Effects of atypical antipsychotics and haloperidol on PC12 cells: only aripiprazole phosphorylates AMP-activated protein kinase.

By converting changes in intracellular energy status to changes in cell membrane polarization, ATP-sensitive K(+) (K(ATP)) channels in hypothalamic appetite-regulating neurons play a critical role in linking neuronal electrochemical function, metabolic and energy status, and feeding behavior. Most atypical antipsychotics (AAPs) increase the appetite of patients with schizophrenia and thus cause obesity. This study aimed to explain the mechanism underlying AAP-induced appetite stimulation, based on the fact that the efficiency of fatty acid uptake into mitochondria generating ATP through β-oxidation is determined by the rate of fatty acid synthesis.

Risperidone reduces mRNA expression levels of Sulfonylurea Receptor 1 and TASK1 in PC12 cells.

Electrophysiological and immunohistochemical studies have demonstrated that glucose-sensing neurons in the hypothalamus contain both ATP-sensitive K(+) (K(ATP)) and tandem-pore K(+) (TASK1 and TASK3) channels and that glucose-induced depolarization or hyperpolarization of these neurons function as an important link between glucose-excited or glucose-inhibited neurons and feeding behavior. Medication with atypical antipsychotics increases the appetite of schizophrenic patients and thus causes increases in body weight. Therefore, the present study investigates mRNA expression levels of the genes encoding the components of these K(+) channel subsets in PC12 cells cultured with risperidone (an atypical antipsychotic) and in the hypothalami of rats subcutaneously injected for 21 consecutive days with 0.