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Roy A Wise - One of the best experts on this subject based on the ideXlab platform.
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Supplemental morphine infusion into the posterior Ventral Tegmentum extends the satiating effects of self-administered intravenous heroin.
Pharmacology biochemistry and behavior, 2015Co-Authors: S. Steidl, Stephanie E. Myal, Roy A WiseAbstract:Rats learn to self-administer intravenous heroin; well-trained animals lever-press at a slow and regular pace over a wide range of intravenous doses. The pauses between successive earned infusions are proportional to the dose of the previous injection and are thought to reflect periods of drug satiety. Rats will also self-administer opiates by microinjection directly into sites in the posterior regions of the Ventral Tegmentum. To determine if the pauses between self-administered intravenous injections are due to opiate actions in posterior Ventral Tegmentum, we delivered supplemental morphine directly into this region during intravenous self-administration sessions in well-trained rats. Reverse dialysis of morphine into the posterior Ventral Tegmentum increased the intervals between earned injections. The inter-response intervals were greatest for infusion into the most posterior Ventral tegmental sites, sites in a region variously known as the tail of the Ventral tegmental area or as the rostromedial tegmental nucleus. These sites at which morphine prolongs inter-response intervals, correspond to the sites at which opiates have been found most effective in reinforcing instrumental behavior.
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Place preference conditioning with Ventral tegmental injections of cytisine
Life Sciences, 2002Co-Authors: Enrico Museo, Roy A WiseAbstract:Abstract The present experiment was designed to determine whether Ventral tegmental injections of the nicotinic agonist cytisine can establish place preferences. Two groups of rats were tested: one group received injections into the Ventral Tegmentum and a second group received injections into sites dorsal to the Ventral Tegmentum; this latter group was used to assess whether the diffusion of drug into sites dorsal to the Ventral Tegmentum might in itself be sufficient to account for the effects associated with injections into the Ventral Tegmentum. A total of eight sets of injections were made. On days 1, 3, 5, and 7, animals were injected with cytisine (10 nmol per 0.5 μl per side) and placed in one of the two main compartments of a place-preference apparatus. On days 2, 4, 6, and 8, injections of physiological saline, the drug vehicle, were paired with the other main compartment. Animals that received Ventral tegmental injections of cytisine spent significantly more time in the cytisine-paired compartment than in the saline-paired compartment. Animals given cytisine injections into sites dorsal to the Ventral Tegmentum did not show a preference for the cytisine-paired compartment. These findings provide additional evidence in support of the hypothesis that nicotinic actions at the level of the Ventral Tegmentum contribute to the reinforcing actions of systemic injections of nicotine.
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Cytisine-induced behavioral activation: delineation of neuroanatomical locus of action.
Brain Research, 1995Co-Authors: Enrico Museo, Roy A WiseAbstract:Systemic injections of nicotine increase locomotor activity. The present study was designed to determine whether there is a circumscribed region in the Ventral Tegmentum that mediates the locomotor-activating effects of nicotine. The mapping technique was used to delineate this region: bilateral injections of cytisine (1 nmol/0.5 μl per side) were made into sites in and around the Ventral Tegmentum and the amount of locomotion associated with each site was quantified. The distribution of injection sites spanned between 0.8 and 4.6 mm posterior to bregma. The amount of locomotion varied with relation to the area into which cytisine was injected and a region was identified within which injections of cytisine preferentially increased locomotion. This region appears to have reasonably well-defined anterior and posterior boundaries. Since a portion of the delineated area overlaps the dopamine-containing cell-body region, the possibility remains that the activation of the mesolimbic dopamine system may contribute to the behavioral activation associated with Ventral tegmental injections of cytisine. This same system may contribute to the locomotor-activating effects associated with systemic injections of nicotine.
