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G Dines

Publications and source records attributed to G Dines.

3 recordsLinked to original sources
PubMed1990

16,16-Dimethyl prostaglandin E2 induces villus contraction in rats without affecting intestinal restitution.

In a previous study we found that 16,16-dimethyl prostaglandin E2 protects the small intestine against chenodeoxycholic acid injury in the rat. One possible explanation for prostaglandin's protective action may be that prostaglandin-induced villus contraction accelerates mucosal restitution. This hypothesis was tested in rats by perfusing intestinal segments in vivo in a single-pass fashion with 0.125-0.5 micrograms/L of 16,16-dimethyl prostaglandin E2. These studies showed a dose-dependent, reversible contraction of intestinal villi and crypts. To test the effect of this contraction on mucosal restitution, standardized intestinal injury was produced in indomethacin-pretreated rats perfused in vivo with 5 mmol/L chenodeoxycholic acid. The rats were then perfused with bile acid-free buffer containing either 0.5 microgram/mL of 16,16-dimethyl prostaglandin E2 or vehicle. This study showed that despite decreasing villus height after bile acid injury, 16,16-dimethyl prostaglandin E2 did not significantly affect the rate of morphologic (assessed by villus denudation) or functional (assessed by mannitol and water absorption) restitution of the injured intestinal mucosa. Thus, although 16,16-dimethyl prostaglandin E2 causes villus contraction, this effect does not result in more rapid restitution of the injured intestinal mucosa and is not a likely mechanism for prostaglandin-mediated protection of the intestinal mucosa.

16,16-Dimethylprostaglandin E2↗
PubMed1985

Slow and multiple unit potentials in trace and temporal conditioning controlled by electrical reward in the rat.

Rats trained to expect medial forebrain bundle electrical reward every 17 sec acquire, in their visual cortex, a linear gradient of increasing negative potential over the prereinforcement half of the interval. The postreinforcement half of the interval is occupied by a less linear reversal of the negative shift. Integrated multiple unit activity from the same electrodes shows for the same half intervals, respectively, acquisition of progressive increase and sudden decrease. Behaviorally, naive subjects are most active following the reinforcement, becoming progressively less active in the second half of the interreinforcement interval. After training, the above pattern is reversed with sudden cessation of activity following reinforcement and progressive increase beginning about 5 sec later and continuing to the time of reinforcement. Slopes for the negative anticipatory potential gradient (APG) ranged from 8 to 28 microV/sec in different subjects on the 17 sec interreinforcement interval. Doubling the interval halved the slope, the maximum prereinforcement negative voltage remaining constant. The phenomenon thus appears as a relative or pacing dynamic rather than as an absolute or fixed microvolts/second function. Making the interreinforcement interval variable caused loss of both the anticipatory gradient and the integrated multiple unit increment. Trace conditioning with variable intertrial interval restored an anticipatory gradient and multiple unit increment. The specific dissociation of unit firing activity during the APG previously reported in the quietly expectant cat is not seen in this study owing to the excited expectancy in the rat anticipating MFB reward. Although the longer periods of negative potential gradient and unit action potential activity appear associated rather than dissociated, transient dissociations in patterns were observed during shorter duration shifts in the slow potential. Resolution of these variations must await more definitive study of unit activity and sustained potential genesis.

Action Potentials↗