Preincubation (3 h) with melatonin (10−7 and 10−9 M). Incubation with 6-OHDA (25, 50, 100, and 250 M).
Melatonin prevented the loss of cell viability and apoptosis induced by 6-OHDA. Melatonin also protected the reduction of mRNAs of antioxidant enzymes evoked by 6-OHDA.
Unilateral injection of 6-OHDA (20 g in 5 L) into the right striatum. Melatonin (3 and 10 mg/kg, i.p.) was administrated 1 h before and immediately and 1 and 2 h after 6-OHDA injection. After that, the animals received a daily administration of melatonin in the next 3 days.
Melatonin treatment recovered the 6-OHDA-induced changes in striatal MDA and DA levels and TH activity.
Unilateral injection of 6-OHDA (8 g in 2 L) into the right SNC. Melatonin treatment (50 ± 7.5 g/h, s.c.) started immediately after 6-OHDA injection and it was maintained for 7 days.
Melatonin treatment prevented apomorphine-induced rotational behaviour and loss of complex I activity induced by 6-OHDA.
Unilateral injection of 6-OHDA into the right striatum (two injections of 12 g in 1 g of saline). Posttreatment (1 h) with melatonin (2, 5, 10, and 25 mg/kg, i.p.), daily for 7 days.
Melatonin prevented 6-OHDA-induced depletion of striatal DA and serotonin levels. Melatonin blocked the apomorphine-induced rotational behaviour.
Pretreatment with melatonin (0.5 mg/kg, i.p.) for 7 days. On day 8, animals received an unilateral injection of 6-OHDA (8 g) into the lateral striatum.
Melatonin treatment prevented motor deficits (observed in the apomorphine-induced rotational behaviour, staircase test, disengage time, stepping test, initiation time, and postural balance test) induced by 6-OHDA administration.
Unilateral injection of 6-OHDA (8 g) into the right medial forebrain bundle (MFB). Melatonin treatment (10 mg/kg, p.o.) began four days after 6-OHDA injection and continued for 30 days.
Melatonin treatment improved motor performance without evoking dyskinesia. Melatonin also protected TH-positive neurons and neuronal ultrastructure of striatum.
Unilateral injection of 6-OHDA (12 g) into the right MFB. Melatonin (10 mg/kg/day, i.p.) was administrated 23 days before and 7 days after (pre- and posttreatment) or only 7 days after (posttreatment) the injection of 6-OHDA.
Melatonin decreased COX and caspase-3 activity and PGE2 levels and increased Bcl-2 levels that have been altered by 6-OHDA injection. Melatonin also prevented the loss of DAergic neurons in SNc.
Unilateral injection of 6-OHDA (20 g in 5 L) into the right striatum. Melatonin (3 and 10 mg/kg, i.p.) was administrated 1 h before and immediately and 1 and 2 h after 6-OHDA injection. After that, the animals received a daily administration of melatonin in the next 3 days.
Melatonin treatment reduced motor deficits and protected against 6-OHDA-induced loss of DAergic neurons in SNc and in dorsolateral striatum.
Unilateral injection of 6-OHDA (12 g) into the right MFB. Melatonin (10 mg/kg/day) was administrated 23 days before and 7 days after (pre- and posttreatment) or only 7 days after (posttreatment) the injection of 6-OHDA.
Melatonin treatment protected against the 7-OHDA-induced loss of DAergic neurons, increased antioxidant enzyme activities (SOD, catalase and GPx), and decreased lipid peroxidation. The pretreatment with melatonin was more effective in protecting against the 6-OHDA-induced deficits.
Pretreatment (30 min) with melatonin (10 mg/kg, i.p.). Unilateral injection of MPP+ (7.4 g) into the right SNc. Animals were subjected to an acute or chronic posttreatment with melatonin.
Melatonin treatment reduced lipid peroxidation and protected against DAergic neuronal loss induced by MPP+.
Unilateral injection of MPP+ (0.1 mol) into the right striatum. Melatonin (10 mg/kg, i.p.) was administrated 1 h before and 1, 3, and 5 h after MPP+ administration.
Melatonin reduced the MPP+-induced DAergic toxicity and recovered the GSH levels.
Coincubation with MPP+ (200 M) and melatonin (1 mM) at the same time.
Melatonin protected cell viability and prevented apoptosis. Melatonin also reduced cdk5 expression and the cleavage of cdk5-35 to cdk5-25 induced by MPP+.
Injection of 1 L of 50 mM MPP+ into the right striatum. Melatonin (10 mg/mL, i.p.) was administrated 0, 1, 2, 3, 4, 24, 48, and 72 h after MPP+ injection.
