Methamphetamine decreases K⁺ channel function in human fetal astrocytes by activating the trace amine-associated receptor type-1.

ABSTRACT: Methamphetamine (Meth) is a potent and commonly abused psychostimulant. Meth alters neuron and astrocyte activity; yet the underlying mechanism(s) is not fully understood. Here we assessed the impact of acute Meth on human fetal astrocytes (HFAs) using whole-cell patch-clamping. We found that HFAs displayed a large voltage-gated K⁺ efflux (I_Kv ) through K_v /K_v -like channels during membrane depolarization, and a smaller K⁺ influx (I_kir ) via inward-rectifying K_ir /K_ir -like channels during membrane hyperpolarization. Meth at a 'recreational' (20 μM) or toxic/fatal (100 μM) concentration depolarized resting membrane potential (RMP) and suppressed I_Kv/Kv-like . These changes were associated wit

SUBMITTER: Dave S 

PROVIDER: S-EPMC6522225 | biostudies-literature | 2019 Jan

REPOSITORIES: biostudies-literature