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Sensitization of locomotion following repeated Ventral tegmental injections of cytisine
Pharmacology Biochemistry and Behavior, 1994Co-Authors: Enrico Museo, Roy A WiseAbstract:Abstract Systemic injections of nicotine increase locomotion, and repeating these injections brings about a sensitization of the locomotor response. Ventral tegmental injections of the nicotinic agonist cytisine also increase locomotion. In the present study cytisine was administered repeatedly into the Ventral Tegmentum to determine whether sensitization of its locomotor-activating effects would develop. Four groups of animals were tested; each group received a total of six injections at a rate of one injection every 48 h. Two of these groups received injections of cytisine (10 nmol/side): one group received injections into the Ventral Tegmentum, and, to insure the anatomical specificity of the locomotor effect, a second group received injections dorsal to the Ventral Tegmentum. The remaining two groups received vehicle injections: one group received injections into the Ventral Tegmentum, and the other received injections into more dorsal sites. The group of animals that received injections of cytisine into the Ventral Tegmentum locomoted more than any other group. In addition, only with this group was a progressive increase in the locomotor response evident across test days. These findings raise the possibility that a neural substrate in the Ventral Tegmentum mediates the locomotor-activating and sensitizing effects associated with the systemic administration of nicotine.
Enrico Museo - One of the best experts on this subject based on the ideXlab platform.
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Place preference conditioning with Ventral tegmental injections of cytisine
Life Sciences, 2002Co-Authors: Enrico Museo, Roy A WiseAbstract:Abstract The present experiment was designed to determine whether Ventral tegmental injections of the nicotinic agonist cytisine can establish place preferences. Two groups of rats were tested: one group received injections into the Ventral Tegmentum and a second group received injections into sites dorsal to the Ventral Tegmentum; this latter group was used to assess whether the diffusion of drug into sites dorsal to the Ventral Tegmentum might in itself be sufficient to account for the effects associated with injections into the Ventral Tegmentum. A total of eight sets of injections were made. On days 1, 3, 5, and 7, animals were injected with cytisine (10 nmol per 0.5 μl per side) and placed in one of the two main compartments of a place-preference apparatus. On days 2, 4, 6, and 8, injections of physiological saline, the drug vehicle, were paired with the other main compartment. Animals that received Ventral tegmental injections of cytisine spent significantly more time in the cytisine-paired compartment than in the saline-paired compartment. Animals given cytisine injections into sites dorsal to the Ventral Tegmentum did not show a preference for the cytisine-paired compartment. These findings provide additional evidence in support of the hypothesis that nicotinic actions at the level of the Ventral Tegmentum contribute to the reinforcing actions of systemic injections of nicotine.
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Cytisine-induced behavioral activation: delineation of neuroanatomical locus of action.
Brain Research, 1995Co-Authors: Enrico Museo, Roy A WiseAbstract:Systemic injections of nicotine increase locomotor activity. The present study was designed to determine whether there is a circumscribed region in the Ventral Tegmentum that mediates the locomotor-activating effects of nicotine. The mapping technique was used to delineate this region: bilateral injections of cytisine (1 nmol/0.5 μl per side) were made into sites in and around the Ventral Tegmentum and the amount of locomotion associated with each site was quantified. The distribution of injection sites spanned between 0.8 and 4.6 mm posterior to bregma. The amount of locomotion varied with relation to the area into which cytisine was injected and a region was identified within which injections of cytisine preferentially increased locomotion. This region appears to have reasonably well-defined anterior and posterior boundaries. Since a portion of the delineated area overlaps the dopamine-containing cell-body region, the possibility remains that the activation of the mesolimbic dopamine system may contribute to the behavioral activation associated with Ventral tegmental injections of cytisine. This same system may contribute to the locomotor-activating effects associated with systemic injections of nicotine.
