Differences in Neurodegeneration Between Kainic Acid-Injected GAERS and Wistar Rats.

AIM: To compare neurodegenerative changes using the Fluoro-Jade B staining, following status epilepticus induced by intraamygdaloid injection of kainic acid in Genetic Absence Epilepsy Rats from Strasbourg (GAERS) and non-epileptic control Wistar rats. MATERIAL AND METHODS: A single unilateral intra-amygdaloid kainic acid (750 ng) was administered in adult male GAERS and Wistar rats to induce status epilepticus. We recorded electroencephalogram (EEG) and behavioral changes throughout the experiments. After 1 week of the kainic acid injection, rats were sacrificed, and the brains were removed. We obtained 20λm sections and processed them for Fluoro-Jade B and Nissl staining, which were evaluated semi-quantitatively. RESULTS: Following kainic acid injections, status epilepticus developed in all rats. In GAERS rats, motor seizures were considerably delayed, with no statistically significant difference in the number of seizures. However, statistically significant differences were observed in the Fluoro-Jade B staining in GAERS rats between contralateral and ipsilateral sides of the CA3, CA1, somatosensory cortex, entorhinal cortex, piriform cortex, reticular nucleus, putamen, and claustrum. In Wistar rats, the CA3, CA1, somatosensory cortex, entorhinal cortex, piriform cortex, reticular nucleus, amygdala, and laterodorsal nucleus exhibited significant differences. Comparing GAERS and Wistar rats, a statistically significant difference was observed for both sides of CA1. In both groups, the staining was prominent ipsilaterally, except for the claustrum in GAERS rats. However, the motor cortex remained unaffected in both groups. Neurodegenerative changes were not associated with the severity of seizures in both groups following the intra-amygdaloid kainic acid administration. CONCLUSION: This study demonstrates that CA1 is the only region exhibiting a statistically significant difference between Wistar and GAERS rats.

Effects of Injection of Gamma-Aminobutyric Acid Agonists into the Nucleus Accumbens on Naloxone-Induced Morphine Withdrawal.

AIMS: This study was to investigate the effects of local administration of gamma-aminobutyric acid (GABA) agonists into the nucleus accumbens (NAc) on naloxone-induced morphine withdrawal symptoms. METHODS: Bilateral guide cannulas were stereotaxically implanted in the shell or core regions of the NAc of Sprague-Dawley rats. After a recovery period, 3 morphine pellets, each consisting of 75 mg morphine base, were placed subcutaneously on the first and third days of the study with the rats under mild ether anaesthesia. The GABA agonists, baclofen hydrochloride or muscimol hydrobromide, were injected into the NAc, and morphine withdrawal was induced by naloxone on the fifth day. RESULTS: Administration of baclofen to the shell or core regions of the NAc of Sprague-Dawley rats led to statistically significant decreases in both behavioural and locomotor activity parameters during the morphine withdrawal period, compared to the control group. However, there were no statistically significant changes in locomotor activity or withdrawal behavioural parameters, with the exception of wet dog shakes, between control and muscimol-treated groups. CONCLUSION: These findings show that GABAergic conduction in the NAc is effective on the morphine withdrawal symptoms, and that both the shell and core regions of the NAc are associated with this effect.

Localized cortical injections of ethosuximide suppress spike-and-wave activity and reduce the resistance to kindling in genetic absence epilepsy rats (GAERS).

Models of genetic absence epilepsy are resistant to secondary generalization of focal limbic seizures. This correlates with the postnatal development of spike-and-wave discharges (SWDs), a hallmark of absence seizures arising from a cortical focus in the perioral region of somatosensory cortex. Ethosuximide injected at this site suppresses SWDs. The effect of this suppression on kindling in "Genetic Absence Epilepsy Rats from Strasbourg" (GAERS), has been compared for postnatal 30 day (PN30) rats having immature SWDs and adult (>4 months) rats having mature SWDs. Non-epileptic Wistar and GAERS rats were implanted with a basolateral amygdaloid stimulation electrode, bilateral injection cannulas into the cortical perioral focus, and cortical recording electrodes. Following recovery cortical injections of ethosuximide or saline were made and after 30min rats were given 36 stimulations or until Racine's stage 5 seizures were produced. All Wistar rats (PN30 and adult) treated with saline or ethosuximide reached stage 5. Of GAERS given saline, 33% (PN30) and 43% (adults) were resistant to kindling; after ethosuximide pups behaved like Wistars, but adults showed a delay in kindling relative to Wistars. These findings imply that mechanisms underlying kindling resistance are related but not limited to SWD activity in animals with genetic absence epilepsy.