Hippocampal interneuron activity has been linked to epileptogenesis, seizures and the oscillatory synaptic activity detected in behaving rats. Interneurons fire at specific times in the rhythmic cycles that comprise these oscillations; however, the mechanisms controlling these firing patterns remain unclear. We have examined the role of synaptic input in modulating the firing of spontaneously active rat hippocampal interneurons. We find that synaptic glutamate receptor currents of 20-30 pA increase instantaneous firing frequency and reset the phase of spontaneously firing CA1 stratum oriens interneurons. Kainate receptor (KAR)-mediated currents are particularly effective at producing this phase reset, while AMPA receptor currents are relatively ineffective. The efficacy of KAR-mediated currents is probably due to their 3-fold longer decay. Given the small amplitude of the currents needed for this phase reset, coincident activation of only a few KAR-containing synapses could synchronize firing in groups of interneurons. These data suggest that KARs are potent modulators of circuit behaviour and their activation alters hippocampal interneuron output.
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http://dx.doi.org/10.1113/jphysiol.2006.118448 | DOI Listing |
Neuron
January 2025
Department of Biology, Washington University in Saint Louis, St. Louis, MO, USA. Electronic address:
In this issue of Neuron, Ruggiero et al. demonstrate that hippocampal networks maintain a stable mean firing rate despite unstable individual units. This homeostatic control operates through NMDAR-eEF2K-BDNF signaling in parvalbumin interneurons.
View Article and Find Full Text PDFBrain
January 2025
Department of Neurology, The First Affiliated Hospital, Guangzhou Medical University, Guangzhou 510120, China.
Epilepsy is a network disorder, involving neural circuits at both the micro- and macroscale. While local excitatory-inhibitory imbalances are recognized as a hallmark at the microscale, the dynamic role of distinct neuron types during seizures remain poorly understood. At the macroscale, interactions between key nodes within the epileptic network, such as the central median thalamic nucleus (CMT), are critical to the, hippocampal epileptic process.
View Article and Find Full Text PDFCell Rep
January 2025
Nash Family Department of Neuroscience, The Friedman Brain Institute, Icahn School of Medicine at Mount Sinai, New York, NY, USA. Electronic address:
Temporal lobe epilepsy (TLE) causes pervasive and progressive memory impairments, yet the specific circuit changes that drive these deficits remain unclear. To investigate how hippocampal-entorhinal dysfunction contributes to progressive memory deficits in epilepsy, we performed simultaneous in vivo electrophysiology in the hippocampus (HPC) and medial entorhinal cortex (MEC) of control and epileptic mice 3 or 8 weeks after pilocarpine-induced status epilepticus (Pilo-SE). We found that HPC synchronization deficits (including reduced theta power, coherence, and altered interneuron spike timing) emerged within 3 weeks of Pilo-SE, aligning with early-onset, relatively subtle memory deficits.
View Article and Find Full Text PDFNeuropsychopharmacology
January 2025
Grupo de Neurociencia de Sistemas, Departamento de Ciencias Fisiológicas, Facultad de Ciencias Médicas, Universidad de Buenos Aires, Buenos Aires, Argentina.
Emotion recognition is fundamental for effective social interactions among conspecifics. Impairments in affective state processing underlie several neuropsychiatric disorders, including schizophrenia, although the neurobiological substrate of these deficits remains unknown. We investigated the impact of early NMDA receptor hypofunction on socio-affective behaviors.
View Article and Find Full Text PDFAdv Sci (Weinh)
January 2025
Department of Neurology, Institute of Neuroscience, Key Laboratory of Neurogenetics and Channelopathies of Guangdong Province and the Ministry of Education of China, The Second Affiliated Hospital, Guangzhou Medical University, Guangzhou, 510260, China.
Fragile X syndrome (FXS) is an inherited neurodevelopmental disorder characterized by a range of clinical manifestations with no effective treatment strategy to date. Here, transplantation of GABAergic precursor cells from the medial ganglionic eminence (MGE) is demonstrated to significantly improve cognitive performance in Fmr1 knockout (KO) mice. Within the hippocampus of Fmr1-KO mice, MGE-derived cells from wild-type donor mice survive, migrate, differentiate into functionally mature interneurons, and form inhibitory synaptic connections with host pyramidal neurons.
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