The Experts below are selected from a list of 225 Experts worldwide ranked by ideXlab platform
Robert H Roth - One of the best experts on this subject based on the ideXlab platform.
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effects of repeated nicotine administration and Footshock stress on rat mesoprefrontal dopamine systems evidence for opioid mechanisms
Neuropsychopharmacology, 2000Co-Authors: Tony P George, Christopher D Verrico, Li Xu, Robert H RothAbstract:We have examined the effects of nicotine pre-treatment on mesoprefrontal dopamine (DA) function in the presence and absence of acute stress, and the involvement of endogenous opiate peptide systems (EOPS). Acute electrical Footshock stress preferentially increases DA utilization in medial prefrontal cortex (mPFC) compared to nucleus accumbens (NAS) and striatal terminal fields, and this is correlated with profound locomotor immobility. Our recent studies have demonstrated that repeated, but not acute, nicotine pre-treatment significantly reduced mPFC DA utilization and Footshock stress-induced immobility responses. There is increasing evidence that the biochemical and behavioral effects of nicotine are mediated by EOPS, and we hypothesized that the stress-reducing effects of repeated nicotine administration in these studies were mediated by EOPS. Accordingly, rats pre-treated subcutaneously with repeated nicotine were given a single dose of the opiate receptor antagonist naloxone (0.1–10.0 mg/kg, i.p.) or saline as a co-treatment with nicotine or saline 10 min prior to acute Footshock stress. Naloxone had no effects on non-stressed or acute Footshock stress-induced mPFC DA utilization, but dose-dependently antagonized repeated nicotine's attenuation of stress-induced mesoprefrontal DA utilization and immobility responses. Furthermore, naloxone dose-dependently blocked repeated nicotine's augmentation of accumbal DA utilization. These results suggest that EOPS may be involved in mediating repeated nicotine administration effects on mesoprefrontal dopaminergic and immobility responses to acute Footshock stress.
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effects of repeated nicotine pre treatment on mesoprefrontal dopaminergic and behavioral responses to acute Footshock stress
Brain Research, 1998Co-Authors: Tony P George, Christopher D Verrico, Robert H RothAbstract:The effects of acute and repeated nicotine administration on the stress response of rat mesoprefrontal dopaminergic pathways were examined. Rats were given daily injections of nicotine (0.15 or 0.60 mg/kg, s.c., freebase) or saline for 4 days, then challenged with either nicotine or saline. A regimen of inescapable electrical Footshocks or no Footshocks was then administered. Thirty minutes after final injection, rats were sacrificed, brains removed and dopamine (DA) and its metabolite dihydroxy-O-phenylacetic acid (DOPAC) were extracted from medial prefrontal cortex (mPFC), nucleus accumbens septi (NAS) and dorsolateral striatum and quantified by high performance liquid chromatography with electrochemical detection. Acute administration of low dose nicotine (0.15 mg/kg) produced an increase in DA utilization (increased DOPAC/DA ratio) in mPFC and NAS, but not striatum. High dose nicotine (0.60 mg/kg) produced activation in NAS, but not mPFC or striatum. Repeated low dose nicotine pre-treatment produced tolerance to the effects of nicotine challenge in the mPFC, and reduced its effects in NAS. Footshock stress preferentially increased DA utilization in mPFC and associated Footshock stress-induced immobility responses, and these were reduced by low, but not high, dose repeated nicotine pre-treatment. Further, a single dose of the nicotinic acetylcholine receptor (nAChR) antagonist mecamylamine (MCA) 30 min prior to nicotine challenge dose-dependently blocked the reduction of mesoprefrontal DA stress responsivity and immobility responses produced by repeated nicotine pre-treatment. These results indicate that: (1) there are dose-dependent differential effects of acute and repeated nicotine pre-exposure on regional DA utilization; (2) low, but not high, dose repeated nicotine reduces both the mesoprefrontal DA and behavioral effects of acute Footshock stress; and (3) these effects of repeated nicotine may depend on mecamylamine-sensitive nAChR stimulation. These results may have relevance to acute stress and nicotine dependence, particularly in schizophrenic disorders, which have high prevalence rates of co-morbid nicotine dependence, stress-induced symptom exacerbation and prefrontal cortical dysfunction.
Tony P George - One of the best experts on this subject based on the ideXlab platform.
