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首页> 外文期刊>The European Journal of Neuroscience >The supramammillary nucleus contributes to associative EPSP-spike potentiation in the rat dentate gyrus in vivo.
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The supramammillary nucleus contributes to associative EPSP-spike potentiation in the rat dentate gyrus in vivo.

机译：上乳头状核在体内有助于大鼠齿状回中的相关EPSP-穗增强。

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摘要

The supramammillary nucleus (SUM) of the hypothalamus sends neural projections to the hippocampus and is supposed to be involved in learning and memory. To test the possibility that SUM afferents modulate hippocampal functions, we investigated the effect of electrical stimulation of the SUM on the induction of long-term potentiation (LTP) at medial perforant path (PP)--granule cell synapses in the dentate gyrus (DG) of anaesthetized rats. High-frequency stimulation of the SUM (100 pulses at 100 Hz) alone did not change PP--DG field potentials. However, when the SUM stimulation was applied simultaneously with weak tetanic stimulation of the PP (20 pulses at 20 Hz) which alone did not induce any potentiation, it produced a long-lasting potentiation of the population spike, without an accompanying increase in the population excitatory postsynaptic potential (EPSP). The EPSP-spike (E-S) potentiation induced by pairing SUM and PP stimulation was abolished by lesions of the fimbria--fornix, a major pathway of SUM afferents. SUM stimulation applied 1 s before or after PP stimulation failed to produce E-S potentiation, and SUM stimulation augmented PP--DG field potentials during tetanic stimulation. Furthermore, the E-S potentiation was abolished by blocking GABAergic neurotransmission with picrotoxin. These results suggest that coactivation of SUM and PP inputs produces a long-lasting increase of granule cell excitability by modulating GABAergic inhibition. SUM afferents may contribute to associative memory processing by modulating hippocampal excitability.
机译：下丘脑的上乳头核（SUM）将神经投射发送到海马体，并被认为与学习和记忆有关。为了测试SUM传入调节海马功能的可能性，我们研究了SUM的电刺激对齿状回（DG）内侧齿孔通路（PP）-颗粒细胞突触的长时程增强（LTP）诱导的影响）的麻醉大鼠。仅对SUM进行高频刺激（在100 Hz时产生100个脉冲）并不会改变PP-DG场电势。但是，当同时施加SUM刺激和PP的弱强直性刺激（20 Hz的20个脉冲）时，单独不会产生任何增强作用，它会产生种群尖峰的持久增强作用，而不会伴随种群的增加兴奋性突触后电位（EPSP）。联合SUM和PP刺激引起的EPSP增强（E-S）增强被SUM传入的主要途径-穹ni-穹隆的病变所消除。在PP刺激未能产生E-S增强之前或之后1 s施加SUM刺激，并且在强直性刺激期间SUM刺激增强了PP-DG场电势。此外，通过用微毒素阻断GABA能神经传递，消除了E-S增强作用。这些结果表明，通过调节GABA能抑制，SUM和PP输入的共激活会长期增加颗粒细胞的兴奋性。 SUM传入可能通过调节海马兴奋性来促进联想记忆处理。

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