Whole-cell patch clamp recordings of neurones in the suprachiasmati'/> Synaptic inhibition: its role in suprachiasmatic nucleus neuronal thermosensitivity and temperature compensation in the rat
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Synaptic inhibition: its role in suprachiasmatic nucleus neuronal thermosensitivity and temperature compensation in the rat

机译:突触抑制:其在大鼠上视交叉核神经元热敏感性和温度补偿中的作用

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摘要

class="enumerated" style="list-style-type:decimal">Whole-cell patch clamp recordings of neurones in the suprachiasmatic nucleus (SCN) from rat brain slices were analysed for changes in spontaneous synaptic activity during changes in temperature. While recent studies have identified temperature-sensitive responses in some SCN neurones, it is not known whether or how thermal information can be communicated through SCN neural networks, particularly since biological clocks such as the SCN are assumed to be temperature compensated.Synaptic activity was predominantly inhibitory and mediated through GABAA receptor activation. Spontaneous inhibitory postsynaptic potentials (IPSPs) and currents (IPSCs) were usually blocked with perifusion of 10–50 μm bicuculline methiodide (BMI). BMI was used to test hypotheses that inhibitory synapses are capable of either enhancing or suppressing the thermosensitivity of SCN neurones.Temperature had opposite effects on the amplitude of IPSPs and IPSCs. Warming decreased IPSP amplitude but increased IPSC amplitude. This suggests that thermally induced changes in IPSP amplitude are primarily influenced by resistance changes in the postsynaptic membrane. The thermal effect on IPSP amplitude contributed to an enhancement of thermosensitivity in some neurones.In many SCN neurones, temperature affected the frequency of IPSPs and IPSCs. An increase in IPSP frequency with warming and a decrease in frequency during cooling made several SCN neurones temperature insensitive, allowing these neurones to maintain a relatively constant firing rate during changes in temperature. This temperature-adjusted change in synaptic frequency provides a mechanism of temperature compensation in the rat SCN.
机译:class =“ enumerated” style =“ list-style-type:decimal”> <!-list-behavior =枚举前缀-word = mark-type = decimal max-label-size = 0-> 分析大鼠脑片上slice神经上核(SCN)中神经元的全细胞膜片钳记录,以观察温度变化过程中自发突触活性的变化。尽管最近的研究已经确定了某些SCN神经元中的温度敏感响应,但尚不清楚是否可以通过SCN神经网络传递热信息,或者如何通过SCN神经网络传递热信息,特别是因为假定诸如SCN之类的生物钟是温度补偿的。突触活性主要是抑制性的,并通过GABAA受体激活介导。自发抑制突触后电位(IPSPs)和电流(IPSCs)通常会因10–50μm双小分子甲硫脲(BMI)的灌注而被阻断。 BMI用来检验抑制性突触能够增强或抑制SCN神经元的热敏性的假设。 温度对IPSP和IPSC的振幅具有相反的影响。变暖会降低IPSP幅度,但会增加IPSC幅度。这表明热诱导的IPSP振幅变化主要受突触后膜电阻变化的影响。对IPSP振幅的热效应有助于提高某些神经元的热敏性。 在许多SCN神经元中,温度影响IPSP和IPSC的频率。随着变暖IPSP频率的增加和冷却过程中频率的降低使多个SCN神经元对温度不敏感,从而使这些神经元在温度变化期间可以保持相对恒定的放电速率。突触频率的温度调节变化为大鼠SCN提供了温度补偿机制。

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