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effects of repeated nicotine administration and Footshock stress on rat mesoprefrontal dopamine systems evidence for opioid mechanisms
Neuropsychopharmacology, 2000Co-Authors: Tony P George, Christopher D Verrico, Li Xu, Robert H RothAbstract:We have examined the effects of nicotine pre-treatment on mesoprefrontal dopamine (DA) function in the presence and absence of acute stress, and the involvement of endogenous opiate peptide systems (EOPS). Acute electrical Footshock stress preferentially increases DA utilization in medial prefrontal cortex (mPFC) compared to nucleus accumbens (NAS) and striatal terminal fields, and this is correlated with profound locomotor immobility. Our recent studies have demonstrated that repeated, but not acute, nicotine pre-treatment significantly reduced mPFC DA utilization and Footshock stress-induced immobility responses. There is increasing evidence that the biochemical and behavioral effects of nicotine are mediated by EOPS, and we hypothesized that the stress-reducing effects of repeated nicotine administration in these studies were mediated by EOPS. Accordingly, rats pre-treated subcutaneously with repeated nicotine were given a single dose of the opiate receptor antagonist naloxone (0.1–10.0 mg/kg, i.p.) or saline as a co-treatment with nicotine or saline 10 min prior to acute Footshock stress. Naloxone had no effects on non-stressed or acute Footshock stress-induced mPFC DA utilization, but dose-dependently antagonized repeated nicotine's attenuation of stress-induced mesoprefrontal DA utilization and immobility responses. Furthermore, naloxone dose-dependently blocked repeated nicotine's augmentation of accumbal DA utilization. These results suggest that EOPS may be involved in mediating repeated nicotine administration effects on mesoprefrontal dopaminergic and immobility responses to acute Footshock stress.
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effects of repeated nicotine pre treatment on mesoprefrontal dopaminergic and behavioral responses to acute Footshock stress
Brain Research, 1998Co-Authors: Tony P George, Christopher D Verrico, Robert H RothAbstract:The effects of acute and repeated nicotine administration on the stress response of rat mesoprefrontal dopaminergic pathways were examined. Rats were given daily injections of nicotine (0.15 or 0.60 mg/kg, s.c., freebase) or saline for 4 days, then challenged with either nicotine or saline. A regimen of inescapable electrical Footshocks or no Footshocks was then administered. Thirty minutes after final injection, rats were sacrificed, brains removed and dopamine (DA) and its metabolite dihydroxy-O-phenylacetic acid (DOPAC) were extracted from medial prefrontal cortex (mPFC), nucleus accumbens septi (NAS) and dorsolateral striatum and quantified by high performance liquid chromatography with electrochemical detection. Acute administration of low dose nicotine (0.15 mg/kg) produced an increase in DA utilization (increased DOPAC/DA ratio) in mPFC and NAS, but not striatum. High dose nicotine (0.60 mg/kg) produced activation in NAS, but not mPFC or striatum. Repeated low dose nicotine pre-treatment produced tolerance to the effects of nicotine challenge in the mPFC, and reduced its effects in NAS. Footshock stress preferentially increased DA utilization in mPFC and associated Footshock stress-induced immobility responses, and these were reduced by low, but not high, dose repeated nicotine pre-treatment. Further, a single dose of the nicotinic acetylcholine receptor (nAChR) antagonist mecamylamine (MCA) 30 min prior to nicotine challenge dose-dependently blocked the reduction of mesoprefrontal DA stress responsivity and immobility responses produced by repeated nicotine pre-treatment. These results indicate that: (1) there are dose-dependent differential effects of acute and repeated nicotine pre-exposure on regional DA utilization; (2) low, but not high, dose repeated nicotine reduces both the mesoprefrontal DA and behavioral effects of acute Footshock stress; and (3) these effects of repeated nicotine may depend on mecamylamine-sensitive nAChR stimulation. These results may have relevance to acute stress and nicotine dependence, particularly in schizophrenic disorders, which have high prevalence rates of co-morbid nicotine dependence, stress-induced symptom exacerbation and prefrontal cortical dysfunction.
Lin Lu - One of the best experts on this subject based on the ideXlab platform.
