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Int Rev Neurobiol. 2016;128:281-342. doi: 10.1016/bs.irn.2016.04.001. Epub 2016 May 13.

BK Channels in the Central Nervous System.

Author information

1
Committee on the Neurobiology of Addictive Disorders, The Scripps Research Institute, La Jolla, CA, United States. Electronic address: contet@scripps.edu.
2
Committee on the Neurobiology of Addictive Disorders, The Scripps Research Institute, La Jolla, CA, United States.
3
Carnegie Mellon University, Pittsburgh, PA, United States.

Abstract

Large conductance Ca(2+)- and voltage-activated K(+) (BK) channels are widely distributed in the postnatal central nervous system (CNS). BK channels play a pleiotropic role in regulating the activity of brain and spinal cord neural circuits by providing a negative feedback mechanism for local increases in intracellular Ca(2+) concentrations. In neurons, they regulate the timing and duration of K(+) influx such that they can either increase or decrease firing depending on the cellular context, and they can suppress neurotransmitter release from presynaptic terminals. In addition, BK channels located in astrocytes and arterial myocytes modulate cerebral blood flow. Not surprisingly, both loss and gain of BK channel function have been associated with CNS disorders such as epilepsy, ataxia, mental retardation, and chronic pain. On the other hand, the neuroprotective role played by BK channels in a number of pathological situations could potentially be leveraged to correct neurological dysfunction.

KEYWORDS:

Action potential; Afterhyperpolarization; Alcoholism; Ataxia; BK channels; Brain; Calcium; Circadian rhythm; Depolarization; Epilepsy; Excitability; Firing; Glaucoma; Ischemia; KCNMA1; Mental retardation; Neurodegeneration; Neurons; Neurotransmission; Neurovascular coupling; Pain; Slo1; Spinal cord; Transmitter release; Tremor; Waveform

PMID:
27238267
PMCID:
PMC4902275
DOI:
10.1016/bs.irn.2016.04.001
[Indexed for MEDLINE]
Free PMC Article

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