Enes Akyuz (Turkey)
University of Health Sciences Department of Biophysics, Faculty of International MedicineAuthor Of 1 Presentation
INVESTIGATING THE ROLE OF MUSCARINIC ACETYLCHOLINE M2 AND SEROTONIN 5-HT2B RECEPTORS, NOREPINEPHRINE TRANSPORTER AND KIR CHANNELS IN A PENTYLENETETRAZOL-KINDLING MODEL OF EPILEPSY
- Villa Chiara (Italy)
Abstract
Background and Aims:
Epilepsy encompasses a group of neurological disorders characterized by an imbalance of electrical activity in the central nervous system (CNS) and recurrent seizures representing the principal clinical manifestation. Acetylcholine (ACh), serotonin, and norepinephrine (NE) may modulate neural activity via several mechanisms, mainly through its receptors/transporter activity and alterations in the extracellular potassium (K+) concentration via inwardly rectifying K+ (Kir) channels. Therefore, the aim of this study was to investigate the immunoreactivity pattern of these neurotransmitter, receptors/transporters and Kir channels in Pentylenetetrazol (PTZ)-kindling rat model, a well-established tool for studying chronic epilepsy.
Methods:
Kindling was chemically induced by intraperitoneally injections of PTZ for one month. Changes in the immunoreactivity of epileptogenesis-related neurotransmitter receptors/transporters (M2, 5-HT2B, and NE transporter) as well as Kir3.1 and Kir6.2 channels were determined in the cortex, hippocampus and medulla of adult Wistar rats by immunohistochemistry analyses.
Results:
Increased immunoreactivity of the NE transporter, M2, and 5-HT2B receptors was witnessed in the cortex and medulla. While the immunoreactivity of the 5-HT2B receptor was found increased in the cortex and medulla, it was decreased in the hippocampus, with no changes observed in the M2 receptor in this region. Kir3.1 and Kir6.2 staining showed increase immunoreactivity in the cerebral cortex, but contrasting findings were found in the hippocampus and medulla.
Conclusions:
Our data suggested significant changes in the neurotransmitter, receptors/transporters and ion channels, that may regulate neurotransmitter levels such as ACh, serotonin, and NE in the cortex, hippocampus, and medulla, thus contributing to epileptogenesis.