The role of axonal voltage-gated potassium channels in tDCS.

Background: Transcranial direct current stimulation (tDCS) is a non-invasive sub-threshold stimulation, widely accepted for its amelioration of distinct neuropsychiatric disorders. The weak electric field of tDCS modulates the activity of cortical neurons, which in turn modifies brain functioning. However, the underlying mechanisms for that are not fully understood.

Calcium channels control tDCS-induced spontaneous vesicle release from axon terminals.

Background: Transcranial direct current stimulation (tDCS) is a subthreshold neurostimulation therapeutic method that ameliorate neuropsychiatric impairments. The most sensitive subcellular compartment for tDCS are the axons that polarize. However, how these relatively small polarizations significantly alter synaptic dynamics is still unknown.

The role of sodium channels in direct current stimulation-axonal perspective.

Transcranial neurostimulation methods are utilized as therapies for various neuropsychiatric disorders. Primarily, they entail the delivery of weak subthreshold currents across the brain, which modulate neuronal excitability. However, it is still a puzzle how such weak electrical fields actuate their effects.

Bioinformatics analyses show dysregulation of calcium-related genes in Angelman syndrome mouse model.

Background: Angelman syndrome (AS) is a genetic neurodevelopmental disorder caused by the loss of function of the UBE3A protein in the brain. In a previous study, we showed that activity-dependent calcium dynamics in hippocampal CA1 pyramidal neurons of AS mice is compromised, and its normalization rescues the hippocampal-dependent deficits. Therefore, we expected that the expression profiles of calcium-related genes would be altered in AS mice hippocampi.

α1-Na/K-ATPase inhibition rescues aberrant dendritic calcium dynamics and memory deficits in the hippocampus of an Angelman syndrome mouse model.

Angelman syndrome (AS) is a neurodevelopmental disorder caused by the loss of function of the maternal copy of the UBE3A gene. Previous studies reported an increase in α1-Na/K-ATPase (α1-NaKA) expression in the AS hippocampus at the age of 2 weeks as the initial and isolated molecular alteration. This increase was further implied upon actuating much of the hippocampal-related deficits in an AS mouse model, although the underlying mechanism was never investigated.

Selective ligands for Na/K-ATPase α isoforms differentially and cooperatively regulate excitability of pyramidal neurons in distinct brain regions.

Sodium-potassium ATPase (NaKA) is a plasma membrane enzyme responsible for influencing membrane physiology by direct electrogenic activity. It determines cellular excitability and synaptic neurotransmission, thus affecting learning and memory processes. A principle catalytic α subunit of NaKA has development-specific expression pattern.