Leite-Panissi Christie Ramos Andrade, Coimbra Norberto Cysne, Menescal-de-Oliveira Leda
Department of Physiology, Faculty of Medicine of Ribeirão Preto, University of São Paulo, 14049-900 Ribeirão Preto, SP, Brazil.
Brain Res Bull. 2003 Apr 15;60(1-2):167-78. doi: 10.1016/s0361-9230(03)00031-5.
Tonic immobility (TI), also known as death feigning or animal hypnosis, is a reversible state of motor inhibition that is triggered by postural inversion and/or movement restraining maneuvers but also by repetitive stimulation and pressure on body parts. Our previous studies demonstrated that cholinergic stimulation of the central amygdala (CEA) decreases the duration of TI in guinea pigs. Some reports have demonstrated that electrical or chemical stimulation of the CEA promotes antinociception. Evidence suggests that the CEA performs part of its functions by means of a connection with the ventrolateral periaqueductal gray (vlPAG). In the current study, we investigated the participation of a possible functional and anatomical CEA-vlPAG connection in guinea pigs in the regulation of the TI response and antinociception. Our results showed that the functional CEA-vlPAG connection is essential for the participation of the CEA in the modulation of TI and of antinociception. The reversible exclusion of the vlPAG by means of microinjection of 2% lidocaine blocked the inhibitory effect on TI duration and the antinociceptive effect, as determined by a decrease of the vocalization index (VI) obtained with the administration of carbachol (2.7 nmol/0.2 microl) into the CEA. On the other hand, the exclusion of the CEA by lidocaine did not block the antinociception or the increase in TI induced by microinjection of CCh into the vlPAG. Finally, microinjection of the retrograde neurotracer Fast Blue into the CEA or into the vlPAG demonstrated the existence of a reciprocal anatomical connection between the CEA and vlPAG.
紧张性不动(TI),也被称为装死或动物催眠,是一种可逆的运动抑制状态,它可由体位倒置和/或运动限制操作引发,也可由对身体部位的重复刺激和压力引发。我们之前的研究表明,对豚鼠中央杏仁核(CEA)进行胆碱能刺激可缩短TI的持续时间。一些报告显示,对CEA进行电刺激或化学刺激可促进抗伤害感受。有证据表明,CEA通过与腹外侧导水管周围灰质(vlPAG)的连接来发挥其部分功能。在本研究中,我们调查了豚鼠中可能存在的功能性和解剖学上的CEA-vlPAG连接在TI反应和抗伤害感受调节中的参与情况。我们的结果表明,功能性CEA-vlPAG连接对于CEA参与TI调节和抗伤害感受至关重要。通过微量注射2%利多卡因可逆性地排除vlPAG,可阻断对TI持续时间的抑制作用和抗伤害感受作用,这是通过向CEA注射卡巴胆碱(2.7 nmol/0.2微升)后发声指数(VI)的降低来确定的。另一方面,利多卡因排除CEA并未阻断抗伤害感受或向vlPAG微量注射氯化乙酰胆碱(CCh)所诱导的TI增加。最后,向CEA或vlPAG微量注射逆行神经示踪剂快蓝证明了CEA和vlPAG之间存在相互的解剖学连接。