Nicotine alters catecholamines and electrocortical activity in perfused mouse brain.
Nicotine differentially altered electrocortical (ECoG) activity and brain catecholamine metabolism in mice (C3H and C57BL) known to differ in behavioral response to nicotine. Nicotine appeared to produce a concentration dependent desynchronization to ECoG activity in isolated perfused mouse brain (IPMB) from C3H mice. Homovanillic acid (HVA) production was unchanged in C3H perfused brains while an apparent reduction in 3-methoxy-4-hydroxyphenethyleneglycol (MPHG) was observed. Brain content of norepinephrine and dopamine remained relatively constant in the various regions tested. In IPMB from C57BL mice, nicotine elicited an enhancement of ECoG amplitude which was accompanied by decreased HVA production rates. A downward trend in MHPG production was also observed. These effects were associated with increased levels of norepinephrine and dopamine in various brain regions.
D000818:Animals; D002395:Catecholamines / Q000378:metabolism*; D002540:Cerebral Cortex / Q000378:metabolism / Q000502:physiology*; D002851:Chromatography, High Pressure Liquid; D004569:Electroencephalography; D006719:Homovanillic Acid / Q000378:metabolism; D008297:Male; D008734:Methoxyhydroxyphenylglycol / Q000096:biosynthesis; D051379:Mice; D008809:Mice, Inbred C3H; D008810:Mice, Inbred C57BL; D009538:Nicotine / Q000494:pharmacology*; D010477:Perfusion
D002395:Catecholamines; D008734:Methoxyhydroxyphenylglycol; D009538:Nicotine; D006719:Homovanillic Acid