Melatonin protected DAergic neurons from apoptosis induced by MPP+. Melatonin recovered mRNA and protein expression of fibroblast growth factor 9 that was reduced by MPP+ injection.
Single injection of MPTP (15 mg/kg, s.c.). Melatonin (5 or 10 mg/kg i.p.), deprenyl (0.37 mg/kg), or deprenyl plus melatonin (0.37 mg/kg and 5 or 10 mg/kg) was administrated 30 min prior to MPTP.
Melatonin was able to protect the mitochondrial complex I activity and the oxidative damage in nigrostriatal neurons. Melatonin treatment also potentiates the protective effect of deprenyl on DA levels and TH activity.
Four injections of MPTP (15 mg/kg, s.c.) with intervals of 2 h. After 24 h, the animals received three additional injections with the same dose and intervals. Melatonin (20 mg/kg s.c.) was administrated 1 h before the first injection of MPTP.
Melatonin treatment prevented the MPTP-induced mitochondrial iNOS in striatum and SNc. Melatonin also protected complex I activity and inhibited lipid peroxidation.
Preincubation with melatonin (50, 100, and 200 M). Incubation with MPTP (400 M).
Melatonin decreased the MPTP-induced oxidative and nitrosative stress, intracellular calcium, and activation of P-p38 MAPK. Melatonin also normalized the levels of inflammatory proteins, mRNA of proinflammatory cytokines, and NF-B.
Ten injections of MPTP (15 mg/kg, i.p.) during 5 weeks (2 injections a week). Melatonin (5 mg/kg, i.p.) was administered 1 week before, 5 weeks during, and 12 weeks after MPTP treatment.
Melatonin recovered mitochondrial respiration, ATP production, and antioxidant enzyme levels. Melatonin also protected against MPTP-induced DAergic neurons loss and locomotor activity deficits.
Four injections of MPTP (20 mg/kg, i.p.) with 2 h between them. Eight days after MPTP injections, animals received L-DOPA/carbidopa (100/10 mg/kg/twice/day, p.o.) and/or melatonin (5 or 10 mg/kg/day, p.o.) for 8 weeks.
Melatonin treatment recovered motor performance, striatal DA level, GSH, and antioxidant enzyme activities and reduced lipid peroxidation. Melatonin also improved the motor response to L-DOPA.
MPTP (30 mg/kg, i.p.) was administrated in two injections (16 h apart). Melatonin treatment (10, 20, and 30 mg/kg, i.p.) 30 min before MPTP administration, followed by four doses of melatonin, at every 10 h.
Melatonin protected against the MPTP-induced TH-positive neurons loss in SNc and enhanced the effects of L-DOPA treatment.
Rotenone injection (6 g in 1 L) into the right SN. Melatonin (10, 20, and 30 mg/kg, i.p.) was administrated 30 min after rotenone injection and was given every 12 h for 4 days.
Melatonin reduced the levels of hydroxyl radicals in the isolated mitochondria and protected GSH levels and antioxidant enzymes activities in SN that were changed by rotenone injection.
Rotenone injection (2.5 mg/kg, i.p.) for 10 days. Melatonin (10 mg/kg, i.p.) was administrated for 28 days after the rotenone injection.
Melatonin treatment protect TH-positive neurons in SNc and striatal levels of dopamine. Melatonin also inhibit the rotenone-induced depressant-like effect.
Three injections of rotenone (4.0 μg in 2.0 L/site) at three points along its rostrocaudal axis. Animals received melatonin (4.0 g/mL) in drinking water, one week before and nine weeks after rotenone injections.
Melatonin treatment protected TH-positive neurons in striatum and SNc. Melatonin also inhibited the rotenone-induced loss in dopamine of SNc and apomorphine-induced rotations.
Melatonin prevented the maneb-induced disruption of the mitochondrial transmembrane potential, activation of caspase-3/7, loss in cell viability, and aggregation of α-synuclein.
Treatment with melatonin (30 mg/kg/day, i.p.) for 9 weeks. Treatment with maneb (30 mg/kg, i.p.) plus paraquat (10 mg/kg, i.p.) twice a week, for 9 weeks, 2 hours after melatonin injection.
Melatonin treatment protected the maneb/paraquat-induced lipid peroxidation, TH-positive neurons degeneration, increased nitrite content and mRNA levels of cytochrome P-450 2E1, GSTA4-4 activity, and increased levels of glutathione-S-transferase, P-p53, Bax, and caspase-9.
Injection with lentiviral vectors encoding A30P mutant human α-synuclein (lenti-A30P) into the right SNc. Melatonin treatment (10 mg/kg/day, i.p.) 2 days before and 8 weeks after the injection of lenti-A30P.
Melatonin treatment prevented the loss of TH-positive neurons induced by injection of lenti-A30P.
