RESUMO
The aim of the present study was to analyze the location of degenerating neurons in the dorsal (insular) claustrum (DCL, VCL) and the dorsal, intermediate and ventral endopiriform nucleus (DEn, IEn, VEn) in rat pups following lithium-pilocarpine status epilepticus (SE) induced at postnatal days [P]12, 15, 18, 21 and 25. The presence of Fluoro-Jade B-positive neurons was evaluated at 4, 12, 24, 48 h and 1 week later. A small number of degenerated neurons was observed in the CL, as well as in the DEn at P12 and P15. The number of degenerated neurons was increased in the CL as well as in the DEn at P18 and above and was highest at longer survival intervals. The CL at P15 and 18 contained a small or moderate number of degenerated neurons mainly close to the medial and dorsal margins also designated as DCl ("shell") while isolated degenerated neurons were distributed in the VCl ("core"). In P21 and 25, a larger number of degenerated neurons occurred in both subdivisions of the dorsal claustrum. The majority of degenerated neurons in the endopiriform nucleus were found in the intermediate and caudal third of the DEn. A small number of degenerated neurons was dispersed in the whole extent of the DEn with prevalence to its medial margin. Our results indicate that degenerated neurons in the claustrum CL and endopiriform nucleus are distributed mainly in subdivisions originating from the ventral pallium; their distribution correlates with chemoarchitectonics of both nuclei and with their intrinsic and extrinsic connections.
Assuntos
Claustrum , Estado Epiléptico , Ratos , Animais , Neurônios , Córtex CerebralRESUMO
Background: Postictal refractoriness, i.e., the inability to elicit a new epileptic seizure immediately after the first one, is present in mature animals. Immature rats did not exhibit this refractoriness, and it is replaced by postictal potentiation. In addition to the immediate postictal potentiation, there is a delayed potentiation present at both ages. These phenomena were studied using cortical epileptic afterdischarges as a model. Objective: We aimed to analyze participation of adenosine A1 receptors in postictal potentiation and depression. Methods: Adenosine A1 receptors were studied by means of Western blotting in the cerebral cortex with a focus on the age groups studied electrophysiologically. Stimulation and recording electrodes were implanted epidurally in 12- and 25-day-old rats. The first stimulation always induced conditioning epileptic afterdischarge (AD), and 1 min after its end, the stimulation was repeated to elicit the second, testing AD. Then, the drugs were administered and paired stimulations were repeated 10 min later. A selective agonist CCPA (0.5 and 1 mg/kg i.p.) and a selective antagonist DPCPX (0.1, 0.5 and 1 mg/kg i.p.) were used to examine the possible participation of adenosine A1 receptors. Results: Control younger animals exhibited potentiation of the testing AD and a moderate increase in both conditioning and testing ADs after an injection of saline. The A1 receptor agonist CCPA shortened both post-drug ADs, and neither potentiation was present. The administration of an antagonist DPCPX resulted in marked prolongation of the conditioning AD (delayed potentiation), and the second testing AD was shorter than the post-drug conditioning AD, i.e., there was no longer immediate potentiation of ADs. To eliminate effects of the solvent dimethylsulfoxide, we added experiments with DPCPX suspended with the help of Tween 80. The results were similar, only the prolongation of ADs was not as large, and the testing ADs were significantly depressed. The older control group exhibited a nearly complete suppression of the first testing AD. There was no significant change in the conditioning and testing ADs after CCPA (delayed potentiation was blocked). Both groups of DPCPX-treated rats (with DMSO or Tween) exhibited significant augmentation of delayed potentiation but no significant difference in the immediate depression. Adenosine A1 receptors were present in the cerebral cortex of both age groups, and their quantity was higher in 12- than in 25-day-old animals. Conclusions: An agonist of the A1 receptor CCPA suppressed both types of postictal potentiation in 12-day-old rats, whereas the A1 antagonist DPCPX suppressed immediate potentiation but markedly augmented the delayed one. Immediate postictal refractoriness in 25-day-old rats was only moderately (non-significantly) affected; meanwhile, the delayed potentiation was strongly augmented.