AI Article Synopsis

Article Abstract

Currents arising from T-type Ca2+ channels in nucleus reticularis thalami (nRT) play a critical role in generation of low-amplitude oscillatory bursting involving mutually interconnected cortical and thalamic neurones, and are implicated in the state of arousal and sleep, as well as seizures. Here we show in brain slices from young rats that two kinetically different T-type Ca2+ currents exist in nRT neurones, with a slowly inactivating current expressed only on proximal dendrites, and fast inactivating current predominantly expressed on soma. Nickel was about twofold more potent in blocking fast (IC50 64 microM) than slow current (IC50 107 microM). The halogenated volatile anaesthetic enflurane blocked both currents, but only the slowly inactivating current was affected in voltage-dependent fashion. Slow dendritic current was essential for generation of low-threshold Ca2+ spikes (LTS), and both enflurane and nickel also suppressed LTS and neuronal burst firing at concentrations that blocked isolated T currents. Differential kinetic properties of T currents expressed in cell soma and proximal dendrites of nRT neurones indicate that various subcellular compartments may exhibit different membrane properties in response to small membrane depolarizations. Furthermore, since blockade of two different T currents in nRT neurones by enflurane and other volatile anaesthetics occurs within concentrations that are relevant during clinical anaesthesia, our findings suggest that these actions could contribute to some important clinical effects of anaesthetics.

Download full-text PDF

Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1464735PMC
http://dx.doi.org/10.1113/jphysiol.2005.086579DOI Listing

Publication Analysis

Top Keywords

t-type ca2+
12
nrt neurones
12
inactivating current
12
kinetic properties
8
ca2+ currents
8
thalamic neurones
8
slowly inactivating
8
current expressed
8
proximal dendrites
8
currents
7

Similar Publications

Dopamine Drives Feedforward Inhibition to Orexin Feeding System, Mediating Weight Loss Induced by Morphine Addiction.

Adv Sci (Weinh)

January 2025

Department of Anesthesiology and Perioperative Medicine, Xijing Hospital, The Fourth Military Medical University, Xi'an, 710032, China.

Feeding behavior changes induced by opioid addiction significantly contribute to the worsening opioid crisis. Activation of the reward system has shown to provoke binge eating disorder in individuals with opioid use disorder, whereas prolonged opioid exposure leads to weight loss. Understanding the mechanisms underlying these phenomena is essential for addressing this pressing societal issue.

View Article and Find Full Text PDF

Interstitial cells of Cajal in the plane of the myenteric plexus (ICC-MY) serve as electrical pacemakers in the stomach and small intestine. A similar population of cells is found in the colon, but these cells do not appear to generate regular slow wave potentials, as characteristic in more proximal gut regions. Ca handling mechanisms in ICC-MY of the mouse proximal colon were studied using confocal imaging of muscles from animals expressing GCaMP6f exclusively in ICC.

View Article and Find Full Text PDF

Background: Several chemical studies described the physiological efficacy of 1,4- dihydropyridines (DHPs). DHPs bind to specific sites on the α1 subunit of L-type calcium channels, where they demonstrate a more pronounced inhibition of Ca2+ influx in vascular smooth muscle compared to myocardial tissue. This selective inhibition is the basis for their preferential vasodilatory action on peripheral and coronary arteries, a characteristic that underlies their therapeutic utility in managing hypertension and angina.

View Article and Find Full Text PDF

Involvement of Ca3.2 T-type Ca channels and cystathionine-β-synthase in colitis-related visceral hypersensitivity in mice.

J Pharmacol Sci

December 2024

Laboratory of Pharmacology and Pathophysiology, Faculty of Pharmacy, Kindai University, 3-4-1 Kowakae, Higashi-Osaka, 577-8502, Japan. Electronic address:

We tested the hypothesis that Ca3.2 T-type Ca channels, which can be rebooted by sulfides from Zn inhibition under physiological conditions, and sulfide-generating enzymes including cystathionine-β-synthase (CBS) would participate in the colitis-related visceral pain in mice treated with 2,4,6-trinitrobenzene sulfonic acid (TNBS). The visceral hypersensitivity following TNBS-induced colitis was abolished by an inhibitor or genetic deletion of Ca3.

View Article and Find Full Text PDF

In congenital stationary night blindness, type 2 (CSNB2)-a disorder involving the Ca1.4 (L-type) Ca channel-visual impairment is mild considering that Ca1.4 mediates synaptic release from rod and cone photoreceptors.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!