Association between carotid plaque and Parkinson's disease.

Background: Epidemiological studies show that patients with Parkinson's disease (PD) are prone to have a reduced incidence of ischemic cerebrovascular disease. Previous studies show the correlation between PD and the lipids serum levels. The PD,s patients are found with a reduced serum level of triglyceride and low-density lipoprotein cholesterol (LDL-C); thus, the level of serum uric acid (UA) is closely related to the occurrence and development of PD.

Amitriptyline modulates calcium currents and intracellular calcium concentration in mouse trigeminal ganglion neurons.

Migraine is increasingly recognized as a channelopathy, and abnormalities of voltage-activated ionic channels could represent the molecular basis for the altered neuronal functioning. The high-voltage-activated (HVA) Ca(2+) channels in the trigeminovascular system play a role in the pathophysiology of migraine. In the present study, effects of amitriptyline (AMT), a commonly used migraine prophylactic drug, on the HVA calcium currents (I(Ca)) were examined in mouse trigeminal ganglion neurons using whole-cell patch clamp technique.

Flunarizine inhibits sensory neuron excitability by blocking voltage-gated Na+ and Ca2+ currents in trigeminal ganglion neurons.

Background: Although flunarizine has been widely used for migraine prophylaxis with clear success, the mechanisms of its actions in migraine prophylaxis are not completely understood. The aim of this study was to investigate the effects of flunarizine on tetrodotoxin-resistant Na(+) channels and high-voltage activated Ca(2+) channels of acutely isolated mouse trigeminal ganglion neurons.

Methods: Sodium currents and calcium currents in trigeminal ganglion neurons were monitored using whole-cell patch-clamp recordings.

Flunarizine blocks voltage-gated Na(+) and Ca(2+) currents in cultured rat cortical neurons: A possible locus of action in the prevention of migraine.

Although flunarizine (FLN) has been widely used for migraine prophylaxis with clear success, the mechanisms of its actions in migraine prophylaxis are not completely understood. It has been hypothesized that migraine is a channelopathy, and abnormal activities of voltage-gated Na(+) and Ca(2+) channels might represent a potential mechanism of cortical hyperexcitability predisposing to migraine. The aim of the present study was to investigate the effects of FLN on Na(+) and Ca(2+) channels of cultured rat cortical neurons.