In:
Journal of Neurophysiology, American Physiological Society, Vol. 95, No. 3 ( 2006-03), p. 1537-1544
Abstract:
Spiny neurons in the neostriatum are highly vulnerable to ischemia. Enhancement of excitatory synaptic transmissions has been implicated in ischemia-induced excitotoxic neuronal death. Here we report that evoked excitatory postsynaptic currents in spiny neurons were potentiated after transient forebrain ischemia. The ischemia-induced potentiation in synaptic efficacy was associated with an enhancement of presynaptic release as demonstrated by an increase in the frequency of miniature excitatory postsynaptic currents (mEPSCs) and a decrease in the paired-pulse ratio. The amplitude of inward currents evoked by exogenous application of glutamate did not show significant changes after ischemia, suggesting that postsynaptic mechanism is not involved. The ischemia-induced increase in mEPSCs frequency was not affected by blockade of voltage-gated calcium channels, but it was eliminated in the absence of extracellular calcium. Bath application of ATP P2X receptor antagonist pyridoxal-phosphate-6-azophenyl-2′,4′-disulfonic acid (PPADS) significantly reduced mEPSC frequency in ischemic neurons but had no effects on the control ones. Furthermore, the inhibitory effect of PPADS on ischemic neurons was abolished in Ca 2+ -free external solution. These results indicate that excitatory synaptic transmissions in spiny neurons are potentiated after ischemia via presynaptic mechanisms. Activation of P2X receptors and the consequent Ca 2+ influx might contribute to the ischemia-induced facilitation of glutamate release.
Type of Medium:
Online Resource
ISSN:
0022-3077
,
1522-1598
DOI:
10.1152/jn.01166.2005
RVK:
XA 10000 ; XA 552555
Language:
English
Publisher:
American Physiological Society
Publication Date:
2006
detail.hit.zdb_id:
80161-6
detail.hit.zdb_id:
1467889-5
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