Drugs online research references
Pancreas. 1999 Apr;18(3):300-7.
Modulation of external pancreatic secretion by endogenous norepinephrine: study with a norepinephrine uptake blocker in the rat.
Nagain-Domaine C, Presset O, Chariot J, Roze C.
INSERM U410, Faculte de Medecine Xavier Bichat, Paris, France.
The effect of endogenous catecholamines on pancreatic secretion was analyzed with nisoxetine, a specific norepinephrine uptake blocker, and specific adrenoceptor antagonists in anesthetized acute fistula rats. Nisoxetine was administered alone or with alpha-1 (prazosin), alpha-2 (idazoxan or yohimbine), or beta (propranolol) adrenoceptor antagonists. Pancreatic secretion was measured in basal conditions or after stimulation by 2-deoxy-D-glucose (2DG), electrical vagal stimulation, or acetylcholine. (a) Basal. Nisoxetine alone had no effect. Associated with idazoxan or yohimbine, nisoxetine produced a dose-related stimulation (p < 0.01) of water and electrolyte without changing protein output. Addition of propranolol abolished this stimulation. (b) 2DG. Nisoxetine inhibited 2DG-induced secretion (p < 0.01). Idazoxan or yohimbine suppressed the nisoxetine inhibition of water and electrolyte output (p < 0.01) but had no effect on protein output, which was restored only by adding a mixture of idazoxan, prazosin, and propranolol. (c) Electrical stimulation. Nisoxetine did not modify water and electrolyte but inhibited protein response by 75%. Adding idazoxan to nisoxetine significantly increased (p < 0.01) water and bicarbonate response and partly restored protein response. Water and bicarbonate response was restored by propranolol, whereas protein response was only restored by adding a mixture of idazoxan, prazosin, and propranolol. (d) Nisoxetine did not modify pancreatic response to acetylcholine. In conclusion, endogenous norepinephrine affects the response to vagally mediated effects through several subtypes of adrenoceptors, without changing basal or acetylcholine stimulated secretion.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10206489&dopt=Abstract
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J Neurosci. 1998 Jul 1;18(13):4854-60.
Quantitative evaluation of 5-hydroxytryptamine (serotonin) neuronal release and uptake: an investigation of extrasynaptic transmission.
Bunin MA, Wightman RM.
Curriculum in Neurobiology and Department of Chemistry, University of North Carolina at Chapel Hill, Chapel Hill, North Carolina 27599-3290, USA.
Whether neurotransmitters are restricted to the synaptic cleft (participating only in hard-wired neurotransmission) or diffuse to remote receptor sites (participating in what has been termed volume or paracrine transmission) depends on a number of factors. These include (1) the location of release sites with respect to the receptors, (2) the number of molecules released, (3) the diffusional rate away from the release site, determined by both the geometry near the release site as well as binding interactions, and (4) the removal of transmitter by the relevant transporter. Fast-scan cyclic voltammetry allows for the detection of extrasynaptic concentrations of many biogenic amines, permitting direct access to many of these parameters. In this study the hypothesis that 5-hydroxytryptamine (5-HT) transmission is primarily extrasynaptic in the substantia nigra reticulata, a terminal region with identified synaptic contacts, and the dorsal raphe nucleus, a somatodendritic region with rare synaptic incidence, was tested in brain slices prepared from the rat. Using carbon fiber microelectrodes, we found the concentration of 5-HT released per stimulus pulse in both regions to be identical when elicited by single pulse stimulations or trains at high frequency. 5-HT efflux elicited by a single stimulus pulse was unaffected by uptake inhibition or receptor antagonism. Thus, synaptic efflux is not restricted by binding to intrasynaptic receptors or transporters. The number of 5-HT molecules released per terminal was estimated in the substantia nigra reticulata and was considerably less than the number of 5-HT transporter and receptor sites, reinforcing the hypothesis that these sites are extrasynaptic. Furthermore, the detected extrasynaptic concentrations closely match the affinity for the predominant 5-HT receptor in each region. Although they do not disprove the existence of classical synaptic transmission, our results support the existence of paracrine neurotransmission in both serotonergic regions.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9634551&dopt=Abstract
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Int J Neurosci. 1998 Apr;93(3-4):163-79.
Behavioral tolerance to and withdrawal from multiple fluoxetine administration.
Bjork JM, Gaytan O, Patt N, Swann AC, Dafny N.
Department of Neurobiology and Anatomy, University of Texas-Houston, Medical School of Houston, 77025, USA.
The objective of this study was to characterize the lasting effects of fluoxetine on the locomotor behavior of rats using a computerized activity-monitoring system. Challenge dosages (8, 16, and 24 mg/kg i.p.) of fluoxetine 2 h into the dark phase resulted in dose-dependent suppression of locomotor activity for 4 h following injection. Escalating (10-30 mg/kg i.p.) semidaily fluoxetine administration for the next five days resulted in decreasing locomotor activity during the multiple-administration period relative to saline control. Circadian activity patterns at the conclusion of the regimen were unchanged in shape, but featured uniform decreases in locomotor activity at every hour which were more significant during the phase. Upon discontinuation, fluoxetine-treated rats showed a significant increase in activity during the first 4 h following the first "missed" dose which was not seen in subsequent washout. Ninety-six h after the final maintenance dose, the initial three dosages were readministered, and the locomotor activity suppression in response to the rechallenge dose of fluoxetine was significantly lessened compared to initial challenge. These findings suggest that tolerance and withdrawal were obtained.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9639233&dopt=Abstract
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