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Sensitization of locomotion following repeated Ventral tegmental injections of cytisine
Pharmacology Biochemistry and Behavior, 1994Co-Authors: Enrico Museo, Roy A WiseAbstract:Abstract Systemic injections of nicotine increase locomotion, and repeating these injections brings about a sensitization of the locomotor response. Ventral tegmental injections of the nicotinic agonist cytisine also increase locomotion. In the present study cytisine was administered repeatedly into the Ventral Tegmentum to determine whether sensitization of its locomotor-activating effects would develop. Four groups of animals were tested; each group received a total of six injections at a rate of one injection every 48 h. Two of these groups received injections of cytisine (10 nmol/side): one group received injections into the Ventral Tegmentum, and, to insure the anatomical specificity of the locomotor effect, a second group received injections dorsal to the Ventral Tegmentum. The remaining two groups received vehicle injections: one group received injections into the Ventral Tegmentum, and the other received injections into more dorsal sites. The group of animals that received injections of cytisine into the Ventral Tegmentum locomoted more than any other group. In addition, only with this group was a progressive increase in the locomotor response evident across test days. These findings raise the possibility that a neural substrate in the Ventral Tegmentum mediates the locomotor-activating and sensitizing effects associated with the systemic administration of nicotine.
Joseph F. Debold - One of the best experts on this subject based on the ideXlab platform.
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Bicuculline infused into the hamster Ventral Tegmentum inhibits, while sodium valproate facilitates, sexual receptivity
Pharmacology biochemistry and behavior, 1993Co-Authors: Cheryl A. Frye, P.g. Mermelstein, Joseph F. DeboldAbstract:Progesterone's (P) actions on both the Ventral medial nucleus of the hypothalamus (VMH) and the Ventral tegmental area (VTA) are essential for sexual receptivity in female hamsters. Evidence suggests that progesterone's actions in the hamster VMH may be genomic while those in the VTA may be mediated nongenomically, via GABAA. Ovariectomized female hamsters were bilaterally implanted with cannulae aimed toward the VTA. One week after surgery, animals were SC injected with 10 μg estradiol benzoate (EB) and 40 h later with 200 or 500 μg P. At hour 43.5, 50 ng bicuculline, a GABAA antagonist, was infused into each available cannula. Control animals received 0.5 μl sterile saline vehicle, or no infusion. At hour 44, animals were tested for sexual receptivity in an observation arena with a sexually experienced male. Histology revealed that only animals with bicuculline infused into the VTA had reduced lordosis durations compared to controls. Other animals, primed with EB and 200 μg progesterone, showed a facilitation of sexual receptivity after infusion into the VTA of 50 μg sodium valproate, a GABAA transaminase inhibitor. These results suggest that GABAA plays a necessary role in the mechanism of progesterone's actions on sexual receptivity in hamster VTA.
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Muscimol facilitates sexual receptivity in hamsters when infused into the Ventral Tegmentum
Pharmacology biochemistry and behavior, 1992Co-Authors: Cheryl A. Frye, Joseph F. DeboldAbstract:Progestogenic stimulation of both the Ventral medial nucleus of the hypothalamus (VMH) and the Ventral tegmental area (VTA) within the midbrain is critical for normal receptivity in female hamsters. However, few estrogen-induced progestin receptors have been found in the midbrain. In addition, recent evidence suggests that progestin's action in the VTA is mediated nongenomically at the membrane. The present experiment investigated the possible role of GABAA receptors in mediating the effects of progesterone in this brain region. Ovariectomized female hamsters were bilaterally implanted with chronic cannulae aimed toward the Ventral mesencephalon. Five days after surgery, animals were injected with 10 μg estradiol benzoate SC. Forty hours later, the same animals were injected with either 25 or 100 μg progesterone and at hour 43.5, 50 ng muscimol was infused in 0.5 μl. Control animals received 0.5 μl vehicle, sterile saline, or no infusion. At hour 44, animals were tested for sexual receptivity by placing them in an observation arena with a sexually experienced male for 10 min, during which lordosis duration was recorded. The following week, the same regimen was given with the alternate dose of progesterone. Histology revealed that only those animals that were infused with muscimol into the VTA had total lordosis durations that were significantly longer than the controls. Implants that missed the Ventral tegmental area were much less effective. These results indicate that GABA might play a facilitatory role in enhancing the efficacy of threshold doses of progesterone. Whether this interaction is due to a direct effect of progestins on the GABAA receptor complex awaits further study.
