期刊
JOURNAL OF NEUROPHYSIOLOGY
卷 93, 期 5, 页码 3001-3006出版社
AMER PHYSIOLOGICAL SOC
DOI: 10.1152/jn.00546.2004
关键词
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Although bilateral fimbria-fornix (FF) lesioning impairs spatial performance in animals, the literature is equivocal regarding its effects on hippocampal long-term potentiation (LTP). We examined the effects of FF lesioning on LTP induction in the Schaffer collateral - CA1 pathway in vivo with a protocol that delivered theta burst stimulation (TBS) trains of increasing length until a sufficient length was reached to induce LTP of the monosynaptic field excitatory postsynaptic potential (fEPSP). Experiments were performed in urethan-anesthetized Long-Evans rats either 4 or 12 - 16 wk after lesioning. In sham-operated controls, TBS trains ranging from 4 to 12 bursts were sufficient to induce robust LTP [ 170 +/- 10% ( mean +/- SF) of control fEPSP slope; n = 8]. Four-week post - FF-lesioned animals also displayed clear LTP ( 167 +/- 12% of control fEPSP slope; n = 4) that did not differ from the shams ( P > 0.05). In contrast, animals in the 12- to 16-wk post-lesion group showed a highly significant deficit in LTP induction ( 95 +/- 3% of control fEPSP slope; n = 8; <= 28 burst TBS trains tested; P < 0.001 vs. sham- and 4-wk post-FF-lesion groups). Other quantitative measures of synaptic excitability (i.e., baseline fEPSP slope and input-output relation) did not differ between the sham- and the 12- to 16-wk post-FF-lesion groups. These results indicate that the FF lesion leads to an enduring defect in hippocampal long-term synaptic plasticity that may relate mechanistically to the cognitive deficits characterized in this model.
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