Topic: hippocampal CA1 pyramidal neurons

Epilepsy is a chronic neurological disorder characterized by recurrent seizures resulting from abnormal electrical activity in the brain. All experimental models for seizure generation are based on the administration of drugs (e.g. pilocarpine), on artificial increase in the concentrations of extracellular K+ (Ko) or on direct electric stimulation, to name a few. However, all these approaches may not accurately reflect the in vivo conditions, where otherwise normal neuronal activity can generate occasional seizures. It is thus important to better understand the pathological changes that may be

The overload of glutamate transporters by excessive extracellular glutamate leads to excitotoxic cell death in multiple neurodegenerative diseases as well as stroke, hypoxia and traumatic brain injury. The sustained activation of extrasynaptic N-methyl-D-aspartate (NMDA) receptors by excess extracellular glutamate has been implicated in multiple disease models in vitro and in vivo. Pathological levels of extracellular glutamate arise from compromised or even reversed function of excitatory amino acid transports (EAATs) in a brain region and subtype dependent manner. We have used whole cell pat

While neuronal activity is important for synapse refinement and maintenance, its contribution to synapse formation and dendritic arborization remains unclear. Our previous work in dissociated hippocampal neurons identified a timeframe prior to the establishment of synapses during which spontaneous glutamate release facilitates the branching of dissociated hippocampal neurons by targeting NMDA receptors (NMDARs). We now demonstrate the role of NMDARs in synapse formation and dendritic maturation in hippocampal CA1 pyramidal neurons in cultured slices and in vivo. To test whether NMDARs guide sy

Hippocampal CA1 pyramidal neurons receive excitatory inputs from both ipsi- and contralateral CA3 and CA2 regions. While synaptic plasticity at the intrahippocampal Schaffer collateral synapses has been extensively described, synaptic plasticity mechanisms at interhippocampal commissural fiber synapses are less well understood. In this project, we investigate cyclic adenosine monophosphate (cAMP)-dependent plasticity at commissural synapses in the CA1 region. We performed in vivo stereotactic injections of AAVs to express ChrimsonR unilaterally in CA3/CA2 glutamatergic neurons of one hippocamp