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The present study used the conditioned place preference (CPP) paradigm to examine the neural mechanisms underlying morphine's rewarding effect in the rat. Of thirteen sites tested with intra-cerebral morphine injections, only the ventral tegmental area (VTA) and periaqueductal gray (PAG) produced a CPP, suggesting that morphine's rewarding effect is initiated by an action at these sites. The CPPs induced by intra-VTA and intra-PAG morphine may be produced by different mechanisms because animals conditioned with these two injections exhibited different patterns of behaviour during testing. Injections of a quaternary opioid antagonist into either the VTA or PAG blocked a CPP to systemic morphine, confirming that opiate-induced reward is mediated via opioid receptors in these sites. Lesions of the pedunculopontine tegmental nucleus (PPT$ rm sb{g}),$ ventral striatum (VS), PAG, or fornix reduced a CPP to morphine, although PAG and fornix lesioned animals displayed a CPP when tested in a drugged state. These findings suggest that PPT$ rm sb{g}$ and VS lesions reduce the rewarding effect of morphine, and that PAG and fornix lesions disrupt the ability to retrieve information about the relationship between conditioned and unconditioned stimuli.

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The role of the dorsal hippocampus, entorhinal cortex, amygdala and fimbria fornix in spatial discrimination was investigated using temporary inactivation and lesioning methods. Spatial learning was tested in a conditioned cue preference (CCP) paradigm involving three phases of behavioral testing on an 8-arm radial maze. In the first phase (pre-exposure) rats were given unreinforced pre-exposure trials in which they were free to move on two adjacent arms of the maze on three consecutive days. Rats were then alternately confined to the ends of the arms for eight days (training), one arm that contained food (Paired-arm) and one that did not (Unpaired-arm). The rats were then given a choice between the two arms with no food present. Only when given unreinforced pre-exposure trials did rats spend more time in the Paired-arm than in the Unpaired-arm, a CCP. Rats with muscimol induced inactivation of the dorsal hippocampus during unreinforced pre-exposure acquired a CCP for the Paired-arm but were impaired with hippocampal inactivation during training or testing. Inactivation of the entorhinal cortex resulted in impairment in all phases of the paradigm. Inactivation of the dorsal hippocampus in the Unpaired but not Paired-arm only resulted in impairment. The effects of dorsal hippocampus inactivation in either the Paired or Unpaired arms were reversed in rats with combined amygdala lesions\dorsal hippocampus inactivation. Rats with fimbria fornix\entorhinal cortex disconnections during pre-exposure were also impaired. These results reveal that spatial learning may rely on the interactions between the hippocampus, entorhinal cortex, amygdala, and fimbria fornix and that the dogma that the hippocampus mediates all forms of spatial learning requires revision.

Young female Sprague-Dawley rats ( 50 gm., body weight-BW) were conditioned to treadmill activity (13.4 m•min -1; 0% grade) over a 12 d. period and then randomly assigned to groups combining exercise (E) and diabetes (D) with appropriate normal-sedentary controls (Sd). The diabetic condition was induced by I.V. injection of Streptozotocin (70 mg/kg BW) in citrate buffer and was evidenced by hyperglycemia (>330 mg. glucose/dl), polyuria and polydipsia. The E program was conducted 6 d./wk. Intensity and duration were progressively increased and reached 20% grade at 26.8 m•min-1 with 45 sec. sprints at 40.2 m-min-1 at 5 min. intervals. Total daily E time reached 60 min. for 8 wks. of training at which time experimental and appropriate control animals were sacrificed. Paramenters studied included in vitro capacity of slow oxidative (SO), fast oxidative. glycolytic (FOG), and fast glycolytic (FG) tissues to oxidize (Q02) pyruvate and palmitate. A 2x2 factorial ANOVA was used to detect E/Sd (Factor A) effects, D/non-D (Factor B) effects, and interaction (AxB) effects. A Student-Newman-Keuls multiple range test was employed to determine which experimental groups differed from each other. Results indicate a complex interaction of treatment effects depending upon muscle type. For the most part, E resulted in a reduction or modification of U effects. The DE group was not significantly different from either Sd or E controls for pyruvate 002 for all 3 muscle types. However, DS was significantly depressed below DE and controls for SO and FG tissues (pyruvate Q02). For palmitate 002 DE was significantly greater than both DSd and CSd groups for FOG tissue, (3244μ a 02/hr./gm vs. 2538 and 2555μl 02/hr/gm). Also both DE and CE were greater than both Sd groups for FG tissue (1925 and 1664μl 02/hr/gm vs. 1352 and 1283μ1 02/hr/gm, respectively). There were no significant differences between groups for SO tissue (palmitate Q02).

Nitric oxide, a short-lived free radical and neurotransmitter, is responsible for decreased smooth muscle contractility in vitro. When in excess, NO can cause hypotension and is believed to mediate altered intestinal motility. Not enough evidence is available for morphological changes in gastrointestinal smooth muscle and its correlation with motility disorders caused by Escherichia coli-induced NO production. Male Lewis rats were treated with injections of 10 mg/kg LPS from E. coli with or without 12.5 mg/kg of NOS inhibitor, LNMMA. Eighteen to 24 hours following injection, duodenum, ileum, colon, liver, and spleen were harvested for histological analysis. Urine and fecal analysis assessed functional aspects in control and treatment groups. Muscularis externa measurements revealed significant increase in muscle thickness of LPS + LNMMA injected group compared to control and LPS group. However, the average values in control and LPS group were not significantly different. Fecal consistency was significant in all 3 groups. Mean urinary nitrite in the LPS group was 44 times higher than control and 52 times higher than the inhibitor-treated group. / Department of Physiology and Health Science