Shock stress protects mice against amphetamine-induced dopaminergic toxicity.
The effect of tail shock (ten, 2.0 mA/0.15 s shocks) on amphetamine-induced dopaminergic toxicity in adult, male BALB/c mice was assessed. Fifteen minutes following a single shock session, mice received amphetamine (50-mg/kg) or saline as follows: Shock/Saline; NoShock/Saline; Shock/Amphetamine; No Shock/Amphetamine. Amphetamine caused a 60% dopamine depletion in the No Shock/Amphetamine group. Tail shock provided neuroprotection against amphetamine-induced dopamine depletion, an effect likely related to the stress response.
Carlson
Kirsten M
KM
Department of Psychology, Busch Campus, Rutgers University, New Brunswick, NJ 08854, USA.
Wagner
George C
GC
D000661:Amphetamine / Q000633:toxicity*; D000818:Animals; D015306:Biogenic Monoamines / Q000378:metabolism; D001921:Brain / Q000187:drug effects*; D000697:Central Nervous System Stimulants / Q000633:toxicity*; D004298:Dopamine / Q000378:metabolism*; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D009474:Neurons / Q000187:drug effects; D013312:Stress, Physiological / Q000209:etiology / Q000378:metabolism*
D015306:Biogenic Monoamines; D000697:Central Nervous System Stimulants; D000661:Amphetamine; D004298:Dopamine