Dependence on morphine impairs the induction of long-term potentiation in the CA1 region of rat hippocampal slices
Dependence on morphine impairs the induction of long-term potentiation in the CA1 region of rat hippocampal slices
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DOI：
10.1016/s0006-8993(02)04144-6
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发表时间：
2003-03
期刊：
影响因子：
2.9
通讯作者：
F. Salmanzadeh;Y. Fathollahi;S. Semnanian;M. Shafizadeh
中科院分区：
文献类型：
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作者：
F. Salmanzadeh;Y. Fathollahi;S. Semnanian;M. Shafizadeh
在体外研究慢性吗啡处理对海马CA 1区长时程增强（LTP）的影响。在对照组和吗啡依赖大鼠脑片上，刺激Schaffer侧支，在CA 1区放射层记录到场兴奋性突触后电位（fEPSP）。为了诱导LTP，使用100-Hz预激爆发刺激（PB）。长期接触吗啡的大鼠切片显示对基线突触反应没有影响。来自对照大鼠或暴露于ACSF中的慢性吗啡与吗啡或纳洛酮的大鼠的切片也对基线突触反应没有影响。用含有吗啡或纳洛酮以及这两种药物的培养基灌注的对照切片表现出海马CA 1 LTP。同样，吗啡依赖大鼠的脑片在ACSF中与纳洛酮或仅吗啡自由ACSF一起维持也表现出海马CA 1 LTP。然而，吗啡依赖大鼠脑片维持在ACSF与吗啡显着衰减海马CA 1 LTP。这些发现表明，海马CA 1-LTP仍然可以实现从吗啡依赖的大鼠表现出吗啡戒断通过阿片类药物暴露的抑制机制的切片。这些研究有助于理解阿片类药物成瘾者记忆缺陷的神经生理学基础。
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.