Table 1.

Summary of the principal findings of the cited literature on 6-OHDA effects on SNpc DAergic neuron functional properties.

Type of Study	[6-OHDA]	Treatment	Modified Parameters in SNpc DAergic Neuron	Molecular Mechanisms	Reference
Ex vivo, rat	0.2, 0.5, 1, 2 (mM)	5 or 10 min	Inhibition of spontaneous firing; Rm drop; Ca2+ accumulation	D2-GIRK and KATP channels activation; mitochondrial release of Ca2+ ions	[23]
Ex vivo, rat	0.5, 1, 2 (mM)	3–5 min	Inhibition of spontaneous firing; Ca2+ accumulation	N-type VGCC current amplitude increase	[24]
In vitro organotypic culture, rat	25 µM	12 or 18 h	Irregular firing/bursting; depolarized RMP	Increased AHP and IAHP mediated by SK channels	[25]
In vivo, mouse	1.5 µg/µL (1.6 µL)	1 injection, SNpc	1 to 8 weeks after lesion; Lack of maturation of Rm, AP half-width, steady-state I(-100mV)		[26]
In vivo, rat	4 µg/4 µL	1 injection, MFB; tested 16–20 days after lesion	Increase in firing rate, n. of bursting neurons and n. spikes/burst	Release of glutamate and mGluR activation (rescue by MPEP)	[27]
In vivo, rat	4 µg/2 µL	1 injection, MFB, 4–6 weeks after lesion	Decreased n. of active neurons; no significant difference in firing rate nor bursting; higher CV	Rearrangements of circuitry to compensate for neuronal loss	[28]
In vivo, rat	8 µg/4 µL	1 injection, MFB	32 days after lesion, 76% reduction in firing rate	Excessive GABA release by reactive astrocytes, rescued by MAO inhibitor safinamide	[7]
Ex vivo	Ipsilateral slices from in vivo lesioned rat		Increase tonic GABAA current; no difference in sIPSC amplitude or frequency	Rescued by bicuculline and safinamide	[7]