Abstract
Co-release of acetylcholine (ACh) and glutamate has been found in a number of cases including Xenopus tadpole spinal cord and hindbrain interneurons, neonatal mouse motoneuron central synapses and rat basal forebrain cholinergic neurons. It is not clear at present whether the co-release is restricted to certain developmental stages. The significance of co-release of both excitatory transmitters may include complex interactions between cholinergic and glutamatergic transmissions during normal functions or development. In Xenopus tadpole spinal cord, co-released ACh from glutamatergic excitatory interneurons (dINs) activate the nicotinic receptors which may help maintain tonic NMDA receptor mediated membrane potential depolarization that is critical for persistent swimming. Nicotinic excitation in early development may also help facilitate the maturation of glutamatergic transmission at dIN synapses.
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