Valjakka A, Lukkarinen K, Koivisto E, Riekkinen P, Miettinen R, Airaksinen M M, Lammintausta R, Riekkinen P
Department of Neurology, University of Kuopio, Finland.
Brain Res Bull. 1991 May;26(5):739-45. doi: 10.1016/0361-9230(91)90169-k.
The hippocampal EEG recording electrodes were implanted bilaterally in the hilus of the dentate gyrus (DG) and the stratum radiatum layer of the CA1 area in young (2-3-month-old) and aged (17-20-month-old) rats. In the subgroups of rats, brain noradrenaline (NA) was depleted by DSP-4 neurotoxin (50 mg/kg, IP). The aged animals were included in DSP-4-lesioned group in order to diminish the plastic regeneration of the noradrenergic system which may be more effective in young subjects. All the EEG recordings, after the administration of different agents or vehicle, were made while rats were awake and immobile. Approximately 40% decrease of brain NA had no noticeable effects on the nonrhythmical hippocampal EEG in either age group. In all the rats, compared to the baseline recordings, scopolamine hydrobromide (2 mg/kg, IP, a muscarinic antagonist) increased the incidence of spontaneous EEG spikes, while tetrahydroaminoacridine (THA, 12.5 mg/kg, IP, an acetylcholine esterase inhibitor) decreased the spike activity and induced theta rhythm. Atipamezole (3 mg/kg, SC), a noradrenergic alpha 2-antagonist, increased the baseline amplitude of the nonrhythmical EEG in the DG and increased slightly the spike activity in the CA1 area. The combined blockade of muscarinic receptors by scopolamine (2 mg/kg) and noradrenergic alpha 2-receptors by atipamezole (3 mg/kg) resulted in irregular EEG pattern and corresponding power spectra differed from the scopolamine spectra. The last combination treatment suggests that the effect of atipamezole was not mediated by the secondary cholinergic activation. In the DG, the spectral power increase caused by atipamezole may be related to the increased excitability/bursting liability of granular cells because NA turnover is increased by this agent and NA increases the excitability of granular cells.(ABSTRACT TRUNCATED AT 250 WORDS)
在年轻（2 - 3月龄）和老年（17 - 20月龄）大鼠双侧齿状回（DG）的门区和CA1区的辐射层植入海马脑电记录电极。在大鼠亚组中，用DSP - 4神经毒素（50 mg/kg，腹腔注射）使脑去甲肾上腺素（NA）耗竭。老年动物被纳入DSP - 4损伤组，以减少去甲肾上腺素能系统的可塑性再生，这在年轻个体中可能更有效。在给予不同药物或赋形剂后，所有脑电记录均在大鼠清醒且静止时进行。脑NA减少约40%对两个年龄组的非节律性海马脑电均无明显影响。在所有大鼠中，与基线记录相比，氢溴酸东莨菪碱（2 mg/kg，腹腔注射，一种毒蕈碱拮抗剂）增加了自发脑电尖峰的发生率，而他克林（THA，12.5 mg/kg，腹腔注射，一种乙酰胆碱酯酶抑制剂）降低了尖峰活动并诱发了θ节律。阿替美唑（3 mg/kg，皮下注射），一种去甲肾上腺素能α2拮抗剂，增加了DG中非节律性脑电的基线振幅，并略微增加了CA1区的尖峰活动。东莨菪碱（2 mg/kg）对毒蕈碱受体的联合阻断和阿替美唑（3 mg/kg）对去甲肾上腺素能α2受体的联合阻断导致脑电模式不规则，相应的功率谱与东莨菪碱谱不同。最后这种联合治疗表明阿替美唑的作用不是由继发性胆碱能激活介导的。在DG中，阿替美唑引起的频谱功率增加可能与颗粒细胞兴奋性/爆发倾向增加有关，因为该药物增加了NA周转率，而NA增加了颗粒细胞的兴奋性。（摘要截选至250字）