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region specific effects of brain corticotropin releasing factor receptor type 1 blockade on Footshock stress or drug priming induced reinstatement of morphine conditioned place preference in rats
Psychopharmacology, 2006Co-Authors: Jishi Wang, Qin Fang, Lin LuAbstract:Systemic injections of the selective corticotropin-releasing factor 1 (CRF1) receptor antagonist CP-154,526 attenuate Footshock-stress-induced reinstatement of heroin and cocaine seeking and morphine conditioned place preference (CPP). Intracranial injections of the nonselective CRF receptor antagonist d-Phe-CRF into the bed nucleus of the stria terminalis (BNST), but not the amygdala, attenuate Footshock-induced reinstatement of cocaine seeking. However, the brain sites involved in the effect of CP-154,526 on Footshock-induced reinstatement of opiate seeking are unknown. We used a CPP version of the reinstatement model to examine the role of CRF1 receptors in the BNST, amygdala, and nucleus accumbens (NAc) in Footshock- or drug-priming-induced reinstatement of extinguished morphine CPP. Rats acquired morphine CPP over a period of 8 days during which they were given four morphine (10 mg/kg s.c.) and four saline injections and were subsequently confined to distinct chambers for 50 min. Subsequently, the morphine CPP was extinguished in 14 daily sessions during which rats were given saline injections and given access to both the saline- and morphine-paired chambers. The rats were then tested for reinstatement of morphine CPP induced by priming injections of morphine (0 or 3.0 mg/kg s.c.) or by exposure to intermittent Footshock (15 min, 0.5 mA). Prior to the test sessions, the rats were given intracranial injections of CP-154,526 (1.0 μg) or vehicle into the BNST, amygdala, or NAc. CP-154,526 injections into the BNST, but not the amygdala or NAc, attenuated Footshock-stress-induced reinstatement of morphine CPP. In contrast, CP-154,526 injections into the amygdala or NAc, but not the BNST, attenuated morphine-priming-induced reinstatement of morphine CPP. The present results demonstrate dissociable roles of CRF1 receptors in the BNST, amygdala, and NAc in Footshock-stress- vs morphine-priming-induced reinstatement of drug CPP.
Christopher D Verrico - One of the best experts on this subject based on the ideXlab platform.
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effects of repeated nicotine administration and Footshock stress on rat mesoprefrontal dopamine systems evidence for opioid mechanisms
Neuropsychopharmacology, 2000Co-Authors: Tony P George, Christopher D Verrico, Li Xu, Robert H RothAbstract:We have examined the effects of nicotine pre-treatment on mesoprefrontal dopamine (DA) function in the presence and absence of acute stress, and the involvement of endogenous opiate peptide systems (EOPS). Acute electrical Footshock stress preferentially increases DA utilization in medial prefrontal cortex (mPFC) compared to nucleus accumbens (NAS) and striatal terminal fields, and this is correlated with profound locomotor immobility. Our recent studies have demonstrated that repeated, but not acute, nicotine pre-treatment significantly reduced mPFC DA utilization and Footshock stress-induced immobility responses. There is increasing evidence that the biochemical and behavioral effects of nicotine are mediated by EOPS, and we hypothesized that the stress-reducing effects of repeated nicotine administration in these studies were mediated by EOPS. Accordingly, rats pre-treated subcutaneously with repeated nicotine were given a single dose of the opiate receptor antagonist naloxone (0.1–10.0 mg/kg, i.p.) or saline as a co-treatment with nicotine or saline 10 min prior to acute Footshock stress. Naloxone had no effects on non-stressed or acute Footshock stress-induced mPFC DA utilization, but dose-dependently antagonized repeated nicotine's attenuation of stress-induced mesoprefrontal DA utilization and immobility responses. Furthermore, naloxone dose-dependently blocked repeated nicotine's augmentation of accumbal DA utilization. These results suggest that EOPS may be involved in mediating repeated nicotine administration effects on mesoprefrontal dopaminergic and immobility responses to acute Footshock stress.
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effects of repeated nicotine pre treatment on mesoprefrontal dopaminergic and behavioral responses to acute Footshock stress
Brain Research, 1998Co-Authors: Tony P George, Christopher D Verrico, Robert H RothAbstract:The effects of acute and repeated nicotine administration on the stress response of rat mesoprefrontal dopaminergic pathways were examined. Rats were given daily injections of nicotine (0.15 or 0.60 mg/kg, s.c., freebase) or saline for 4 days, then challenged with either nicotine or saline. A regimen of inescapable electrical Footshocks or no Footshocks was then administered. Thirty minutes after final injection, rats were sacrificed, brains removed and dopamine (DA) and its metabolite dihydroxy-O-phenylacetic acid (DOPAC) were extracted from medial prefrontal cortex (mPFC), nucleus accumbens septi (NAS) and dorsolateral striatum and quantified by high performance liquid chromatography with electrochemical detection. Acute administration of low dose nicotine (0.15 mg/kg) produced an increase in DA utilization (increased DOPAC/DA ratio) in mPFC and NAS, but not striatum. High dose nicotine (0.60 mg/kg) produced activation in NAS, but not mPFC or striatum. Repeated low dose nicotine pre-treatment produced tolerance to the effects of nicotine challenge in the mPFC, and reduced its effects in NAS. Footshock stress preferentially increased DA utilization in mPFC and associated Footshock stress-induced immobility responses, and these were reduced by low, but not high, dose repeated nicotine pre-treatment. Further, a single dose of the nicotinic acetylcholine receptor (nAChR) antagonist mecamylamine (MCA) 30 min prior to nicotine challenge dose-dependently blocked the reduction of mesoprefrontal DA stress responsivity and immobility responses produced by repeated nicotine pre-treatment. These results indicate that: (1) there are dose-dependent differential effects of acute and repeated nicotine pre-exposure on regional DA utilization; (2) low, but not high, dose repeated nicotine reduces both the mesoprefrontal DA and behavioral effects of acute Footshock stress; and (3) these effects of repeated nicotine may depend on mecamylamine-sensitive nAChR stimulation. These results may have relevance to acute stress and nicotine dependence, particularly in schizophrenic disorders, which have high prevalence rates of co-morbid nicotine dependence, stress-induced symptom exacerbation and prefrontal cortical dysfunction.
