15 results on '"Racagni G."'
Search Results
2. Behavioural and biochemical effects in the adult rat after prolonged postnatal administration of clozapine
- Author
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Cuomo, V., Cagiano, R., Mocchetti, I., Coen, E., Cattabeni, F., and Racagni, G.
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- 1983
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Catalog
3. Enduring behavioural and biochemical effects in the adult rat after prolonged postnatal administration of haloperidol
- Author
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Cuomo, V., Cagiano, R., Coen, E., Mocchetti, I., Cattabeni, F., and Racagni, G.
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- 1981
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4. Modulation of neuronal plasticity following chronic concomitant administration of the novel antipsychotic lurasidone with the mood stabilizer valproic acid
- Author
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Calabrese, F., primary, Luoni, A., additional, Guidotti, G., additional, Racagni, G., additional, Fumagalli, F., additional, and Riva, M. A., additional
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- 2012
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5. Behavioural responsiveness to muscimol and apomorphine 2 months after prolonged treatment with estradiol in rats
- Author
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Cuomo, V., Cagiano, R., Apud, J., Masotto, C., and Racagni, G.
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- 1984
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6. A single cocaine exposure disrupts actin dynamics in the cortico-accumbal pathway of adolescent rats: modulation by a second cocaine injection.
- Author
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Caffino L, Giannotti G, Racagni G, and Fumagalli F
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- Analysis of Variance, Animals, Central Nervous System Stimulants pharmacology, Cocaine administration & dosage, Cocaine-Related Disorders metabolism, Disease Models, Animal, Male, Neuronal Plasticity drug effects, Nucleus Accumbens drug effects, Rats, Rats, Sprague-Dawley, Reward, Actins drug effects, Cocaine pharmacology, Prefrontal Cortex drug effects
- Abstract
Rationale and Objectives: Among the changes caused by repeated exposure to drugs of abuse, structural rearrangements play a critical role, setting the stage for maladaptive responses to environmental challenges and sustaining drug-taking and drug-seeking behaviors. Given that adolescents are more vulnerable to drug abuse than adults and based on our recent data showing that a single exposure to cocaine during adolescence is sufficient to change the adolescent brain, we decided to investigate whether acute cocaine exposure may alter actin remodeling in reward-related brain regions., Methods: Accordingly, we decided to evaluate if F-actin/G-actin ratio was altered by a single injection of cocaine (20 mg/kg) at postnatal day 35. We also evaluated whether the first administration of cocaine influences such a ratio in response to a second injection (10 mg/kg) provided 24 h or 7 days later., Results: Within the medial prefrontal cortex, a single cocaine injection increases the F-actin/G-actin ratio. This effect lasts 1 week, and it is not affected by the second injection of cocaine, indicating a persistent effect of the first exposure. In the nucleus accumbens, cocaine reduces the F-actin/G-actin ratio 24 h later. Seven days later, instead, such a ratio is markedly increased: notably, the additional exposure to the psychostimulant normalizes the F-actin/G-actin ratio., Conclusions: These results suggest that a single cocaine injection during adolescence causes possible changes in actin dynamics and influences the response to a second challenge of the psychostimulant, indicating that early cocaine priming might affect mechanisms regulating synaptic structural plasticity in specific brain regions. more...
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- 2017
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7. Region-specific effects of developmental exposure to cocaine on fibroblast growth factor-2 expression in the rat brain.
- Author
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Giannotti G, Caffino L, Mottarlini F, Racagni G, and Fumagalli F
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- Amygdala metabolism, Animals, Brain metabolism, Fibroblast Growth Factor 2 metabolism, Hippocampus drug effects, Male, Nucleus Accumbens drug effects, Prefrontal Cortex drug effects, RNA, Messenger metabolism, Rats, Rats, Sprague-Dawley, Reward, Ventral Tegmental Area metabolism, Brain drug effects, Cocaine pharmacology, Dopamine Uptake Inhibitors pharmacology, Fibroblast Growth Factor 2 biosynthesis
- Abstract
Rationale: Adolescence is a period of high vulnerability to drugs of abuse and alterations of the proper developmental trajectory via psychostimulant exposure might change the physiological brain homeostasis., Objective: By microdissection of brain areas via punching, we investigated whether repeated exposure to cocaine during adolescence (from postnatal day 28 [PND28] to PND42) has altered fibroblast growth factor-2 (FGF-2) messenger RNA (mRNA) levels in selected brain subregions critical for the action of cocaine., Results: We found a reduction of FGF-2 mRNA levels in ventral tegmental area (VTA), where mesocortical and mesolimbic pathways originate. The analysis of the trophic factor levels in the distal projecting regions revealed a selective reduction of FGF-2 mRNA levels in infralimbic (IL) subregion of the medial prefrontal cortex (the terminal region of the mesocortical pathway) and in the nucleus accumbens core (cNAc) (the terminal region of the mesolimbic pathway). Last, we found reduced FGF-2 mRNA levels also in brain regions which, although in a different manner, contribute to the reward system, i.e., the central nucleus of amygdala (cAmy) and the ventral portion of hippocampus (vHip)., Conclusion: The widespread and coordinated reduction of FGF-2 mRNA levels across the brain's reward neurocircuitry might represent a defensive strategy set in motion to oppose to the psychostimulant properties of cocaine. Moreover, given the role of FGF-2 in modulating mood disorders, the reduced trophic support here observed might sustain the negative emotional state set in motion by repeated exposure to cocaine. more...
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- 2016
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8. A single exposure to cocaine during development elicits regionally-selective changes in basal basic Fibroblast Growth Factor (FGF-2) gene expression and alters the trophic response to a second injection.
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Giannotti G, Caffino L, Malpighi C, Melfi S, Racagni G, and Fumagalli F
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- Animals, Brain growth & development, Brain metabolism, Female, Fibroblast Growth Factor 2 genetics, Gene Expression drug effects, Male, Models, Animal, RNA, Messenger genetics, RNA, