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Mormyrid鱼电感受叶神经元可塑性的研究
The electrosensory system in mormyrid fish serves three functions: ac tive electrolocation, in which external object are sensed by the distortions of the electric field of the fish's electric organ discharge (EOD);electrocommuni cation, in which EODs convey information between fish;and passive electrolocati on, in which the low frequency electric fields from other animals in the water a re sensed. These functions are served by three classes of electroreceptors in th e fish skin. The primary afferents from these electroreceptors terminate in diff erent regions of the electrosensory lobe (ELL). ELL is a cerebellum like structu re which is also strongly affected by descending electric organ corollary discha rge signal (EOCD) associated with the motor command signals that drives EOD. Thu s, the descending EOCD signal and the EOD electrosensory input converge onto the ELL.In vivo studies have indicated that the EOCD signal generates negative images of predictable features in the sensory inflow in mormyrid ELL. Addition of such negative images to the actual or concurrent sensory input minim izes the predictable features and allows novel or unexpected inputs to stand out more clearly. The generation of negative images is largely due to plasticity at the parallel fiber synapses onto Purkinje-like cell in ELL.The present study extended these in vivo findings to in vitro slice pr eparation. The basic features and mechanisms of such plasticity were studied in ELL slices with the intracellular recording method. The plasticity was rapidly e stablished by pairing the electric-activated parallel fiber epsp with a post-s ynaptic broad spike evoked by depolarizing current pulse in a Purkinje-like cel l, at 1 Hz for 5 min at 0 to 50 ms delays. After such pairing, the parallel fibe r epsp was depressed by 25%～30% for over 30 min. This depression was blocked by adding NMDA receptor antagonist AP5 to the bath or injecting calcium chelator B APTA into the recorded cell. The depression could be reversed by stimulating the parallel fiber at 1 Hz without pairing with post-synaptic broad spike, this hap pens under natural physiological conditions. It is hypothesized that the broad s pike leads to calcium influx through NMDA receptors during pairing. The elevatio n in post-synaptic calcium in turn leads to the depression of synaptic transmis sion in the post-synaptic cell by activating different protein kinases. Such re versibility and a narrow timing window are the most important features of this p lasticity and has not been demonstrated in any system of its kind, including the mammalian cerebellum. The reversibility allows the neuron to "forget" the pas t event and get ready for a new task. The narrow timing window renders the cell able to selectively "remember" some information, not every single input signal .
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电鱼小脑浦肯野细胞对急性缺氧的功能反应
目的:通过研究急性缺氧对电鱼(mormyrid electric fish)小脑浦肯野细胞(Purkinje cell,PC)的功能影响,阐明缺氧耐受动物神经元在缺氧条件下的电生理特征.方法:采用全细胞膜片钳记录法,观察急性缺氧对电鱼小脑主神经元PC膜电位、兴奋性和平行纤维(parallel fiber,PF)-PC突触传递的影响.结果:(1)短暂缺氧使电鱼小脑PC膜电位发生迅速而持久的超极化,可持续30 min以上,同时伴随自发放电频率的显著下降.谷氨酸AMPA受体阻断剂CNQX不影响PC缺氧性超极化的产生,但可阻断缺氧性超极化的持续存在；而GABAA受体阻断剂Bicuculline则完全阻断缺氧性超极化的产生,并使膜电位在缺氧开始后发生短暂的去极化.(2)缺氧使PC诱发动作电位的阈值增高,频率减低,幅值减小.(3)急性缺氧使刺激PF诱发的PC兴奋性突触后电流(excitatory postsynaptic current,EPSC)呈现长时程增强(long term potentiation,LTP),同时使EPSC双脉冲增强现象(pair-pulse facilitation,PPF)显著衰减.CNQX逆转了PF EPSC的缺氧性LTP,表现为长时程抑制(Long Term Depression,LTD);而Bicuculline则使PF EPSC的缺氧性LTP增强.结论:耐缺氧动物电鱼小脑神经元的缺氧反应特征与哺乳类动物显著不同,AMPA受体和GABAA受体均参与电鱼小脑PC的缺氧性超极化和PF LTP的产生,表明维持GABA能突触和谷氨酸能突触活动的适度平衡,可能是电鱼以及其他耐缺氧动物脑保护机制的关键.
