Related Experiment Video
Updated: May 29, 2026

Development of a Unilaterally-lesioned 6-OHDA Mouse Model of Parkinson's Disease
Published on: February 14, 2012
L-type Cav1.2 calcium channel is involved in 6-hydroxydopamine-induced neurotoxicity in rats
Rong Wang1, Zegang Ma, Jun Wang
1Department of Physiology, Shandong Provincial Key Laboratory of Pathogenesis and Prevention of Neurological Disorders and State Key Disciplines: Physiology, Medical College of Qingdao University, Qingdao 266071, China.
Abstract:
Evidence suggested that L-type calcium channels may play a key role in the pathogenesis of dopaminergic neuron degeneration. In the present study, effects of L-type Cav1.2 calcium channel on 6-hydroxydopamine (6-OHDA)-induced neurotoxicity were investigated. By the semi-quantitative reverse transcription polymerase chain reaction (RT-PCR) studies, we showed that the expression of L-type Cav1.2 calcium channel α1 subunit mRNA increased in the substantia nigra (SN) of 6-OHDA-lesioned rats. Treatment with nifedipine could improve the apomorphine-induced rotation behavior in 6-OHDA-lesioned rats. Using high-performance liquid chromatography electrochemical detection, we also observed that nifedipine partly restored 6-OHDA-induced dopamine depletion in the striatum of rats. These results suggest that the L-type Cav1.2 calcium channel is associated with the development and progression of dopaminergic neuron degeneration.
Related Concept Videos
Ligand-Gated Ion Channel Receptor: Gating Mechanism
Voltage-gated Ion Channels
Generally, all voltage-gated ion channels have a 'voltage-sensing domain' that spans the lipid bilayer. The charged residues in the sensor move in response to the membrane potential changes that open the channel allowing ions movement. There are several types of...
Antihypertensive Drugs: Action of Calcium Channel Blockers

