Zn2+ Ions: Modulators of Excitatory and Inhibitory Synaptic Activity  

Oleh:

Smart, Trevor G. ; Hosie, Alastair M. ; Miller, Paul S.

Jenis: Article from Journal - ilmiah internasional
Dalam koleksi: The Neuroscientist vol. 10 no. 5 (Okt. 2007), page 432–442.
Topik: Zinc; Synaptic transmission; GABA; Glutamate
Fulltext: 432TN105.pdf (360.63KB)

Isi artikel

The role of Zn2+ in the CNS has remained enigmatic for several decades. This divalent cation is accumulated by specific neurons into synaptic vesicles and can be released by stimulation in a Ca2+-dependent manner. Using Zn2+ fluorophores, radiolabeled Zn2+, and selective chelators, the location of this ion and its release pattern have been established across the brain. Given the distribution and possible release under physiological conditions, Zn2+ has the potential to act as a modulator of both excitatory and inhibitory neurotransmission. Excitatory N-methyl-D-aspartate (NMDA) receptors are directly inhibited by Zn2+, whereas non-NMDA receptors appear relatively unaffected. In contrast, inhibitory transmission mediated via GABAA receptors can be potentiated via a presynaptic mechanism, influencing transmitter release; however, although some tonic GABAergic inhibition may be suppressed by Zn2+, most synaptic GABA receptors are unlikely to be modulated directly by this cation. In the spinal cord, glycinergic transmission may also be affected by Zn2+ causing potentiation. Recently, the penetration of synaptically released Zn2+ into neurons suggests that this ion has the potential to act as a direct transmitter, by affecting postsynaptic signaling pathways. Taken overall, present studies are broadly supportive of a neuromodulatory role for Zn2+ at specific excitatory and inhibitory synapses.

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