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ISSN 0022-1295
EISSN 1540-7748

Research News

Mice lacking BK channels are weak because of reduced vesicle release at neuromuscular junctions.


SCN2A mutations can cause early-onset epilepsy. Thompson et al. examined these human mutations in neonatal versus adult channel isoforms.

This study by Tóth et al. has defined that the N-terminal MHR1/2 domain is a conserved ADPR binding site in TRPM2 from ancient cnidarians to vertebrate, and that it is the key ligand binding site for invertebrate TRPM2 channel activation by ADPR, the same as observed in human and zebrafish TRPM2.

Research Articles

TRPM2 cation channels are activated by ADP ribose (ADPR), which binds to two distinct locations in the N- and C-terminal cytosolic domains. Tóth et al. selectively determine the ligand-binding affinities of these two binding sites in sea anemone TRPM2 and provide insights into the mechanistic contributions of several amino acids within the N-terminal site.

D1R density changes are associated with cognitive disorders. McCarthy et al. demonstrate that D1R constitutive activity increases CaV2.2 current in prefrontal cortex pyramidal neurons and a heterologous expression system, requiring active Gs protein and D1R-CaV2.2 interaction.

In several preparations, it has been found that synaptic vesicles can be released either quickly or slowly in response to a strong stimulus. Blanchard et al. differentially modify the proportion of quick versus slow vesicles by prior subthreshold or suprathreshold stimulations.


Voltage-sensing phosphatases (VSPs) can be used to experimentally manipulate cellular phosphoinositide levels. Kawanabe et al. describe an enhanced VSP based on the zebrafish orthologue Dr-VSP and developed by the introduction of a mutation into a membrane-interacting site and fusion with the N-terminal cytoplasmic region of sea squirt VSP.

Mice lacking BK potassium channels have weakness with stimulation of peripheral nerve, but not muscle, which is caused by a defect in neuromuscular transmission. Prolonging the motor neuron action potential fully normalizes in vivo strength.

Methods and Approaches

Channelrhodopsin-2 is the key ion channel in optogenetics. Walther et al. demonstrate that coupling channelrhodopsin-2 to the β1 subunit of voltage-gated sodium channels allows action potentials to be triggered by blue-light illumination of Xenopus laevis oocytes coexpressing different types of sodium channel α subunits.

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