The Experts below are selected from a list of 1086 Experts worldwide ranked by ideXlab platform
Roger L. Albin - One of the best experts on this subject based on the ideXlab platform.
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A novel device for chronic Intracranial Drug delivery via microdialysis.
Journal of neuroscience methods, 1991Co-Authors: Terence J. Bazzett, Jill B. Becker, Roger L. AlbinAbstract:A system is described for chronic Intracranial Drug Administration in the rat using a modified in vivo microdialysis probe coupled to an Alzet model 2002 osmotic minipump. The results presented demonstrate that this system can be used for the chronic Administration of quinolinic acid with minimal non-specific damage. Each pump delivered approximately 225 ~1 of solution over a period of 19-20 days when tested in vitro. The dialysis units were uniform in function, delivering > 93% of the [3H]quinolinic acid initially loaded into the minipump. For in vivo analysis of this apparatus the dose of quinolinic acid tested produced extensive destruction of the striatum. The present system allows reliable Drug diffusion over a relatively large area without pressure injection variability. In conclusion, we have developed a simple and inexpensive technique for Administration of Drugs into brain parenchyma with substantial advantages over previously used techniques.
Terence J. Bazzett - One of the best experts on this subject based on the ideXlab platform.
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A novel device for chronic Intracranial Drug delivery via microdialysis.
Journal of neuroscience methods, 1991Co-Authors: Terence J. Bazzett, Jill B. Becker, Roger L. AlbinAbstract:A system is described for chronic Intracranial Drug Administration in the rat using a modified in vivo microdialysis probe coupled to an Alzet model 2002 osmotic minipump. The results presented demonstrate that this system can be used for the chronic Administration of quinolinic acid with minimal non-specific damage. Each pump delivered approximately 225 ~1 of solution over a period of 19-20 days when tested in vitro. The dialysis units were uniform in function, delivering > 93% of the [3H]quinolinic acid initially loaded into the minipump. For in vivo analysis of this apparatus the dose of quinolinic acid tested produced extensive destruction of the striatum. The present system allows reliable Drug diffusion over a relatively large area without pressure injection variability. In conclusion, we have developed a simple and inexpensive technique for Administration of Drugs into brain parenchyma with substantial advantages over previously used techniques.
Jill B. Becker - One of the best experts on this subject based on the ideXlab platform.
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A novel device for chronic Intracranial Drug delivery via microdialysis.
Journal of neuroscience methods, 1991Co-Authors: Terence J. Bazzett, Jill B. Becker, Roger L. AlbinAbstract:A system is described for chronic Intracranial Drug Administration in the rat using a modified in vivo microdialysis probe coupled to an Alzet model 2002 osmotic minipump. The results presented demonstrate that this system can be used for the chronic Administration of quinolinic acid with minimal non-specific damage. Each pump delivered approximately 225 ~1 of solution over a period of 19-20 days when tested in vitro. The dialysis units were uniform in function, delivering > 93% of the [3H]quinolinic acid initially loaded into the minipump. For in vivo analysis of this apparatus the dose of quinolinic acid tested produced extensive destruction of the striatum. The present system allows reliable Drug diffusion over a relatively large area without pressure injection variability. In conclusion, we have developed a simple and inexpensive technique for Administration of Drugs into brain parenchyma with substantial advantages over previously used techniques.
Thomas M. Tzschentke - One of the best experts on this subject based on the ideXlab platform.
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Measuring reward with the conditioned place preference paradigm: a comprehensive review of Drug effects, recent progress and new issues.
Progress in neurobiology, 1998Co-Authors: Thomas M. TzschentkeAbstract:This review gives an overview of recent findings and developments in research on brain mechanisms of reward and reinforcement from studies using the place preference conditioning paradigm, with emphasis on those studies that have been published within the last decade. Methodological issues of the paradigm (such as design of the conditioning apparatus, biased vs unbiased conditioning, state dependency effects) are discussed. Results from studies using systemic and local (Intracranial) Drug Administration, natural reinforcers, and non-Drug treatments and from studies examining the effects of lesions are presented. Papers reporting on conditioned place aversion (CPA) experiments are also included. A special emphasis is put on the issue of tolerance and sensitization to the rewarding properties of Drugs. Transmitter systems that have been investigated with respect to their involvement in brain reward mechanisms include dopamine, opioids, acetylcholine, GABA, serotonin, glutamate, substance P, and cholecystokinin, the motivational significance of which has been examined either directly, by using respective agonist or antagonist Drugs, or indirectly, by studying the effects of these Drugs on the reward induced by other Drugs. For a number of these transmitters, detailed studies have been conducted to delineate the receptor subtype(s) responsible for the mediation of the observed Drug effects, particularly in the case of dopamine, the opioids, serotonin and glutamate. Brain sites that have been implicated in the mediation of Drug-induced place conditioning include the 'traditional' brain reward sites, ventral tegmental area and nucleus accumbens, but the medial prefrontal cortex, ventral pallidum, amygdala and the pedunculopontine tegmental nucleus have also been shown to play important roles in the mediation of place conditioning induced by Drugs or natural reinforcers. Thus, although the paradigm has also been criticized because of some inherent methodological problems, it is clear that during the past decade place preference conditioning has become a valuable and firmly established and very widely used tool in behavioural pharmacology and addiction research.
