Biphasic effects of chronic nicotine treatment on hypothalamic immunoreactive beta-endorphin in the mouse.
Hypothalamic but not pituitary immunoreactive beta-endorphin (beta-E) was significantly reduced (37%) in mice 24 hr following 30 daily doses of nicotine (1200 micrograms/kg, SC). Hypothalamic beta-E returned towards normal levels within 7 days and was observed to rise 50% above normal 14 days after the cessation of nicotine treatment. None of the other neuropeptides measure, substance P, neurotensin, or [met5]-enkephalin was altered by nicotine treatment. The data suggest that the hypothalamic beta-E containing neurons were unable to adapt to nicotine's repeated effects on this system.
J A
JA
Rosecrans
J S
JS
Hendry
J S
JS
Hong
D000818:Animals; D004723:Endorphins / Q000032:analysis / Q000378:metabolism*; D004744:Enkephalin, Methionine / Q000032:analysis; D006801:Humans; D007031:Hypothalamus / Q000032:analysis*; D008297:Male; D051379:Mice; D008813:Mice, Inbred ICR; D009496:Neurotensin / Q000032:analysis; D009538:Nicotine / Q000009:adverse effects / Q000494:pharmacology*; D010902:Pituitary Gland / Q000032:analysis*; D013373:Substance P / Q000032:analysis; D013375:Substance Withdrawal Syndrome; D001615:beta-Endorphin
D004723:Endorphins; D013373:Substance P; D009496:Neurotensin; D004744:Enkephalin, Methionine; D001615:beta-Endorphin; D009538:Nicotine