phorbol 12,13-dibutyrate (PDB) and inhibited by tetrodotoxin. Ca(2+)-chelator BAPTA-AM did not attenuate this Li-evoked [3H]NE release. After application of 3,4-diaminopyridine to evoke [3H]NE release and PDB to enhance this release, the Li(+)-evoked [3H]NE release was significantly inhibited. The findings suggest that the liberation of internal Ca2+ stores was not involved in this release process.
Related Concept Videos
Long-term Depression
Long-term depression, or LTD, is one of the ways by which synaptic plasticity—changes in the strength of chemical synapses—can occur in the brain. LTD is the process of synaptic weakening that occurs over time between pre and postsynaptic neuronal connections. The synaptic weakening of LTD works in opposition to synaptic strengthening by long-term potentiation (LTP) and together are the main mechanisms that underlie learning and memory.
Long-term Depression
Long-term depression, or LTD, is one of the ways by which synaptic plasticity—changes in the strength of chemical synapses—can occur in the brain. LTD is the process of synaptic weakening that occurs over time between pre and postsynaptic neuronal connections. The synaptic weakening of LTD works in opposition to synaptic strengthening by long-term potentiation (LTP) and together are the main mechanisms that underlie learning and memory.
Calcium Ion Concentration Mechanism
If over time, all...
Calcium Ion Concentration Mechanism
If over time, all...


