CDPPB (1-30 mg/kg, s.c., 20 min prior to Amphetamine injection (locomotor test) or 20 min after Amphetamine injection (PPI test)) suppresses Amphetamine-induced locomotor activity without affecting spontaneous locomotor activity and reverses Amphetamine-induced deficits in PPI in rats[1].
CDPPB (10 mg/kg/day, i.p., 14 days) improves Phencyclidine-induced cognitive deficits in mice[4].
CDPPB (5 mg/kg, i.p., 14 days) improves cognitive impairment and partially reverses the lesion-induced changes in eNOS and nNOS expressions in olfactory bulbectomized rats[5].
CDPPB (1.5 mg/kg, s.c., 18 weeks) ameliorates pathology and phenotypic signs of Huntington's disease mice[6].
CDPPB (20 mg/kg, p.o., single) attenuates depressive-like behavior induced by repeated social defeat stress in mice[7].
CDPPB (10 mg/kg, i.p., adolescence) reverses MK-801 (HY-15084B)-induced locomotor hyperactivity and anhedonia in mice[8].
CDPPB (1-5 mg/kg, i.p., 8 days) improves neuronal survival and prevents memory deficits in C57BL/6 mice injected intrahippocampally with Aβ. [9].
| Animal Model: | Male Sprague-Dawley rats (250–300 g at the time of surgery, age not specified in this context for this part) with olfactory bulbectomy[5] |
| Dosage: | 2.5 or 5 mg/kg, dissolved in 0.5% methylcellulose |
| Administration: | Intraperitoneal injection (i.p.), once daily for 14 days |
| Result: | Reversed the cognitive impairment in the passive avoidance test at 5 mg/kg.
Partially abolished the lesion-induced increase in total eNOS protein in the prefrontal cortex.
Reversed the lesion - induced changes in both total eNOS protein and D/M ratio in the striatum.
Had no impact on the lesion - induced decrease in total nNOS protein in the hippocampus but counteracted the lesion - induced increase in total nNOS protein in the striatum.
Decreased DDAH1 expression in the hippocampus and striatum of lesioned animals and reduced RAGEs expression in the hippocampi of sham animals and in the striata of OB animals.
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