Ventrolateral Periaqueductal Gray Matter Neurochemical Lesion Facilitates Epileptogenesis and Enhances Pain Sensitivity in Epileptic Rats. (15th July 2019)

• Record Type: Journal Article
• Authors: Wang, Lei; Shen, Jie; Cai, Xin-Ting; Tao, Wei-Wei; Wan, Ya-Di; Li, Dong-Lin; Tan, Xiu-Xiu; Wang, Yu
• Is Part Of: Neuroscience. Volume 411(2019)
• Page Start: 105
• Page End: 118
• Publication Date: 2019-07-15
• Subjects: dPAG dorsal periaqueductal gray matter -- EEG electroencephalography -- GABA gamma-aminobutyric acid -- i.p intraperitoneal -- MAP2 microtubule-associated protein 2 -- NMDA N-methyl-D-aspartic acid -- PAG periaqueductal gray matter -- PPN pedunculopontine nucleus -- RPO reticularis pontis oralis -- SE status epilepticus -- SRS spontaneous recurrent seizures -- TUNEL terminal deoxynucleotidyl transferase (TdT)-mediated dUTP nick end labeling -- vGLUT1 vesicular glutamate neurotransmitter transporter 1 -- vGAT vesicular γ-aminobutyric acid neurotransmitter transporter -- vlPAG ventrolateral periaqueductal gray matter; comorbidity -- epilepsy -- epileptogenesis -- migraine -- pain sensitivity -- ventrolateral periaqueductal gray matter; Neurochemistry -- Periodicals; Neurophysiology -- Periodicals; Neurology -- Periodicals; Neurochimie -- Périodiques; Neurophysiologie -- Périodiques; Neurochemistry; Neurophysiology; Electronic journals; Periodicals; Electronic journals; 612.8
• DOI: 10.1016/j.neuroscience.2019.05.027
• Languages: English
• ISSNs: 0306-4522

Abstract

Abstract: The ventrolateral periaqueductal gray matter (vlPAG) plays a critical role in the pathogenesis of migraine and few studies have shown that vlPAG might be involved in the pathophysiology of epilepsy. But its roles in epileptogenesis and comorbid relationship between migraine and epilepsy have never been reported. In this study, the impairments of vlPAG neuronal network during spontaneous recurrent seizure (SRS) development after status epilepticus (SE) were investigated, and the pain sensitivity as well as the SRS investigated after neurochemical lesion to vlPAG to determine the role of vlPAG in epileptogenesis and in migraine comorbidity with epilepsy. Neuronal loss and alterations of excitatory and inhibitory neural transmission within vlPAG accompanied the development of epileptogenesis induced by SE. On the other hand, neurochemical lesion to vlPAG enhanced frequency and duration of spontaneous seizure event and frequency of epileptiform inter-ictal spike discharges in electroencephalography (EEG), but decreased pain threshold in epileptic rats. This indicates an involvement of the pain regulating structure, vlPAG, in the pathogenesis of epilepsy. This may imply that vlPAG network alterations could be a possible underlying mechanism of the interactive comorbid relationship between epilepsy and migraine. Highlights: Neuronal loss in vlPAG accompanied the processes of epileptogenesis. Excitatory transmission was inferior to inhibitory transmission in later stage of epileptogenesis. vlPAG neurochemical lesion caused an enhanced development of epileptogenesis. vlPAG neurochemical lesion caused an increased pain sensitivity in epileptic rats.