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首页> 外文期刊>The European Journal of Neuroscience >Endogenous acetylcholine lowers the threshold for long-term potentiation induction in the CA1 area through muscarinic receptor activation: in vivo study.
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Endogenous acetylcholine lowers the threshold for long-term potentiation induction in the CA1 area through muscarinic receptor activation: in vivo study.

机译：体内研究表明，内源性乙酰胆碱可通过毒蕈碱受体激活降低CA1区长期增强诱导的阈值。

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Abstract Little is known how synaptically released endogenous ACh affects hippocampal synaptic plasticity in vivo. Here, we examined the role of cholinergic drive in the regulation of the induction of long-term potentiation (LTP) at basal dendrites in the CA1 area of the anaesthetized rat hippocampus. The non-subtype selective muscarinic acetylcholine receptor antagonist, scopolamine, (0.3 mg/kg, i.p.) inhibited the induction of LTP by weak, but not strong, high frequency conditioning stimulation. A relatively M(1) subtype-selective receptor antagonist, pirenzepine, (50 nmol/5 micro L, i.c.v.) also inhibited LTP induction by the weak protocol. As the medial septum (MS) is a major source of endogenous ACh in the hippocampus, we also examined the effect of high frequency pre-conditioning stimulation of the MS on LTP induction. The pre-conditioning MS tetanus reduced the threshold for LTP induction at basal synapses in a narrow time window. Such an effect of MS pre-conditioning was prevented by scopolamine, strong evidence of a direct MS control of LTP threshold through a mechanism dependent on muscarinic receptor activation. These results suggest that the cholinergic drive to the hippocampus is critically involved in the control of the LTP induction threshold in vivo. To the extent that LTP mechanisms may underlie certain types of learning and memory, the septo-hippocampal cholinergic regulation of synaptic plasticity may constitute an important target for the treatment of cognitive disorders associated with ACh deficits.
机译：摘要人们尚不知道突触释放的内源性ACh在体内如何影响海马突触可塑性。在这里，我们检查了胆碱能驱动在麻醉大鼠海马CA1区基底树突中长期增强（LTP）诱导调控中的作用。非亚型选择性毒蕈碱型乙酰胆碱受体拮抗剂东pol碱（0.3 mg / kg，腹腔注射）通过弱但不强的高频调节刺激抑制LTP的诱导。相对M（1）亚型选择性受体拮抗剂pirenzepine（50 nmol / 5 micro L，i.c.v.）也通过弱方案抑制LTP诱导。由于内侧隔膜（MS）是海马内源性ACh的主要来源，因此我们还研究了MS的高频预处理刺激对LTP诱导的影响。预先治疗的MS破伤风可以在很短的时间范围内降低基础突触处LTP诱导的阈值。东pol碱可预防MS预处理的这种作用，东pol碱是通过依赖毒蕈碱受体激活的机制直接控制LTP阈值的有力证据。这些结果表明，对海马的胆碱能驱动与体内LTP诱导阈值的控制密切相关。在一定程度上，LTP机制可能是某些类型的学习和记忆的基础，隔垫-海马胆碱能调节突触可塑性可能是治疗与ACh缺陷相关的认知障碍的重要目标。

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