Yavin Shaham - One of the best experts on this subject based on the ideXlab platform.
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time dependent changes in extinction behavior and stress induced reinstatement of drug seeking following withdrawal from heroin in rats
Psychopharmacology, 2001Co-Authors: Uri Shalev, Marisela Morales, Bruce T Hope, Yavin ShahamAbstract:Rationale and objectives: Footshock stress reliably reinstates heroin seeking in rats, but the time course of the development of this effect following drug withdrawal is not known. Here we studied the effect of intermittent Footshock stress on reinstatement of heroin seeking following different withdrawal periods (1–66 days). We also studied whether changes in corticotropin-releasing factor (CRF) mRNA in the central nucleus of the amygdala (CeA) and the bed nucleus of the stria terminalis (BNST) are correlated with this reinstatement after 1 day and 6 days of heroin withdrawal. Methods: Rats were trained to self-administer heroin (9 h/day; 0.1 mg/kg per infusion) for 10 days. Tests for extinction behavior and Footshock-induced reinstatement of heroin seeking were then conducted after 1, 6, 12, 25, or 66 days of heroin withdrawal. On the test day, rats were given five to ten 60-min extinction sessions until they reached the extinction criterion of less than 15 responses per 60 min on the lever previously associated with heroin. Rats were then exposed to intermittent Footshock (0.8 mA; 10 min), and lever-pressing behavior was recorded for 120 min. Results: Reinstatement of lever-pressing behavior by Footshock followed an inverted U-shaped curve with maximal responding after 6 days and 12 days of heroin withdrawal. Surprisingly, Footshock did not reinstate lever-pressing behavior on day 1 of withdrawal. Lever pressing during extinction, prior to exposure to Footshock, also followed an inverted U-shaped curve, with higher responding after 6, 12, and 25 days of heroin withdrawal. Finally, compared with control groups not exposed to shock, CRF mRNA levels in response to Footshock were increased in the CeA (day 1 of withdrawal) and the dorsal BNST (day 1 and day 6), but not in the ventral BNST. Conclusions: The duration of the heroin withdrawal period is an important factor in the manifestation of (1) Footshock stress-induced reinstatement of heroin seeking and (2) extinction of the heroin-reinforced behavior. Finally, the time-dependent changes in Footshock stress-induced reinstatement following withdrawal from heroin were not correlated with alterations in CRF mRNA in the CeA and BNST.
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Alpha-2 Adrenergic Receptor Agonists Block Stress-Induced Reinstatement of Cocaine Seeking
Neuropsychopharmacology, 2000Co-Authors: Paul K Hitchcott, Yavin Shaham, Heshmat Rajabi, Devin Mueller, Jane StewartAbstract:The alpha -2 adrenergic receptor agonists, clonidine, lofexidine and guanabenz, blocked stress- but not cocaine-induced reinstatement of cocaine seeking at doses that suppressed Footshock-induced release of noradrenaline in prefrontal cortex and amygdala. Rats were trained to self-administer cocaine (0.5 mg/kg/infusion, i.v; 10–12 days) and, after a drug-free period (7–13 days), were returned to the self-administration chambers for daily extinction and reinstatement test sessions. Both intermittent Footshock (15 min, 0.6 mA) and cocaine priming (20 mg/kg, i.p.) reinstated extinguished drug seeking. Pretreatment with either clonidine (20, or 40 μg/kg, i.p.) or lofexidine (50, 100, 150, or 200 μg/kg, i.p.) attenuated Footshock- but not cocaine-induced reinstatement of cocaine seeking. Guanabenz (640 μg/kg, i.p.), an alpha -2 agonist with low affinity for imidazoline type-1 receptors, also attenuated Footshock- but not cocaine-induced reinstatement of cocaine seeking. The results point to an important role for NE systems in the effects of Footshock on relapse to cocaine seeking.