Please use this identifier to cite or link to this item: https://une.intersearch.com.au/unejspui/handle/1959.11/381
Title: Long-Lasting Synaptic Modification in the Rat Hippocampus Resulting From NMDA Receptor Blockade During Development
Contributor(s): Bellinger, FP (author); Wilce, PA (author); Bedi , KS (author); Wilson, P (author)
Publication Date: 2002
DOI: 10.1002/syn.10020
Handle Link: https://hdl.handle.net/1959.11/381
Abstract: Recent reports have suggested that proper maturation of synapses in the hippocampus requires activation of NMDA receptors. We previously demonstrated that neonatal ethanol exposure results in a lasting reduction in synaptic strength in the hippocampus. To determine if this reduction was due to ethanol's effects on NMDA receptors, we investigated long-term changes in synaptic properties resulting from administration of NMDA receptor antagonists to neonatal animals. Rats were injected daily from PND 4-9 with either the noncompetitive NMDA receptor antagonist MK-801, the competitive NMDA receptor antagonist CPP, or the AMPA receptor antagonist NBQX. Control rats were either injected daily with physiological saline during the same period or left to develop normally. Hippocampal slices were prepared from nembutal-anesthetized animals between PND 35 and PND 40. The maximum pEPSP and PS values were not significantly different between controls and NMDA antagonist-treated animals. However, slices from animals injected with NMDA receptor antagonists required higher stimulus currents to attain comparable pEPSPs. The ratio of the slope of the pEPSP to the amplitude of the presynaptic volley was also reduced, as were pEPSP responses to specific stimulus currents. None of these effects were observed in slices prepared from animals treated with the AMPA receptor antagonist NBQX. Glutamate receptor antagonism did not produce lasting changes in long-term potentiation or paired-pulse facilitation. These results indicate activation of NMDA receptors during development is necessary for proper development of synapses. Synapse 43:95-101, 2002. © 2001 Wiley-Liss, Inc.
Publication Type: Journal Article
Source of Publication: Synapse, 43(2), p. 95-101
Publisher: John Wiley & Sons Inc
Place of Publication: New York, United States of America
ISSN: 0887-4476
Field of Research (FOR): 110903 Central Nervous System
Peer Reviewed: Yes
HERDC Category Description: C1 Refereed Article in a Scholarly Journal
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