A novel bioelectronic glucose sensor to process distinct electrical activities of pancreatic beta-cells.

Glucose sensors have improved and facilitated therapy for type 1 diabetes. However, they are still not capable to sense all physiological signals and to act in a closed-loop. Pancreatic β-cells have been shaped during evolution as biological sensors and offer the advantage to integrate all physiological signals in addition to glucose.

Nimodipine inhibits AP firing in cultured hippocampal neurons predominantly due to block of voltage-dependent potassium channels.

L-type calcium channels (LTCC) are important functional elements of hippocampal neurons contributing to processes like memory formation and gene expression. Mice lacking the Ca(V)1.2 channel in hippocampal pyramidal cells exhibited defects in spatial memory (Moosmang et al.

Ca(v)1.3 and BK channels for timing and regulating cell firing.

L-type Ca(2+) channels (LTCCs, Ca(v)1) open readily during membrane depolarization and allow Ca(2+) to enter the cell. In this way, LTCCs regulate cell excitability and trigger a variety of Ca(2+)-dependent physiological processes such as: excitation-contraction coupling in muscle cells, gene expression, synaptic plasticity, neuronal differentiation, hormone secretion, and pacemaker activity in heart, neurons, and endocrine cells. Among the two major isoforms of LTCCs expressed in excitable tissues (Ca(v)1.