Table 3.

Pre-clinical studies targeting CCBs in HD.

Disorder	Drug, Dose/Concentration	Pre-Clinical Model/ In Vivo/In Vitro	Results	Refs.
HD	ω-conotoxin GVIA 50 nM	Striatal synaptosomes from BACHD mice/ in vitro	↓ striatal glutamate release observed in BACHD mice	[13]
HD	Isradipine 1 nM	Corticostriatal neurons from BACHD mice/ in vitro	Neuronal protection against glutamate toxicity	[14]
HD	Felodipine 1 and 5 μM	HD transgenic mice (B6HD mice) / in vivo	Felodipine induces autophagy and clear aggregate-prone, neurodegeneration disease-associated proteins (mhtt).	[147]
HD	Nimodipine, 2, 4, and 10 mg/kg, i.p.	Male Sprague-Dawley rats/ in vivo	No beneficial effect against quinolinic acid striatal lesion	[156]
HD	Nifedipine 5 μM	Cocultured striatal and cortical neurons/ in vitro	Mixed solution with memantine rescued neurons from NMDA-mediated toxicity	[158]
HD	Nimodipine 12 mg/kg	Male Sprague-Dawley rats/ in vivo	Protective against oxidative stress	[159]
HD	Nifedipine 10 μM	Cortical pyramidal neurons from R6/2 mouse mice/ in vitro	Nifedipine significantly ↓ both somatic Ca2+transient amplitude and area	[160]

Note: Isradipine, Felodipine, Nimodipine= L-type blocker; Mibefradil=T-type blocker; ω-conotoxin GVIA= N-type blocker; ML218= T-type blocker; s.c.= subcutaneous; i.p= intraperitoneal; ↓= decrease; ↑= increase; TH= tyrosine hydroxylase; SNpc= substantia nigra pars compacta; ω-agatoxin IVA= P/Q blocker; SNX-482 (R-type blocker); Dantrolene= ryanodine receptor (RyR) antagonist; STN=subthalamic nucleus.