Periadolescent nicotine exposure produces sensitization to reinforcement by diazepam in the rat.

Epidemiologic studies establish a relationship between nicotine use by adolescents and a subsequent involvement with drugs of abuse in adulthood. Recent research implicates the periadolescent period as a crucial time in development, during which nicotine use produces persistent adaptations that serve to predispose an individual to substance use. The present investigation evaluated the effects of periadolescent nicotine priming on young adult sensitization to reinforcement by a drug of abuse. Nicotine (0.4 mg/kg, intraperitoneal), mecamylamine (2 mg/kg, subcutaneous), mecamylamine and nicotine, or saline was administered as a once-daily injection to periadolescent (postnatal days 35-44) Sprague-Dawley male rats. The effects of periadolescent nicotine priming on reinforcement parameters in the young adult animal (postnatal day 80) were measured by conditioning a place preference with diazepam (1 mg/kg, subcutaneous). Rats were tested for place conditioning in a drug-free state. In contrast to other periadolescent treatment groups, rats treated with only nicotine during periadolescence showed a heterologous sensitization to the subthreshold dose of diazepam utilized during conditioning. Pretreatment with mecamylamine before periadolescent nicotine priming prevented the enhanced response to diazepam observed in the young adult animal. Priming with nicotine during late adolescence (postnatal days 60-69) failed to sensitize the adult rats to diazepam. This study supports a relationship between periadolescent nicotine priming and the production of persistent, behavioral adaptations in the young adult animal.

The effect of oral consumption of perchlorate, alone and in combination with ethanol, on plasma thyroid hormone and brain catecholamine concentrations in the rat.

Literature has reported a controversy concerning the effects of the environmental pollutant perchlorate on pertinent physiological systems. However, no research to date has evaluated the effect of concomitant consumption of perchlorate and an additional environmental contaminant on physiological systems. The present preliminary investigation served to assess the effects of oral consumption of perchlorate, alone and in combination with ethanol, on thyroid hormone and brain catecholamine concentrations in female rats of gestational age. Forty, female Myers' high ethanol-preferring rats were randomly assigned to 1 of 7 groups that received: (1) deionized water, both bottles (2) deionized water and 10% ethanol (v/v), two separate bottles (3) 300 microg/l perchlorate solution in deionized water, both bottles (4) 300 microg/l perchlorate in deionized water and in 10% ethanol (v/v), two separate bottles (5) 3000 microg/l perchlorate solution in deionized water, both bottles (6) 3000 microg/l perchlorate in deionized water and in 10% ethanol (v/v), two separate bottles (7) 0.01% propylthiouracil solution in deionized water, both bottles. At cessation of the treatment period, plasma triiodothyronine (T3) and thyroxine (T4) levels were measured by radioimmunoassay and brain area concentrations of dopamine, 3,4-dihydroxyphenylacetic acid (DOPAC), and norepinephrine were measured by high performance liquid chromatography. Perchlorate consumption, alone and/or in combination with ethanol consumption, failed to produce significant alterations from control values for triiodothyronine, thyroxine, dopamine, DOPAC, or norepinephrine. The data suggest that the no-observed effect level of perchlorate consumption on thyroid hormone and brain catecholamine concentrations is above the 3000 microg/l concentration in the adult female rat.