Brain ? Opioid and A1 Adenosine Receptors in the Status Epilepticus Regulation.
Abstract number :
1.114
Submission category :
Year :
2000
Submission ID :
1219
Source :
www.aesnet.org
Presentation date :
12/2/2000 12:00:00 AM
Published date :
Dec 1, 2000, 06:00 AM
Authors :
Agustina Cano-Martinez, Luisa L Rocha, Rafael Villalobos-Molina, Magdalena Briones, Inst Nacional de Cardiologia and Cinvestav, Mexico, D.f., Mexico; Cinvestav, Mexico D.f., Mexico; Cinvestav, M{exico, D.f., Mexico; Inst Mexicano de Psiquiatria, Mexico, D
RATIONALE: The changes in the ? opioid and A1 adenosine receptors after status epilepticus (SE) induced with kainic acid (KA) in rats suggest that one via for SE regulation from two mediators is by changes in their receptor number. In the present study was evaluated the effect of previous increase in ? and A1 receptors on SE presentation and on postictal period, in association to the quantification of affinity and number receptor after SE in three brain regions. METHODS: The increase in the ? and A1 receptor number was induced by pharmacological strategies (repeated morphine (M) or repeated cyclopentyladenosine (CPA) administrations, measured 48 h after last M or CPA administration in rats). The SE was induced by KA (10 mg/kg., i.p.), 48 h after last M or CPA administration. The affinity and number of receptors were measured by binding assay in membranes from hippocampus (HC), amygdala (AM) and cortex (CX), 24 h after SE presentation. RESULTS: The previous increase in the ? receptor number in the three brain regions analiced was associated with acelerated SE presentation, while same treatment decreases the harmful effects resulting from SE during postictal period, in association to dejected increase in the ? receptor and potentiate increase A1 levels in HC, and a potenctiate increase in both, ? and A1 receptor number in AM and CX. The previous increase in A1 receptor, delayed the SE presentation and accented the depressive characteristics observed after SE in the postictal period, in association with an increase of A1 and a decrease of ? receptors in the three brain regions analiced. No significative changes in the affinity were detected. CONCLUSIONS: Our results are in concordance with the hypothesis about that, opioids and adenosine, via ? and A1 receptors, respectively, my be part of endogenous mechanisms that participate in the SE seizures regulation, to protect of presentation, in seizures termination and/or eviting subsecuent seizures propagation. Apparently, for adenosine, may be protecting in the focus (HC), around (AM) and in periferic (CX) brain regions. While for opioids, may be protecting in the around and periferic regions, but not in the epileptic focus.