Excitatory amino acid receptor-mediated responses in periaqueductal gray neurons are increased during ethanol withdrawal.
Excitatory amino acid receptor-mediated responses in periaqueductal gray neurons are increased during ethanol withdrawal.
复制标题
乙醇戒断期间，导水管周围灰色神经元的兴奋性氨基酸受体介导的反应增加。
DOI：
10.1016/j.neuropharm.2006.09.019
复制
发表时间：
2007
影响因子：
4.7
通讯作者：
StevenEvans,M
中科院分区：
文献类型：
--
作者：
Long,Cheng;Yang,Li;Faingold,CarlL;StevenEvans,M
腹外侧导水管周围灰质（PAG）对于乙醇戒断（ETX）癫痫发作的神经元网络中的传播至关重要，并且已知乙醇会改变谷氨酸的作用。本研究评价了谷氨酸拮抗剂对乙醇处理的大鼠脑片PAG神经生理学的影响。自发性动作电位在对照PAG神经元中罕见，但在ETX期间常见。自发兴奋性突触后电位（EPSP）频率在ETX期间增加，AMPA拮抗剂6，7-二硝基喹喔啉-2，3-二酮（DNQX）比NMDA拮抗剂2-氨基-7-膦酰基庚酸酯（AP 7）更有效地抑制这种活性。在ETX和对照神经元中，AP 7或DNQX可降低刺激背外侧PAG诱发的EPSP。ETX神经元的EPSP对AP 7和DNQX阻断的敏感性显著低于对照组。在ETX期间，EPSP的成对脉冲易化显著增加，但对照组发生成对脉冲抑制。因此，PAG过度兴奋在ETX的结果从NMDA和AMPA受体介导的神经传递，这可能是重要的ETX癫痫发作的改变。这些结果不同于先前的研究结果，在ETX癫痫发作的起始部位，下丘（IC），其中NMDA受体介导的机制主导兴奋性增加在ETX。这种二分法可能与IC和PAG在ETX癫痫发作网络中发挥的不同作用有关。
The ventrolateral periaqueductal gray (PAG) is critical for propagation in the neuronal network for ethanol withdrawal (ETX) seizures, and ethanol is known to alter glutamate effects. This study evaluated changes in glutamate antagonist effects on PAG neurophysiology in brain slices from rats treated with ethanol in vivo. Spontaneous action potentials were rare in control PAG neurons but common during ETX. Spontaneous excitatory postsynaptic potential (EPSP) frequency was increased during ETX, and an AMPA antagonist, 6,7-dinitroquinoxaline-2,3-dione (DNQX) was more effective in suppressing this activity than an NMDA antagonist, 2-amino-7-phosphonoheptanoate (AP7). EPSPs evoked by stimulation of dorsolateral PAG were decreased by AP7 or DNQX in ETX and control neurons. EPSPs of ETX neurons were significantly less sensitive than controls to blockade by AP7 and DNQX. Paired-pulse facilitation of EPSPs was significantly increased during ETX, but paired-pulse inhibition occurred in controls. Thus, PAG hyperexcitability during ETX results from alterations of both NMDA and AMPA receptor-mediated neurotransmission, which may contribute importantly to ETX seizures. These results differ from previous findings in the seizure-initiating site for ETX seizures, inferior colliculus (IC), where NMDA receptor-mediated mechanisms dominate excitability increases during ETX. This dichotomy may be related to the different role played by IC and PAG in the ETX seizure network.