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R B Kaplan

Publications and source records attributed to R B Kaplan.

7 recordsLinked to original sources
PubMed1985

Central action of gamma-aminobutyric acid ligands to alter basal water and electrolyte absorption in the rat ileum.

The gamma-aminobutyric acid agonist muscimol and the gamma-aminobutyric acid antagonist bicuculline were studied to determine their effects on basal net water and electrolyte transport in the rat ileum. Whereas the intraperitoneal injection of muscimol caused a reversible, dose-dependent decrease in net water absorption, bicuculline produced a reversible, dose-dependent increase in net water and ion absorption. The threshold doses of muscimol and bicuculline were greater than 2.1 and 2.2 micrograms/kg, respectively. Lower doses of muscimol (0.1 microgram) or bicuculline (0.3 microgram) administered into the cerebrospinal fluid had the same effect as higher doses given systemically. Vagotomy prevented the effect of intracerebroventricular muscimol. Atropine (6 micrograms intracerebroventricularly) alone did not alter basal water absorption but abolished the muscimol effect, suggesting that muscimol promoted the release of acetylcholine from central cholinergic neurons. Atropine did not prevent the bicuculline effect. We conclude that (a) muscimol decreases ileal water absorption and bicuculline enhances ileal water absorption by an action at a gamma-aminobutyric acid receptor in the central nervous system, (b) the muscimol effect is due to an alteration in parasympathetic vagal outflow to the intestine, (c) the muscimol effect is mediated by a central cholinergic interneuron, and (d) the bicuculline effect is not mediated by the release of acetylcholine from central cholinergic neurons.

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PubMed1984

Role of enkephalins in regulation of basal intestinal water and ion absorption in the rat.

Intraluminal administration of naloxone (10(-4) M), a mu-opiate receptor antagonist, or diprenorphine (10(-6) M), an opiate receptor antagonist with high affinity for both delta- and mu-receptors, decreased basal in vivo water and electrolyte absorption in the jejunum and ileum but not the colon of the rat. Diprenorphine (10(-5) M) decreased basal colonic water transport. These changes were not due to a reduction in mucosal Na-K-ATPase activity. Intravenous atropine prevented as well as abolished the changes in water transport due to naloxone. The diprenorphine-induced changes were not altered by atropine. Naloxone and diprenorphine acted by different receptors. Pretreatment with naloxone (10(-4) M) prevented the increase in water transport due to morphine, a mu-agonist, whereas a higher concentration of naloxone (10(-3) M) was required to inhibit the increase due to D-Ala-methionine-enkephalinamide, a delta-receptor agonist. In contrast, diprenorphine (10(-6) M) abolished the absorption caused by morphine and D-Ala-methionine-enkephalinamide. Diprenorphine (3 X 10(-7) M) partially prevented the morphine-induced increase in water absorption.(ABSTRACT TRUNCATED AT 250 WORDS)

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PubMed1979

Phosphorylcholine-specific helper T cells in mice with an X-linked defect of antibody production to the same hapten.

F1 male mice with the CBA/N X-linked defect that are unable to produce plaque-forming cell responses to phosphorylcholine (PC) provide normal PC-specific helper T-cell activity when compared to F1 female littermates. Inhibition of helper activity with anti-idiotypic antiserum indicates that PC-specific T cells from both NBF1 female and male mice possess predominantly BALB/c myeloma protein HOPC-8 idiotypic determinants. Therefore, the CBA/N defect cannot be explained as a deletion of genes coding for V-region anti-PC specificities. The demonstration of helper activity in NBF1 male mice, which occurs in the absence of anti-PC antibody synthesis, also demonstrates the endogenous origin of the T-cell receptor.

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