1. Calcium channel blockers were tested on excitatory postsynaptic currents (EPSCs) at the synapse formed by the calyx of Held on the principal cells in the medial nucleus of trapezoid body (MNTB) in brainstem slices of 4- to 14-day-old rats. 2. At postnatal day 4-9 (P4-9), EPSCs were irreversibly suppressed by the P/Q-type Ca2+ channel blocker omega-agatoxin-IVA (omega-Aga-IVA, 200 nM) and also by the N-type Ca2+ channel blocker omega-conotoxin GVIA (omega-CgTx, 2 microM). A small fraction of EPSCs was resistant to both toxins but abolished by Cd2+ (100 microM). 3. After P7, the omega-CgTx-sensitive EPSC fraction diminished and eventually disappeared after P10. Concomitantly the fraction insensitive to both toxins decreased and became undetectable after P10. 4. In contrast, the omega-Aga-IVA-sensitive EPSC fraction increased with development and became predominant after P10. All through the developmental period examined, the L-type Ca2+ channel blocker nicardipine (10 microM) had no effect. 5. We conclude that presynaptic Ca2+ channel types triggering transmitter release undergo developmental switching during the early postnatal period.
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http://dx.doi.org/10.1111/j.1469-7793.1998.419bn.x | DOI Listing |
J Gen Physiol
March 2025
Department of Physiology, University of Maryland School of Medicine, Baltimore, MD, USA.
Voltage-gated Ca2+ channels (VGCCs) are highly expressed throughout numerous biological systems and play critical roles in synaptic transmission, cardiac excitation, and muscle contraction. To perform these various functions, VGCCs are highly regulated. Inactivation comprises a critical mechanism controlling the entry of Ca2+ through these channels and constitutes an important means to regulate cellular excitability, shape action potentials, control intracellular Ca2+ levels, and contribute to long-term potentiation and depression.
View Article and Find Full Text PDFFree Radic Res
January 2025
Department of Human and Animal Physiology, Faculty of Biology, M.V. Lomonosov Moscow State University, Moscow, Russia.
Reactive oxygen species (ROS) produced by NADPH oxidase promote contraction of peripheral arteries, which is especially pronounced in early postnatal period in comparison to adulthood, but the mechanisms of such vasomotor influence are poorly understood. We tested the hypothesis that Rho-kinase and protein kinase C (PKC) mediate procontractile influence of NADPH oxidase derived ROS in peripheral artery of early postnatal rats. In addition, we evaluated the involvement Src-kinase and L-type voltage-gated Ca channels (LTCC) into procontractile influence of ROS, produced by NADPH oxidase, because of their known interplay with Rho-kinase and PKC pathways.
View Article and Find Full Text PDFCell Calcium
January 2025
IGBMC (Institut de Génétique et de Biologie Moléculaire et Cellulaire), Inserm U1258, CNRS UMR7104, Université de Strasbourg, 67404 Illkirch, France. Electronic address:
Biochem Soc Trans
January 2025
Departamento de Ciencias Médicas Básicas, Facultad de Ciencias de la Salud-sección Medicina, Universidad de La Laguna, Tenerife, ES-38071, Spain.
Large conductance voltage- and calcium-activated potassium channels (BK channels) are extensively found throughout the central nervous system and play a crucial role in various neuronal functions. These channels are activated by a combination of cell membrane depolarisation and an increase in intracellular calcium concentration, provided by calcium sources located close to BK. In 2001, Isaacson and Murphy first demonstrated the coupling of BK channels with N-methyl-D-aspartate receptors (NMDAR) in olfactory bulb neurons.
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.
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