{'fraction_non_alphanumeric': 0.016867469879518072, 'fraction_numerical': 0.004819277108433735, 'mean_word_length': 5.422680412371134, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Specialized role of Ca2+‐activated K+ channels in signaling responses of different brain cell types

The change in membrane electrical properties is a critical determinant of cellular function. Potassium channels are ubiquitous native membrane proteins and play a role in a variety of cellular functions induced by endogenous or exogenous stimuli. The KCa channels are unique members of voltage‐gated K+ channel family in that they are activated both by voltage and a rise in [Ca2+]i. The KCa channels are important regulators the resting membrane potential and link extracellular signals with intracellular second messenger systems. The KCa channels expressed in astrocytes and neurons are different from those native in cerebral arterial muscle cells (CAMCs) in that they are insensitive to the toxin blockers of KCa channel due to expression of the KCa channel fÒ4 subunit. Blockade of KCa channels results in membrane potential depolarization that permit Ca2+ influx in CAMCs and neurons but not in astrocytes, whereas activation of KCa channels causes membrane potential hyperpolarization in all cell types that inhibits Ca2+ influx in VSMCs and neurons, but facilitates Ca2+ influx in astrocytes that is crucial for neurovascular coupling.