Klockars, Oscar Andreas - One of the best experts on this subject based on the ideXlab platform.
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Identification of central circuitry components mediating anorexigenic properties of oxytocin
The University of Waikato, 2019Co-Authors: Klockars, Oscar AndreasAbstract:Recent years have brought exciting discoveries showing that a neurohormone, oxytocin (OT), acts as an appetite suppressant. Importantly, OT decreases energy needs-driven consumption of high-calorie foods by promoting early satiation, and it terminates intake motivated by palatability related to sweet taste. OT’s anorexigenic effects on both aspects of ingestive behavior are mediated by the OT receptor (OTr) expressed broadly in the brain, however, our understanding of which specific sites relay anorexigenic actions of OT is limited. Thus far, only the nucleus accumbens and ventral tegmental area of the mesolimbic system, and the brainstem’s dorsal vagal complex, have been directly implicated in relaying OT-induced hypophagia. Thus, the overarching goal of this thesis was to examine which discrete components of circuitry expressing the OTr mediate OT’s anorexigenic effects on energy- versus reward-driven feeding. The research approaches included Intracranial Drug Administration, analyses of region-specific expression of genes, neuronal activation mapping, and feeding behavior testing in rats. The first set of studies explored whether extreme overeating induced by a powerful orexigen, butorphanol tartrate (BT), can be alleviated by pharmacologically stimulating the OT receptor in the forebrain versus the hindbrain (via lateral (LV) and fourth ventricular (4V) OT injections, respectively). I established effective doses of BT and LV / 4V OT. Then, I determined doses of LV and 4V OT that reduce hyperphagia produced by BT in sated and deprived rats. Finally, I assessed whether OT’s effects on BT-induced feeding can be suppressed by an OTr antagonist. 4 mg/kg BT increased intake in fed and in deprived rats, whereas LV and 4V OT at 1μg caused a decrease in deprived rats. BT-induced chow intake in hungry and sated animals was suppressed by a very low, 0.1-μg dose of 4V OT, whereas 1μg OT was effective LV. The effect of OT was attenuated by OTr antagonist. The data strongly suggest that while both the forebrain and hindbrain populations of the OTr promote hypophagia, the hindbrain component of the circuitry is particularly sensitive to appetite reducing properties of OT in animals motivated to eat by a potent orexigen, BT. In the second set of studies, I examined whether either of the two populations of the hypothalamic OTr, in the medial preoptic area (MPOA) or the ventromedial hypothalamic nucleus (VMH), mediates OT-driven hypophagia in energy- and reward-related ingestive behaviors. I provide insights into mechanisms underlying OT-driven anorexia mediated by the hypothalamus by (a) defining whether OT MPOA or VMH Administration affects feeding for energy versus palatability; (b) identifying feeding-related sites activated by VMH OT injection; (c) measuring VMH OTr mRNA changes in response to hunger and palatability; and (d) examining how VMH OT affects sweet solution intake in rats. MPOA had no effect on intake of energy-dense chow in deprived rats nor did it decrease intake of calorie-dilute palatable solutions. VMH OT decreased chow intake and the effect was reversed by the antagonist. OT did not affect intakes of saccharin and sucrose solutions. Fos immunoreactivity, a marker of neuronal activation, was elevated in the VMH and energy balance-related paraventricular and arcuate nuclei, but not reward areas. VMH OT receptor expression was higher in hungry than sated rats; saccharin intake had no effect. In sum, MPOA OTr is not involved in OT-driven hypophagia mediated by hypothalamic networks. VMH OT decreases intake driven by energy not by palatability. Finally, I assessed whether the OTr present in the basolateral (BLA) and central amygdala (CNA), sites implicated in emotional/pleasure processing of food intake, is involved in appetite control by OT. I injected OT in the BLA or CNA and assessed intake of chow induced by energy deprivation and intake of sweet solutions in nondeprived rats. I examined whether these effects are reversible by OTr blockade. I determined the effect of energy deprivation and exposure to saccharin on BLA and CNA expression of OTr mRNA. BLA OT at 0.3 μg and CNA OT at 1 μg reduced chow intake after deprivation. Only BLA OT was effective at suppressing consumption of sucrose and saccharin. The anorexigenic effects of BLA and CNA OT were attenuated by an OTr antagonist. BLA OTr mRNA expression was affected by exposure to saccharin, whereas that of CNA OTr, by energy deprivation. The relationship between amygdalar OT and energy- vs palatability-driven intake depends on the discrete localization of the OTr in this complex structure. Overall, these findings shed light on the specific elements of brain circuitry mediating anorexigenic properties of OT. Both the forebrain and hindbrain OTr populations are relevant to feeding control. OT’s inhibitory effects on feeding for energy are mediated by a broader network of sites that includes, aside from the previously reported nucleus accumbens and dorsal vagal complex, the VMH, BLA, and CNA. Only the BLA OT modifies eating for reward. Surprisingly, the OTr in the MPOA is not involved in feeding regulation