Pyramidal Neurons In Hippocampal CA3 Research Articles

Efficacy of dapsone administered alone or in combination with diazepam to inhibit status epilepticus in rats

Status epilepticus (SE) is a serious medical condition, as it may trigger epileptogenesis. SE produces continuous generalized seizures resulting in irreversible brain damage. Therefore, the use of neuroprotective agents to prevent cell damage, may reduce the impact of SE. The use of diazepam (DZP), has shown limited neuroprotective effect in SE patients. According to previous reports, dapsone (DDS) is able to reduce both cell damage and seizures, when administered 30 min before the onset of seizures. This study is aimed to evaluate the ability of DDS, alone or in combination with DZP starting their administration once the SE is onset to evaluate the control of seizures in rats. Results showed a reduced convulsive electrical activity after 30 min, 1 and 2 h after SE induced by kainic acid (KA) administration, in the animals treated with DZP alone or in combination with DDS. At 24 h, we observed electrical activity similar to baseline in all groups receiving treatment. The animals treated with DDS and DZP alone or in combination showed an increase in the number of viable pyramidal cells but only the combination showed a lower number of damaged pyramidal neurons of hippocampal CA3. In conclusion, DDS plus DZP was able to control SE and to prevent SE-induced damage, when administered in combination with DZP. As DDS is already in use for patients with leprosy, that combination may be a safe, good option for human cases of SE.

Prenatal stress causes dendritic atrophy of pyramidal neurons in hippocampal CA3 region by glutamate in offspring rats

A substantial number of human epidemiological data, as well as experimental studies, suggest that adverse maternal stress during gestation is involved in abnormal behavior, mental, and cognition disorder in offspring. To explore the effect of prenatal stress (PS) on hippocampal neurons, in this study, we observed the dendritic field of pyramidal neurons in hippocampal CA3, examined the concentration of glutamate (Glu), and detected the expression of synaptotagmin-1 (Syt-1) and N-methyl-D-aspartate receptor 1 (NR1) in hippocampus of juvenile female offspring rats. Pregnant rats were divided into two groups: control group (CON) and PS group. Female offspring rats used were 30-day old. The total length of the apical dendrites of pyramidal neurons in hippocampal CA3 of offspring was significantly shorter in PS than that in CON (p < 0.01). The number of branch points of the apical dendrites of pyramidal neurons in hippocampal CA3 of offspring was significantly less in PS (p < 0.01). PS offspring had a higher concentration of hippocampal Glu compared with CON (p < 0.05). PS offspring displayed increased expression of Syt-1 and decreased NR1 in hippocampus compared with CON (p < 0.001 and p < 0.01, respectively). The expression of NR1 in different hippocampus subfields of offspring was significantly decreased in PS than that in CON (p < 0.05-0.01). This study shows that PS increases the Glu in hippocampus and causes apical dendritic atrophy of pyramidal neurons of hippocampal CA3 in offspring rats. The decline of NR1 in hippocampus may be an adaptive response to the increased Glu.

Effects of Acute Amphetamine Administration on AMPA-Mediated Synaptic Activity and Expression of AMPA Receptor Subunit 2 of Brain Neurons

We investigated the role of alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionate receptor (AMPAR) in mechanisms underlying the action of amphetamine (Amph) on brain neurons, for AMPAR has been proposed to participate in psychotic and neurodegenerative disorders. In the cultured rat brain cortical neurons pretreated with 1 microM Amph for 1 h, the accumulation of 45Ca2+ driven by 10 min incubation with 100 microM AMPA was reduced by about 36%. This Amph-induced decrease seems to involve L-type voltage-gated Ca2+ channels, because the AMPA-induced 45Ca2+ uptake was blocked by 70% and 80%, respectively, for untreated and Amph-treated neurons in the presence of nifedipine (1 microM), an antagonist to L-type calcium channels. Whole-cell, patch-clamp recording revealed that AMPA-elicited current amplitude became 26% lower than the control in Amph-treated cultured neurons. Moreover, Amph treatment down-regulated the level of flip-form glutamate receptor 2 (GluR2) mRNA by 27% in cultured neurons but did not change the expression of GluR2 proteins and flop-form mRNA, as detected by quantitative immunocytochemistry and in situ hybridization. In contrast, in postnatal day 4 rats at 1 h after receiving one intraperitoneal injection of 5 mg/kg of Amph, levels of flip GluR2 mRNA were up-regulated by 13% and 18% in neurons of motor cortex layer 5 and pyramidal neurons of hippocampal CA3, respectively. The data suggest that acute action of Amph on brain neurons is possibly associated with decreased AMPA-mediated Ca2+ influx and current amplitude, as well as modified expression of the GluR2 mRNA.