Gaetano Di Chiara - One of the best experts on this subject based on the ideXlab platform.
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a dopamine μ1 opioid link in the rat Ventral Tegmentum shared by palatable food fonzies and non psychostimulant drugs of abuse
European Journal of Neuroscience, 1998Co-Authors: Gianluigi Tanda, Gaetano Di ChiaraAbstract:The role of mu1 opioid receptors in the stimulation of dopamine transmission in the rat nucleus accumbens by an unusual palatable food (Fonzies) and non-psychostimulant drugs of abuse was investigated by the use of naloxonazine, a pseudo-irreversible antagonist of mu1 opioid receptors. Feeding of Fonzies stimulated dopamine release in the medial prefrontal cortex and in the shell, but not in the core of the nucleus accumbens. Pretreatment with naloxonazine given systemically (15 mg/kg i.p. 20 h before) completely prevented the stimulation of dopamine release in the shell of the nucleus accumbens by Fonzies without affecting that in the prefrontal cortex. Systemic pretreatment with naloxonazine reduced or, depending on the dose, abolished, the stimulation of dopamine release in the nucleus accumbens shell by morphine, nicotine and ethanol, but did not affect that by haloperidol. Naloxonazine also prevented the stimulatory effects of Fonzies, nicotine and morphine on nucleus accumbens dopamine transmission when infused bilaterally in the Ventral tegmental area. The results indicate that mu1 opioid receptors in the Ventral Tegmentum play a major role in the stimulant effects of food and drugs of abuse on mesolimbic dopamine transmission.
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A dopamine‐μ1 opioid link in the rat Ventral Tegmentum shared by palatable food (Fonzies) and non‐psychostimulant drugs of abuse
The European journal of neuroscience, 1998Co-Authors: Gianluigi Tanda, Gaetano Di ChiaraAbstract:The role of mu1 opioid receptors in the stimulation of dopamine transmission in the rat nucleus accumbens by an unusual palatable food (Fonzies) and non-psychostimulant drugs of abuse was investigated by the use of naloxonazine, a pseudo-irreversible antagonist of mu1 opioid receptors. Feeding of Fonzies stimulated dopamine release in the medial prefrontal cortex and in the shell, but not in the core of the nucleus accumbens. Pretreatment with naloxonazine given systemically (15 mg/kg i.p. 20 h before) completely prevented the stimulation of dopamine release in the shell of the nucleus accumbens by Fonzies without affecting that in the prefrontal cortex. Systemic pretreatment with naloxonazine reduced or, depending on the dose, abolished, the stimulation of dopamine release in the nucleus accumbens shell by morphine, nicotine and ethanol, but did not affect that by haloperidol. Naloxonazine also prevented the stimulatory effects of Fonzies, nicotine and morphine on nucleus accumbens dopamine transmission when infused bilaterally in the Ventral tegmental area. The results indicate that mu1 opioid receptors in the Ventral Tegmentum play a major role in the stimulant effects of food and drugs of abuse on mesolimbic dopamine transmission.
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cannabinoid and heroin activation of mesolimbic dopamine transmission by a common µ1 opioid receptor mechanism
Science, 1997Co-Authors: Gianluigi Tanda, Francesco E Pontieri, Gaetano Di ChiaraAbstract:The effects of the active ingredient of Cannabis , Δ9-tetrahydrocannabinol (Δ9-THC), and of the highly addictive drug heroin on in vivo dopamine transmission in the nucleus accumbens were compared in Sprague-Dawley rats by brain microdialysis. Δ9-THC and heroin increased extracellular dopamine concentrations selectively in the shell of the nucleus accumbens; these effects were mimicked by the synthetic cannabinoid agonist WIN55212-2. SR141716A, an antagonist of central cannabinoid receptors, prevented the effects of Δ9-THC but not those of heroin. Naloxone, a generic opioid antagonist, administered systemically, or naloxonazine, an antagonist of μ1 opioid receptors, infused into the Ventral Tegmentum, prevented the action of cannabinoids and heroin on dopamine transmission. Thus, Δ9-THC and heroin exert similar effects on mesolimbic dopamine transmission through a common μ1 opioid receptor mechanism located in the Ventral mesencephalic Tegmentum.
