Overview
- Wu, W. et al. (2012) Neurosci. Lett. 506, 307.
Alomone Labs Amitriptyline hydrochloride inhibits L-type voltage-gated Ca2+ currents expressed in Xenopus oocytes.A. Time course of CaV1.2/α2-δ1/β1 current inhibition by 800 µM Amitriptyline hydrochloride (#A-155). Currents were elicited by application of voltage ramps from a holding potential of -100 mV to +50 mV (100 msec). B. Superimposed example traces of current responses before and during perfusion of 800 µM Amitriptyline hydrochloride, as indicated.
Voltage-gated L-type CaV1.2 calcium channels couple membrane depolarization to transient increase in cytoplasmic free Ca2+ concentration that initiates a number of essential cellular functions including cardiac and vascular muscle contraction, gene expression, neuronal plasticity, and exocytosis1.
Tricyclic antidepressants (TCAs) are known to inhibit Ca2+ currents, including the L-type CaV1.2 channel in heart myocyte and neurons2. Other known physiological targets of tricyclic antidepressants in the central nervous system are the 5-HT2 serotonin receptors and the α1-adrenergic receptors3.
Amitriptyline hydrochloride, a tricyclic antidepressant, is used for a number of medical conditions including management of depressive, anxiety and bipolar disorders3 and management of chronic pain such as neuropathic pain, diabetic neuropathy, postherpetic neuralgia and fibromyalgia4.
The proposed mechanisms of action for amitriptyline hydrochloride include inhibition of the reuptake of serotonin and norepinephrine, inhibition of NMDA receptors, of voltage-gated ion channels such as Ca2+ and Na+ channels and interaction with adenosine receptors5.
