ABSTRACT
Approximately 53,000 serologic tests and viral isolation studies were performed on 1,700 nonhuman primate specimens for evidence of past and/or current viral infection. Information, other than the requested test, generally was not provided with the specimen. This lack of information does not permit any attempt at interpretation of results. Requested testing included a large number of diverse viral agents in approximately 40 primate species. The resulting data are in keeping with those of previous studies and offer an insight into the needs of colony management, as well as some general information on the overall frequency of infection with the indicated viruses. Inasmuch as the results represent testing of single specimens, they are not to be construed as "diagnostic," and simply indicate past infection as represented by the presence of antibody in the test animal. Viral isolation results are listed, and the number of positive results versus the number of animals tested emphasizes the limitations of the procedure. Investigations such as these continue to assist in the maintenance of healthy nonhuman primate colonies. This information also supports continued use of nonhuman primates for research in human viral infections and may be helpful in terms of animal selection for use in xenotransplants.
Subject(s)
Ape Diseases/virology , Haplorhini/virology , Monkey Diseases/virology , Virus Diseases/veterinary , Animals , Antibodies, Viral/analysis , Ape Diseases/diagnosis , Fluorescent Antibody Technique, Indirect/veterinary , Humans , Immunoblotting/veterinary , Immunoenzyme Techniques/veterinary , Monkey Diseases/diagnosis , Serologic Tests/veterinary , Virus Diseases/diagnosis , Virus Diseases/virology , Viruses/immunology , Viruses/isolation & purificationABSTRACT
The adrenergic agonist norepinephrine can exert its influence on cell function by activating both alpha- and beta-adrenergic receptors. In astrocytes, the alpha-adrenergic receptor activity of norepinephrine is known to inhibit the cyclic AMP response elicited by its action at beta-adrenergic receptors. Pharmacological studies were conducted to identify the subtype of alpha-adrenergic receptor which mediates this inhibitory action. The alpha 2-adrenergic antagonist yohimbine potentiated the cyclic AMP response elicited by norepinephrine, whereas the alpha 1-adrenergic antagonist prazosin did not affect the response. The alpha 2-adrenergic agonist clonidine inhibited the cyclic AMP response elicited by the beta-adrenergic agonist isoproterenol and this inhibition could be blocked by yohimbine but not by prazosin. In contrast, the alpha 1-adrenergic agonist phenylephrine did not inhibit the cyclic AMP response to isoproterenol. These studies indicate that the inhibitory action of norepinephrine is mediated by its action at alpha 2-adrenergic receptors.
Subject(s)
Adenylyl Cyclases/metabolism , Astrocytes/physiology , Prazosin/pharmacology , Receptors, Adrenergic, alpha/physiology , Receptors, Adrenergic, beta/physiology , Yohimbine/pharmacology , Animals , Animals, Newborn , Astrocytes/drug effects , Astrocytes/enzymology , Cells, Cultured , Cerebral Cortex/physiology , Enzyme Activation , Isoproterenol/pharmacology , Rats , Rats, Inbred StrainsABSTRACT
Studies were conducted to determine if alpha agonists could influence the desensitization of the beta-noradrenergic receptor activated adenylate cyclase system. Pretreatment of astrocyte cultures with isoproterenol results in a rapid decrease in the cyclic AMP response to subsequent re-exposure to this agonist. The cyclic AMP response to isoproterenol in astrocytes pre-exposed for 2 h to isoproterenol plus clonidine was 2-3 times higher than in cells pre-exposed to isoproterenol alone. The response in astrocytes pretreated with phenylephrine plus isoproterenol was not different from that in cells pretreated with isoproterenol alone. Cyclic AMP may be involved in the effects elicited by clonidine, since this agonist can inhibit the accumulation of cyclic AMP in these cells. Also pretreatment with isobutylmethylxanthine decreases the cyclic AMP response to isoproterenol. The results suggest that clonidine can effect the desensitization of the noradrenergic receptor coupled adenylate cyclase system independent of effects on neurotransmitter release.
Subject(s)
Adenylyl Cyclases/metabolism , Astrocytes/enzymology , Clonidine/pharmacology , Isoproterenol/pharmacology , Receptors, Adrenergic, beta/drug effects , 1-Methyl-3-isobutylxanthine/pharmacology , Animals , Astrocytes/drug effects , Colforsin/pharmacology , Cyclic AMP/metabolism , Enzyme Activation/drug effects , Rats , Rats, Inbred Strains , Receptors, Adrenergic, beta/metabolismABSTRACT
Capsaicin (CAP) caused a time, concentration and Ca++ dependent increase in cyclic AMP accumulation in tissue slices from rat and guinea pig spinal cord. The CAP-induced increase occurred uniquely in slices from dorsal cord of both rat and guinea pig and the increase was significantly greater in dorsal cord slices from guinea pig vs rat spinal cord. CAP mediated release of substance P does not appear to mediate the CAP-induced increase in cyclic AMP accumulation since the increase in cyclic AMP is significantly less with substance P and the substance P antagonist [D-Pro2, D-Trp7,9]-substance P does not antagonize the CAP-induced increase. The CAP-induced increase in cyclic AMP accumulation appears to be a direct effect. Structural requirements for this effect are both the substituted aromatic and alkyl side chain portion of the CAP molecule. The present results suggest that CAP has the ability to interact with sites in dorsal spinal cord which are linked to the synthesis of cyclic AMP, which could modulate spinal processing of nociceptive information.
