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Your search keyword '"Daw, Michael I."' showing total 3 results
Start Over Author "Daw, Michael I." Topic action potentials
3 results on '"Daw, Michael I."'

1. Coordinated developmental recruitment of latent fast spiking interneurons in layer IV barrel cortex.

Author

Daw MI, Ashby MC, and Isaac JT

Subjects
Age Factors, Animals, Animals, Newborn, Bicuculline pharmacology, Dose-Response Relationship, Radiation, Electric Stimulation methods, Excitatory Postsynaptic Potentials drug effects, Excitatory Postsynaptic Potentials physiology, Excitatory Postsynaptic Potentials radiation effects, GABA Antagonists pharmacology, Green Fluorescent Proteins biosynthesis, Green Fluorescent Proteins genetics, In Vitro Techniques, Mice, Mice, Transgenic, Patch-Clamp Techniques methods, Thalamus anatomy & histology, Action Potentials physiology, Cerebral Cortex cytology, Interneurons physiology, Neural Pathways growth & development, Thalamus physiology
Abstract

Feedforward inhibitory GABAergic transmission is critical for mature cortical circuit function; in the neonate, however, GABA is depolarizing and believed to have a different role. Here we show that the GABAA receptor-mediated conductance is depolarizing in excitatory (stellate) cells in neonatal (postnatal day [P]3-5) layer IV barrel cortex, but GABAergic transmission at this age is not engaged by thalamocortical input in the feedforward circuit and has no detectable circuit function. However, recruitment occurs at P6-7 as a result of coordinated increases in thalamic drive to fast-spiking interneurons, fast-spiking interneuron-stellate cell connectivity and hyperpolarization of the GABAA receptor-mediated response. Thus, GABAergic circuits are not engaged by thalamocortical input in the neonate, but are poised for a remarkably coordinated development of feedforward inhibition at the end of the first postnatal week, which has profound effects on circuit function at this critical time in development.

Published
2007
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2. Reduced local input to fast‐spiking interneurons in the somatosensory cortex in the GABAA γ2 R43Q mouse model of absence epilepsy

Author

Currie, Stephen P., Luz, Liliana L., Booker, Sam A., Wyllie, David J. A., Kind, Peter C., and Daw, Michael I.

Subjects
Male, Analysis of Variance, Patch-Clamp Techniques, Full‐Length Original Research, Action Potentials, Glutamic Acid, Somatosensory Cortex, Development, In Vitro Techniques, Arginine, Receptors, GABA-A, Synapse, Animal models, Mice, Inbred C57BL, Disease Models, Animal, Mice, Animals, Newborn, Epilepsy, Absence, Inhibitory Postsynaptic Potentials, Interneurons, Animals, Point Mutation, Female, Inhibition
Abstract

Summary Objective Absence seizures in childhood absence epilepsy are initiated in the thalamocortical (TC) system. We investigated if these seizures result from altered development of the TC system before the appearance of seizures in mice containing a point mutation in γ‐aminobutyric acid A (GABAA) receptor γ2 subunits linked to childhood absence epilepsy (R43Q). Findings from conditional mutant mice indicate that expression of normal γ2 subunits during preseizure ages protect from later seizures. This indicates that altered development in the presence of the R43Q mutation is a key contributor to the R43Q phenotype. We sought to identify the cellular processes affected by the R43Q mutation during these preseizure ages. Methods We examined landmarks of synaptic development at the end of the critical period for somatosensory TC plasticity using electrophysiologic recordings in TC brain slices from wild‐type mice and R43Q mice. Results We found that the level of TC connectivity to layer 4 (L4) principal cells and the properties of TC synapses were unaltered in R43Q mice. Furthermore, we show that, although TC feedforward inhibition and the total level of GABAergic inhibition were normal, there was a reduction in the local connectivity to cortical interneurons. This reduction leads to altered inhibition during bursts of cortical activity. Significance This altered inhibition demonstrates that alterations in cortical circuitry precede the onset of seizures by more than a week.

Published
2017

3. Asynchronous Transmitter Release from Cholecystokinin-Containing Inhibitory Interneurons Is Widespread and Target-Cell Independent.

Author

Daw, Michael I., Tricoire, Ludovic, Erdelyi, Ferenc, Szabo, Gabor, and McBain, Chris J.

Subjects
*SYNAPSES, *NEUROTRANSMITTERS, *ACTION potentials, *ELECTROPHYSIOLOGY, *INTERNEURONS, *CHOLECYSTOKININ
Abstract

Neurotransmitter release at most central synapses is synchronized to the timing of presynaptic action potentials. Here,we show that three classes of depolarization-induced suppression of inhibition-expressing, cholecystokinin (CCK)-containing, hippocampal interneurons show highly asynchronous release in response to trains of action potentials. This asynchrony is correlated to the class of presynaptic interneuron but is unrelated to their postsynaptic cell target. Asynchronous and synchronous release from CCK-containing interneurons show a slightly different calcium dependence, such that the proportion of asynchronous release increases with external calcium concentration, possibly suggesting that the modes of release are mediated by different calcium sensors. Asynchronous IPSCs include very large (up to 500 pA/7nS) amplitude events, which persist in low extracellular calcium and strontium, showing that they result from quantal transmitter release at single release sites. Finally, we show that asynchronous release is prominent in response to trains of presynaptic spikes that mimic natural activity of CCK-containing interneurons. That asynchronous release from CCK-containing interneurons is a widespread phenomenon indicates a fundamental role for these cells within the hippocampal network that is distinct from the phasic inhibition provided by parvalbumin-containing interneurons. [ABSTRACT FROM AUTHOR]

Published
2009
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