Objective:To investigate the effects of ethanol exposure in adolescent rats during adulthood by assesssing aggression and anxiety-like behaviors and measuring the levels of inflammatory markers.Methods:Groups of male Wistar rats (mean weight 81.4 g, n = 36) were housed in groups of four until postnatal day (PND) 60. From PNDs 30 to 46, rats received one of three treatments: 3 g/kg of ethanol (15% w/v, orally, n = 16), 1.5 g/kg of ethanol (12.5% w/v, PO, n = 12), or water (n = 12) every 48 hours. Animals were assessed for aggressive behavior (resident x intruder test) and anxiety-like behaviors (elevated plus maze) during adulthood.Results:Animals that received low doses of alcohol showed reduced levels of brain-derived neurotrophic factor (BDNF) in the hippocampus as compared to the control group. No significant difference was found in prefrontal cortex.Conclusions:Intermittent exposure to alcohol during adolescence is associated with lower levels of BDNF in the hippocampus, probably due the episodic administration of alcohol, but alcohol use did not alter the level agression toward a male intruder or anxiety-like behaviors during the adult phase.

Adolescence is an important neurodevelopmental stage for brain sites that are related to the impulse control and reward systems. Alcohol abuse during this period may cause irreversible modifications of neural circuits that are linked to impulsivity. The present study evaluated the effects of alcohol ingestion during adolescence in Wistar rats on anxiety, risk-taking, and impulsive behavior parameters during adulthood. Male Wistar rats (n ϭ 40) were randomly assigned to 1 of 3 treatments: 0, 1, and 3 g/kg alcohol administered orally over 9 sessions, from postnatal Day 31 to 50. Anxiety and risk-taking behaviors were assessed in the elevated plus maze soon after adolescence and during adulthood, and impulsivity was assessed in the operant delay-discounting task in adulthood. None of the alcohol treatments altered risk-taking or impulsive behavior compared with the control group. The group that received 3 g/kg alcohol exhibited less anxiety-like behavior in the first exposure to the elevated plus maze compared with the control group. The results are discussed with regard to the doseresponse, frequency, duration, and age of exposure and route of administration.

The therapeutic effects of a number of antineoplastic agents administered subcutaneously to L1210 leukemic mice in silicone polymer (Silastic®, Dow Corning Medical Grade) implants is reported. 1-β-d-arabinofuranosylcytosine (ara-C, cytarabine), two 5′-acylates of ara-C (the 1-adamantanecarboxylate [AdO-ara-C] and acetate [AcO-ara-C]) and two nitrosoureas [l-(2-chloroethyl)-3-cyclohexyl-1-nitrosourea {CCNU} and 1-(2-chloroethyl)-3-trans-4-methylcyclohexyl)-1-nitrosourea {MeCCNU}], when administered in this manner, significantly increased survival time and, in the case of ara-C, CCNU, and MeCCNU, resulted in a considerable number of cures. Silastic cylinders containing ara-C (625 mg ara-C/kg) implanted up to 3 days prior to tumor inoculation yielded significant therapeutic effects, suggesting that ara-C was being released at a slow rate such that cytotoxic levels of ara-C persisted in the mice for several days. This ‘depot’ effect was confirmed by studies of ara-C plasma levels and excretion after administration of ¹⁴C-ara-C in this manner. Silastic cylinders containing CCNU (25 mg CCNU/kg), when implanted 4 h prior to tumor inoculation showed activity, but no therapeutic effect was observed when administration was 24 h prior to inoculation. Studies in which drug implants were removed at various times after implantation indicated that the necessary exposure time (for optimum therapeutic effect) is considerably longer for an S-phase (DNA synthetic) specific agent such as ara-C than for nonphase-specific agents such as CCNU.

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