Drugs online research references
Pharmacol Biochem Behav. 1995 Feb;50(2):253-8.
Dorsomedial hypothalamic GABA regulates anxiety in the social interaction test.
Shekhar A, Katner JS.
Department of Psychiatry, Indiana University School of Medicine, Indianapolis 46202, USA.
Blockade of GABAA function in the region of the dorsomedial hypothalamus (DMH) of rats is known to elicit a constellation of physiologic responses including increases in heart rate (HR), mean arterial blood pressure (BP), respiratory rate, and plasma catecholamine levels, as well as behavioral responses such as increases in locomotor activity and anxiogenic-like effects as measured in a conflict test and the elevated plus-maze test. The aim of the present study was to test the effects of microinjecting GABAA antagonists bicuculline methiodide (BMI) and picrotoxin, as well as the GABAA agonist muscimol, into the DMH of rats placed in the social interaction (SI) test. Muscimol decreased HR and BP but increased SI, whereas the GABA antagonists increased HR and BP but decreased SI time. Blocking the HR changes elicited by GABAergic drugs injected into the DMH with systemic injections of atenolol and atropine methylbromide did not block their effects on SI.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7740065&dopt=Abstract
Neuropsychopharmacology. 1996 Mar;14(3):195-204.
beta-adrenergic antagonism alters the behavioral and neurochemical responses to cocaine.
Harris GC, Hedaya MA, Pan WJ, Kalivas P.
Alcohol and Drug Abuse Program, Washington State University, Pullman, WA 99164-6520, USA.
The effects of the beta-adrenergic antagonist propranolol on the locomotor stimulating, neurochemical, and reinforcing effects of cocaine were examined in rats. In Experiment 1, propranolol (1, 3 and 10 mg/kg, IP) produced a dose-dependent increase in the motor stimulant effects of cocaine without affecting basal motor activity. Atenolol, a peripherally restricted beta 1 antagonist, and (+) propranolol, the inactive isomer of propranolol, did not alter cocaine-induced locomotion. In Experiment 2, propranolol was shown to augment significantly the increase in extracellular dopamine content in the nucleus accumbens that accompanies a cocaine challenge. Experiment 3 demonstrated that propranolol produced a dose-dependent decrease in cocaine self-administration. Atenolol (10 mg/kg, IP) reduced cocaine self-administration but to a much lesser extent than propranolol. Experiment 4 demonstrated that coadministration of propranolol and cocaine did not alter the levels of cocaine in the brain and plasma achieved by cocaine administration alone. These data suggest that the blockade of beta-adrenergic receptors potentiates cocaine-induced elevation of dopamine transmission in the nucleus accumbens, which is associated with an increase in cocaine-induced motor activity and a decrease in cocaine self-administration.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8866703&dopt=Abstract
Proc Natl Acad Sci U S A. 1988 Feb;85(4):1292-6.
Norepinephrine inhibits gamma-interferon-induced major histocompatibility class II (Ia) antigen expression on cultured astrocytes via beta-2-adrenergic signal transduction mechanisms.
Frohman EM, Vayuvegula B, Gupta S, van den Noort S.
Department of Neurology, University of California, Irvine 92717.
The astrocyte is now recognized as a facultative immunocompetent antigen-presenting cell that can initiate intracerebral immune responses. However, despite the presence of activated T lymphocytes and their associated lymphokines within the central nervous system, there is a paucity in the expression of the major histocompatibility (MHC) antigens on normal neural tissue. These membrane-localized glycoproteins are required for the process of antigen presentation and, therefore, for the initiation of immune responses. To date, little is understood regarding the nature of inhibitory mechanisms that might be responsible for maintaining the brain as an immunoprivileged site. In this study we found that norepinephrine, a major brain transmitter, significantly inhibited gamma interferon-induced MHC class II antigen expression on astrocytes derived from neonatal Lewis rats. We show that this inhibition can be attenuated by the addition of a beta-adrenergic antagonist, propranolol, but not by the addition of a beta 1-selective antagonist, atenolol, or by an alpha-adrenergic antagonist, phentolamine. Furthermore, it was found that a similar inhibition could be achieved by the addition of either dibutyryl-cAMP or dipyridimole, a phosphodiesterase inhibitor. Therefore, it seems that norepinephrine-mediated inhibition of MHC class II antigen expression on astrocytes works through beta 2-adrenergic signal transduction pathways. Taken together, these in vitro results suggest that the brain contains inhibitory factors that may play a pivotal role in the regulation of intracerebral immune responses by modulating the expression of MHC antigens on astrocytes.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2829222&dopt=Abstract
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