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Cannabinoid and Heroin Activation of Mesolimbic Dopamine Transmission by a Common µ1 Opioid Receptor Mechanism
Science (New York N.Y.), 1997Co-Authors: Gianluigi Tanda, Francesco E Pontieri, Gaetano Di ChiaraAbstract:The effects of the active ingredient of Cannabis, Delta9-tetrahydrocannabinol (Delta9-THC), and of the highly addictive drug heroin on in vivo dopamine transmission in the nucleus accumbens were compared in Sprague-Dawley rats by brain microdialysis. Delta9-THC and heroin increased extracellular dopamine concentrations selectively in the shell of the nucleus accumbens; these effects were mimicked by the synthetic cannabinoid agonist WIN55212-2. SR141716A, an antagonist of central cannabinoid receptors, prevented the effects of Delta9-THC but not those of heroin. Naloxone, a generic opioid antagonist, administered systemically, or naloxonazine, an antagonist of micro1 opioid receptors, infused into the Ventral Tegmentum, prevented the action of cannabinoids and heroin on dopamine transmission. Thus, Delta9-THC and heroin exert similar effects on mesolimbic dopamine transmission through a common mu1 opioid receptor mechanism located in the Ventral mesencephalic Tegmentum.
L Kokkinidis - One of the best experts on this subject based on the ideXlab platform.
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Infusion of quinpirole and muscimol into the Ventral tegmental area inhibits fear-potentiated startle: implications for the role of dopamine in fear expression.
Brain research, 1997Co-Authors: L J Munro, L KokkinidisAbstract:Dopamine (DA) D2 and gamma-aminobutyric acid (GABA)A somatodendritic receptors tonically inhibit mesolimbic projection neurons in the A10 DA cell grouping of the Ventral Tegmentum. In the present study we determined the contribution of the Ventral tegmental area (VTA) to the expression of a classically conditioned fear-induced increase in the acoustic startle reflex. Saline applied to VTA neurons did not modify the capacity of a light previously associated with footshock to potentiate acoustic startle amplitudes; conversely, bilateral administration of the DA D2/3 agonist quinpirole or the GABAA receptor agonist muscimol into the Ventral Tegmentum blocked fear-potentiated startle without altering baseline acoustic startle responding. It was suggested that DA VTA neurons regulate the excitatory aspects of fear expression by gating levels of aversive emotional arousal within the amygdala-based fear system.
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contribution of Ventral tegmental area dopamine neurons to expression of conditional fear effects of electrical stimulation excitotoxin lesions and quinpirole infusion on potentiated startle in rats
Behavioral Neuroscience, 1996Co-Authors: Thomas Orowski, L KokkinidisAbstract:Potentiated startle was used in this study to determine the fear-motivational functions of the Ventral tegmental area (VTA). In Experiment I, electrical stimulation of the VTA increased acoustic startle amplitudes. In subsequent experiments fear-potentiated startle was assessed following axon-sparing N-methyl-D-aspartic acid (NMDA) lesions of the VTA and after bilateral intra-VTA infusion of the dopamine (DA) D 2/3 receptor agonist quinpirole. The NMDA lesions produced substantial cell loss in the medial Ventral Tegmentum and suppressed fear expression. Similarly, inhibition of DA neuronal activity associated with locally administered quinpirole blocked fear-potentiated startle. It was suggested that VTA neurons and their forebrain DA projections regulate levels of aversive emotional arousal within the amygdala-based fear system.
