Epileptic seizures are associated with neuronal hyperactivity. Here, however, we investigated whether continuous neuronal firing is necessary to maintain electrographic seizures. We studied a class of "low-Ca2+" ictal epileptiform bursts, induced in rat hippocampal slices, that are characterized by prolonged (2-15 s) interruptions in population spike generation. We found that, during these interruptions, neuronal firing was suppressed rather than desynchronized. Intracellular current injection, application of extracellular uniform electric fields, and antidromic stimulation showed that the source of action potential disruption was depolarization block. The duration of the extracellular potassium transients associated with each ictal burst was not affected by disruptions in neuronal firing. Application of phenytoin or veratridine indicated a critical role for the persistent sodium current in maintaining depolarization block. Our results show that continuous neuronal firing is not necessary for the maintenance of experimental electrographic seizures.
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http://dx.doi.org/10.1152/jn.00467.2003 | DOI Listing |
Phys Rev Lett
December 2024
University of Strathclyde, Institute of Photonics, SUPA Dept of Physics, Glasgow, United Kingdom.
We report a spiking flip-flop memory mechanism that allows controllably switching between neural-like excitable spike-firing and quiescent dynamics in a resonant tunneling diode (RTD) neuron under low-amplitude (<150 mV pulses) and high-speed (ns rate) inputs pulses. We also show that the timing of the set-reset input pulses is critical to elicit switching responses between spiking and quiescent regimes in the system. The demonstrated flip-flop spiking memory, in which spiking regimes can be controllably excited, stored, and inhibited in RTD neurons via specific low-amplitude, high-speed signals (delivered at proper time instants) offers high promise for RTD-based spiking neural networks, with the potential to be extended further to optoelectronic implementations where RTD neurons and RTD memory elements are deployed alongside for fast and efficient photonic-electronic neuromorphic computing and artificial intelligence hardware.
View Article and Find Full Text PDFTrends Genet
January 2025
Graduate School of Frontier Biosciences, Osaka University, Suita, Osaka 565-0871, Japan; Institute of Neurological and Psychiatric Disorders, Shenzhen Bay Laboratory, Shenzhen, Guangdong 518132, China. Electronic address:
Neuronal activity, including sensory-evoked and spontaneous firing, regulates the expression of a subset of genes known as activity-dependent genes. A key issue in this process is the activation and accumulation of transcription factors (TFs), which bind to cis-elements at specific enhancers and promoters, ultimately driving RNA synthesis through transcription machinery. Epigenetic factors such as histone modifiers also play a crucial role in facilitating the specific binding of TFs.
View Article and Find Full Text PDFJ Neurophysiol
January 2025
Department of Psychology, University of Wisconsin-Milwaukee, Milwaukee WI, USA.
The hippocampus has a known role in learning and memory, with the ventral subregion supporting many learning tasks involving affective responding, including fear conditioning. Altered neuronal intrinsic excitability reflects experience-dependent plasticity that supports learning-related behavioral changes. Such changes have previously been observed in the dorsal hippocampus following fear conditioning, but little work has examined the effect of fear conditioning on ventral hippocampal intrinsic plasticity.
View Article and Find Full Text PDFJ Neurochem
January 2025
School of Life Science, Nanchang University, Nanchang, China.
Activation of the brain-penetrant beta3-adrenergic receptor (Adrb3) is implicated in the treatment of depressive disorders. Enhancing GABAergic inputs from interneurons onto pyramidal cells of prefrontal cortex (PFC) represents a strategy for antidepressant therapies. Here, we probed the effects of the activation of Adrb3 on GABAergic transmission onto pyramidal neurons in the PFC using in vitro electrophysiology.
View Article and Find Full Text PDFJ Neurochem
January 2025
Molecular Horizons, Faculty of Science, Medicine and Health, University of Wollongong, Wollongong, New South Wales, Australia.
GABA receptor (GABAR) activation is known to alleviate pain by reducing neuronal excitability, primarily through inhibition of high voltage-activated (HVA) calcium (Ca2.2) channels and potentiating G protein-coupled inwardly rectifying potassium (GIRK) channels. Although the analgesic properties of small molecules and peptides have been primarily tested on isolated murine dorsal root ganglion (DRG) neurons, emerging strategies to develop, study, and characterise human pluripotent stem cell (hPSC)-derived sensory neurons present a promising alternative.
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