Leung L S, Martin L A, Stewart D J
Department of Physiology, University of Western Ontario, London, Canada.
Hippocampus. 1994 Apr;4(2):136-47. doi: 10.1002/hipo.450040204.
The effects of ibotenic acid lesion of the septum were studied in rats implanted with chronically indwelling electrodes and septal cannula. Each rat served as its own control and the properties of the hippocampal theta rhythm were studied before and after ibotenic acid and control saline infusion into the medial septal area. Ibotenic acid preferentially killed neurons in the lateral septum, and significantly attenuated the hippocampal theta rhythm about 50% bilaterally, at both surface and deep electrodes. The coherence and the phase of the theta rhythm at the CA1 apical dendrites, with respect to a superficial electrode, also declined significantly after ibotenic acid lesion. Pilocarpine (25 mg/kg i.p.) induced a theta rhythm of 7-9 Hz during immobility in the lesioned rats that was significantly higher in frequency than that induced in intact rats (4-6 Hz). In lesioned rats, the theta rhythm during tail pinch under urethane anesthesia was largely abolished, and the theta during walking was attenuated by atropine sulfate (50 mg/kg i.p.). Phencyclidine (10 mg/kg i.p.) or parachlorophenylalanine (PCPA) alone, which was inferred to abolish an atropine-resistant theta input, did not affect the power of the walking theta rhythm in either the lesioned or the normal rat. It was concluded that the theta in the behaving rats after ibotenic acid lesion in the septum has a strong atropine-sensitive component, and that it is not predominantly atropine-resistant, as suggested previously. The lack of PCPA effect on the theta phase in intact and lesioned rats also suggested a different view of the atropine-resistant theta in hippocampal region CA1. One possible mechanism of the atropine-resistant theta at the distal dendrites of pyramidal cells may result from rhythmic inhibition by stratum lacunosum-moleculare interneurons which may be activated by either serotonergic or cholinergic inputs.
在植入慢性留置电极和隔区套管的大鼠中，研究了隔区鹅膏蕈氨酸损伤的影响。每只大鼠作为自身对照，在向内侧隔区注入鹅膏蕈氨酸和对照生理盐水之前和之后，研究海马θ节律的特性。鹅膏蕈氨酸优先杀死外侧隔区的神经元，并在双侧表面和深部电极处显著衰减海马θ节律约50%。在鹅膏蕈氨酸损伤后，相对于表面电极，CA1顶树突处θ节律的相干性和相位也显著下降。毛果芸香碱（25mg/kg腹腔注射）在损伤大鼠静止期间诱导出7 - 9Hz的θ节律，其频率显著高于完整大鼠诱导出的θ节律（4 - 6Hz）。在损伤大鼠中，乌拉坦麻醉下夹尾时的θ节律基本消失，行走时的θ节律被硫酸阿托品（50mg/kg腹腔注射）减弱。单独使用苯环己哌啶（10mg/kg腹腔注射）或对氯苯丙氨酸（PCPA），推测其可消除对阿托品耐药的θ输入，但对损伤或正常大鼠行走时的θ节律功率均无影响。得出的结论是，隔区经鹅膏蕈氨酸损伤后的行为大鼠中的θ节律有一个强大的对阿托品敏感的成分，且并不像先前认为的那样主要对阿托品耐药。PCPA对完整和损伤大鼠θ相位缺乏影响也提示了对海马CA1区中对阿托品耐药的θ节律的不同看法。锥体细胞远端树突处对阿托品耐药的θ节律的一种可能机制可能源于腔隙-分子层中间神经元的节律性抑制，这些中间神经元可能由5-羟色胺能或胆碱能输入激活。
