Assessment of serotonergic system in formation of memory and learning / Avaliação do sistema serotonérgico na formação de memória e aprendizagem

Abstract We evaluated the involvement of the serotonergic system on memory formation and learning processes in healthy adults Wistar rats. Fifty-seven rats of 5 groups had one serotonergic nuclei damaged by an electric current. Electrolytic lesion was carried out using a continuous current of 2mA during two seconds by stereotactic surgery. Animals were submitted to learning and memory tests. Rats presented different responses in the memory tests depending on the serotonergic nucleus involved. Both explicit and implicit memory may be affected after lesion although some groups showed significant difference and others did not. A damage in the serotonergic nucleus was able to cause impairment in the memory of Wistar. The formation of implicit and explicit memory is impaired after injury in some serotonergic nuclei.

Resumo Avaliar a participação do sistema serotoninérgico em processos de formação de memória e aprendizagem em ratos Wistar adultos saudáveis. Cinquenta e sete ratos de 5 grupos tinham um núcleo serotoninérgico danificado por uma corrente elétrica. A lesão eletrolítica foi realizada utilizando uma corrente contínua de 2 mA durante dois segundos por cirurgia estereotáxica. Os animais foram submetidos a testes de aprendizagem e memória. Os ratos apresentaram respostas diferentes nos testes de memória, dependendo do núcleo serotoninérgica envolvido. A memória explícita e implícita pode ser afetada após a lesão, embora alguns grupos apresentaram diferença significativa e outros não. A lesão no núcleo serotoninérgico foi capaz de causar danos na memória de Wistar. A formação da memória implícita e explícita é prejudicada após a lesão em alguns núcleos serotoninérgicos.

Ginkgo modulates noise induced hippocampal damage in male albino rats: a light and electron microscopic study

Noise has been a major problem to mankind and induces many auditory and extra-auditory hazards. This study was carried out to determine the injurious effects of noise on the hippocampus and to show whether Ginkgo biloba has any modulatory effect on hippocampal injury. Twenty-five adult male albino rats were divided into five groups: a control group; a noise group exposed to 100 dB of sound pressure level white noise 4h/day for 4 weeks; a protected group exposed to the same noise level with the administration of a G. biloba extract [50mg/kg daily] for 4 weeks; a recovery group, which was allowed to recover for 4 weeks after noise cessation; and a treated group, administered the same dose of G. biloba for 4 weeks after noise cessation. In the noise-exposed group, the pyramidal cell layer of CA1 and CA3 and the granular cell layer of the dentate gyrus [DG] showed a decrease in thickness compared with the control group, which showed loss and degeneration of many cells, and evidence of increased apoptosis. The protected and treated groups showed improvement in many parameters compared with the recovery group, that is, an increase in the thickness of CA1, CA3, and DG; increase in the surface area of cells; increased vascularity; and a statistically significant decrease in apoptosis compared with the recovery group. Noise exerted detrimental effects on cells of CA1, CA3, and DG of the hippocampus. Although partial spontaneous recovery may occur after cessation of noise exposure, the administration of G. biloba led to a marked decrease in the injurious effect of noise on the hippocampus. This might suggest the probable usefulness of G. biloba in reducing the central hazardous effects in individuals exposed to noise

Cavernoma de hipocampo associado a epilepsia do lobo temporal refratária / Hippocampal cavernoma associated to refractory temporal lobe epilepsy

Os cavernomas, entre todas as malformações vasculares encontradas no sistema nervoso, constituem os principais causadores de epilepsia. Para ilustrar essa associação, é apresentado o caso de uma paciente com crises convulsivas de início recente, refratárias ao tratamento clínico, ocasionadas por um cavernoma localizado no lobo temporal (hipocampo) direito. A paciente foi submetida a lesionectomia, sem ressecção do córtex temporal adjacente, com resultado pós-operatório positivo. São discutidas as indicações de lesionectomia em indivíduos com epilepsia, com ênfase nos cavernomas, bem como as indicações de corticectomia para o controle das crises e a obtenção de prognóstico favorável.

The cavernomas, of all the vascular malformations found in the nervous system, are the leading cause of epilepsy. To illustrate this association we present the case of a female patient with convulsive crises of recent onset, refractory to clinical treatment, caused by a cavernoma located in the right temporal lobe (hippocampus). The patient was submitted to lesionectomy, without resection of the adjacent temporal cortex, with a positive postoperative outcome. Indications of lesionectomy to individuals with epilepsy are discussed, with an emphasis on cavernomas, as well as indications of corticectomy for the control of crises and the achievement of a favorable prognosis.

Magnesium chloride alone or in combination with diazepam fails to prevent hippocampal damage following transient forebrain ischemia

