C-terminus mediated inhibition is one emerging modality of intervention for L-type Ca2+ channels, which coordinate multiple motifs to acutely tune Ca2+ current and Ca2+ influx down to the lower limits preset by end-stage Ca2+-dependent inactivation.
The 3Å structure and correlated functional analysis of the TRPM2 cation channel from Nematostella vectensis shed light on the molecular mechanisms of TRPM2 regulation by intra- and extracellular Ca2+, and of inactivation of human TRPM2.
Gonzalo Hernandez-Hernandez, Samantha C O'Dwyer ... Colleen E Clancy
A computer model predicts different mechanisms of blood pressure regulation and effective hypertensive therapy for males and females, thereby serving as a foundational tool for improved treatment precision.
Electrophysiological and optical analysis of neurotransmitter release at central synapses reveals that glutamate signalling is not required for the long-term potentiation (LTP) of presynaptic function, and instead only promotes presynaptic long-term depression (LTD).
Kwun Nok Mimi Man, Peter Bartels ... Johannes W Hell
The α1-adrenergic receptor augments the activity of the L-type Ca2+ channel CaV1.2 through PKC and the tyrosine kinases Pyk2 and Src and thereby synaptic plasticity.
Audrey T Medeiros, Scott J Gratz ... Kate M O'Connor-Giles
In vivo analysis of endogenously tagged Ca2+ channel subunits reveals unexpected differences in subunit composition and synapse-specific relationships between channel abundance and synaptic strength.
Three distinct AKT isoforms are found in the brain and show dissimilar patterns of expression, differential roles in the expression of synaptic plasticity, and different roles in neuronal signaling.
Acetylcholine, released from cholinergic fibers originating from the medial septum, shapes social memory, and controls the CA2 hippocampal circuit via nicotinic receptors localized on GABAergic interneurons.
In a mouse model of Sjogren's disease, mitochondrial function and Ca2+ signaling are disrupted resulting in altered coupling between Ca2+ release and Ca2+ activated Cl- channels and salivary gland hypofunction.