The neuronal basis of the excitation received by motoneurones during swimming in curarized Xenopus embryos has been investigated further. Extracellular stimulation of axons in the fibre tracts of the spinal cord has been used to evoke unitary excitatory post-synaptic potentials (p.s.p.s) in motoneurones. The p.s.p.s. had a rise time of 3-5 ms and a long falling phase lasting up to 200 ms. These potentials consist of two components: a 'fast' p.s.p. which is insensitive to 50 microM-(+/-)-2-amino-5-phosphonovaleric acid (APV) but is blocked by 2 mM-cis-2,3-piperidine dicarboxylic acid (PDA) and is therefore probably mediated by kainate/quisqualate receptors, and a 'slow' p.s.p. which is blocked by both APV and PDA and is therefore probably mediated by N-methyl-D-aspartate (NMDA) receptors. Paired intracellular recordings from motoneurones and interneurones have revealed a class of spinal cord interneurone which makes descending excitatory amino-acid-dependent synapses onto motoneurones and commissural interneurones. The p.s.p.s evoked by intracellular stimulation of these excitatory interneurones consist of 'fast' and 'slow' components identical in shape and pharmacological properties to those of the extracellularly evoked potentials. One neurone may, therefore, be able to release a transmitter which activates both NMDA and non-NMDA receptors on the same post-synaptic neurone generating fast and slow post-synaptic potentials. The excitatory interneurones play an important role in the generation of the swimming pattern in the curarized Xenopus embryo. Like motoneurones, they fire once per swimming cycle in phase with the ipsilateral motoneurones and receive a background excitation during swimming that is excitatory amino acid mediated. They are therefore part of the swimming rhythm generator. The temporal summation of the extracellularly evoked p.s.p.s shows that these excitatory interneurones are sufficient to generate the excitatory drive received by motoneurones during swimming.
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http://dx.doi.org/10.1113/jphysiol.1985.sp015694 | DOI Listing |
Brain
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 PDFJ Clin Invest
January 2025
Department of Pharmacology, University of Michigan Medical School, Ann Arbor, United States of America.
Dravet syndrome (DS) is a developmental and epileptic encephalopathy (DEE) that begins in the first year of life. While most cases of DS are caused by variants in SCN1A, variants in SCN1B, encoding voltage-gated sodium channel β1 subunits, are also linked to DS or to the more severe early infantile DEE. Both disorders fall under the OMIM term DEE52.
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.
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January 2025
Network of Immunity in Infection, Malignancy and Autoimmunity (NIIMA), Universal Scientific Education and Research Network (USERN), Children's Medical Center Hospital, Dr. Qarib St, Keshavarz Blvd, Tehran 14194, Iran.
Fast spiking parvalbumin (PV) interneuron is an inhibitory gamma-aminobutyric acid (GABA)ergic interneuron diffused in different brain networks, including the cortex and hippocampus. As a key component of brain networks, PV interneurons collaborate in fundamental brain functions such as learning and memory by regulating excitation and inhibition (E/I) balance and generating gamma oscillations. The unique characteristics of PV interneurons, like their high metabolic demands and long branching axons, make them too vulnerable to stressors.
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January 2025
Department of Bioscience, University of Oslo, Oslo, Norway.
Perineuronal nets (PNNs) are a condensed form of extracellular matrix primarily found around parvalbumin-expressing (PV+) interneurons. The postnatal maturation of PV+ neurons is accompanied with the formation of PNNs and reduced plasticity. Alterations in PNN and PV+ neuron function have been described for mental disorders such as schizophrenia and autism.
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