In the central nervous system, magnesium ion (Mg2+) acts as an endogenous modulator of N-methyl-D-aspartate (NMDA)-coupled calcium channels, and may play a major role in the pathomechanisms of ischemic brain damage. In the present study, we investigated the effects of magnesium chloride (MgCl2, 2.5, 5.0 or 7.5 mmol/kg), either alone or in combination with diazepam (DZ), on ischemia-induced hippocampal cell death. Male Wistar rats (250-300 g) were subjected to transient forebrain ischemia for 15 min using the 4-vessel occlusion model. MgCl2 was applied systemically (sc) in single (1x, 2 h post-ischemia) or multiple doses (4x, 1, 2, 24 and 48 h post-ischemia). DZ was always given twice, at 1 and 2 h post-ischemia. Thus, ischemia-subjected rats were assigned to one of the following treatments: vehicle (0.1 ml/kg, N = 34), DZ (10 mg/kg, N = 24), MgCl2 (2.5 mmol/kg, N = 10), MgCl2 (5.0 mmol/kg, N = 17), MgCl2 (7.5 mmol/kg, N = 9) or MgCl2 (5 mmol/kg) + DZ (10 mg/kg, N = 14). Seven days after ischemia the brains were analyzed histologically. Fifteen minutes of ischemia caused massive pyramidal cell loss in the subiculum (90.3 percent) and CA1 (88.4 percent) sectors of the hippocampus, vehicle vs sham). Compared to the vehicle-treated group, all pharmacological treatments failed to attenuate the ischemia-induced death of both subiculum (lesion: 86.7-93.4 percent) and CA1 (lesion: 85.5-91.2 percent) pyramidal cells. Both DZ alone and DZ + MgCl2 reduced rectal temperature significantly. No animaldeath was observed after drug treatment. These data indicate that exogenous magnesium, when administered systemically post-ischemia even in different multiple dose schedules, alone or with diazepam, is not useful against the histopathological effects of transient global cerebral ischemia in rats

Role of the hippocampus in contextual memory after classical aversive conditioning in pigeons (C. livia)

We investigated the effects of hippocampal lesions with ibotenic acid (IBO) on the memory of the sound-context-shock association during reexposure to the conditioning context. Twenty-nine adult pigeons were assigned to a non-lesioned control group (CG, N = 7), a sham-lesioned group (SG, N = 7), a hippocampus-lesioned experimental group (EG, N = 7), and to an unpaired nonlesioned group (tone-alone exposure) (NG, N = 8). All pigeons were submitted to a 20-min session in the conditioning chamber with three associations of sound (1000 Hz, 85 dB, 1 s) and shock (10 mA, 1 s). Experimental and sham lesions were performed 24 h later (EG and SG) when EG birds received three bilateral injections (anteroposterior (A), 4.5, 5.25 and 7.0) of IBO (1 µl and 1 µg/µl) and SG received one bilateral injection (A, 5.25) of PBS. The animals were reexposed to the training context 5 days after the lesion. Behavior was videotaped for 20 min and analyzed at 30-s intervals. A significantly higher percent rating of immobility was observed for CG (median, 95.1; range, 79.2 to 100.0) and SG (median, 90.0; range, 69.6 to 95.0) compared to EG (median, 11.62; range, 3.83 to 50.1) and NG (median, 7.33; range, 6.2 to 28.1) (P<0.001) in the training context. These results suggest impairment of contextual fear in birds who received lesions one day after conditioning and a role for the hippocampus in the modulation of emotional aversive memories in pigeons

Subicular lesion induced impairment in operant behaviour and altered dendritic morphology of CA1, CA3 hippocampal neurons.

The effects of bilateral electrolytic subicular lesions were examined on the operant behaviour for food reward on a continuous reinforcement schedule as well as the dendritic morphology of CA1 and CA3 hippocampal areas. The subjects were female Wistar rats 20 days of age and were divided into four groups. 1. Age matched control 2. Sham operated 3. Operant behaviour for food reward and 4. Subicular lesion. Animals were starved twenty-four hours prior to operant behaviour training sessions. Two trial sessions with continuous reinforcement (CRF) of 10 min duration/day were done during training sessions following which the rats were allowed CRF for ten minutes per day for ten days. On the eleventh day, the operant behaviour and sham operated animals were taken up for bilateral subicular lesion and sham surgery respectively. After seventy two hours of surgical recovery, operant behavioural testing was done as before for a further period of ten days. Later all the groups of animals were sacrificed and the hippocampi were processed for rapid Golgi staining technique. Our results suggest that subicular lesions do produce a significant reduction in operant learning behaviour for food reward. Further the Golgi studies revealed a reduction in dendritic branching points and intersections of apical and basal CA1, CA3 neurons in lesioned animals.

Cambios en la excitibilidad neuronal y alteraciones en la densidad neuronal del hipocampo inducidos por isquemia focal / Changes in neuronal excitability and modifications in neural population of the hippocampus induce y focal ischemia

Despúes de un periodo de isquemia cerebral se observa aumento en la frecuencia de descarga neuronal de hipocampo y signos electroencefalográficos de actividad paroxística espontánea. Es probable que estos cambios en la excitabilidad se deban a mecanismos de excitotoxicidad que inducen muerte neuronal. En el presente estudio se evaluaron los cambios en la inhibición recurrente así como en la densidad neuronal del hipocampo de ratas sometidas a 5 y 20 min de isquemia focal con un periodo de recuperación de 7 días. El grado de inhibición recurrente se cuantificó mediante el índice de máxima inibición (IMI). La cuantificación neuronal se realizó a través de un sistema de procesamiento digital de imágenes (Imagenia 2000). Se observó aumento en la amplitud del segundo componente del segundo potencial provocado. Al calcular el IMI resultó mayor que 1. La mayor pérdida neuronal se observó en CA1 y CA2, mientras que la mayor vulnerabilidad se observó en el GD, CA3 y CA4. En conclusión, la isquemia focal con recuperación de 7 días provocó disminución en la densidad neuronal así como la aparición de un mecanismo de desinhibición, que condiciona cambios en la excitabilidad neuronal del hipocampo probablemente debido a lesión de interneuronas