In:
European Journal of Neuroscience, Wiley, Vol. 13, No. 12 ( 2001-06), p. 2195-2204
Abstract:
Although glycine receptors (GlyRs) are responsible for the main spinal inhibitory responses in adult vertebrates, in the embryo they have been reported to mediate depolarizing responses, which can sometimes activate dihydropyridine‐sensitive l ‐type calcium channels. However, these channels are not the only targets of dihydropyridines (DHPs), and we questioned whether GlyRs might be directly modulated by DHPs. By whole‐cell recording of cultured spinal neurons, we investigated modulation of glycine responses by the calcium channel antagonists, nifedipine, nitrendipine, nicardipine and ( R )‐Bay K 8644, and by the calcium channel, agonist ( S )‐Bay K 8644. At concentrations between 1 and 10 µ m , all these DHPs could block glycine responses, even in the absence of extracellular Ca 2+ . The block was stronger at higher glycine concentrations, and increased with time during each glycine application. Nicardipine blocked GABA A responses from the same neurons in a similar manner. In addition to their blocking effects, nitrendipine and nicardipine potentiated the peak responses to low glycine concentrations. Both effects of extracellular nitrendipine on glycine responses persisted when the drug was present in the intracellular solution. Thus, these modulations are related neither to calcium channel modulation nor to possible intracellular effects of DHPs. Another type of calcium antagonist, verapamil (10–50 µ m ), also blocked glycine responses. Our results suggest that some of the effects of calcium antagonists, including the neuroprotective and anticonvulsant effects of DHPs, might result partly from their interactions with ligand‐gated chloride channels.
Type of Medium:
Online Resource
ISSN:
0953-816X
,
1460-9568
DOI:
10.1046/j.0953-816x.2001.01599.x
Language:
English
Publisher:
Wiley
Publication Date:
2001
detail.hit.zdb_id:
2005178-5
SSG:
12
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