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首页> 外文期刊>Brain research >Dependence on morphine impairs the induction of long-term potentiation in the CA1 region of rat hippocampal slices.
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Dependence on morphine impairs the induction of long-term potentiation in the CA1 region of rat hippocampal slices.

机译:依赖吗啡会损害大鼠海马切片CA1区的长期增强诱导作用。

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摘要

The effect of chronic morphine treatment on hippocampal CA1-long-term potentiation (LTP) was examined in vitro. The field excitatory postsynaptic potential (fEPSP) was recorded from stratum radiatum of area CA1 following stimulation of Schaffer collaterals in slices taken from control and morphine-dependent rats. To induce LTP, a 100-Hz primed burst stimulation (PBs) was used. Slices from rats exposed to chronic morphine showed no effect on baseline synaptic responses. Slices from control rats or rats exposed to chronic morphine maintained in ACSF with either morphine or naloxone also had no effect on baseline synaptic responses. Control slices perfused with medium containing either morphine or naloxone as well as both drugs exhibited hippocampal CA1 LTP. Similarly, slices from morphine-dependent rats maintained in ACSF with either naloxone or just morphine free ACSF also exhibited hippocampal CA1 LTP. However, slices from morphine-dependent rats maintained in ACSF with morphine significantly attenuated hippocampal CA1 LTP. These findings suggest that hippocampal CA1-LTP can still be achieved in slices from morphine-dependent rats exhibiting morphine withdrawal through mechanisms that may be inhibited by opiate exposure. Such studies can be helpful in understanding the neurophysiological substrate of memory deficits seen in opiate addicts.
机译:在体外检查了慢性吗啡治疗对海马CA1长期增强(LTP)的影响。刺激和控制吗啡依赖性大鼠的切片中的沙弗尔侧支刺激后,从CA1区的放射状区域记录了田间兴奋性突触后电位(fEPSP)。为了诱发LTP,使用了100 Hz的预备爆发刺激(PBs)。暴露于慢性吗啡的大鼠的切片对基线突触反应无影响。对照大鼠或暴露于ACSF中吗啡或纳洛酮的慢性吗啡大鼠的切片对基线突触反应也没有影响。用含有吗啡或纳洛酮以及两种药物的培养基灌注的对照切片均表现出海马CA1 LTP。同样,用纳洛酮或不含吗啡的ACSF维持在ACSF中的吗啡依赖性大鼠的切片也显示出海马CA1 LTP。然而,吗啡依赖大鼠的切片在吗啡中维持在ACSF中,可显着减弱海马CA1 LTP。这些发现表明,在吗啡依赖大鼠的切片中仍可实现海马CA1-LTP的表达,而吗啡依赖大鼠的吗啡戒断可能是通过鸦片暴露抑制的机制。此类研究有助于了解鸦片成瘾者所见的记忆缺陷的神经生理学基础。

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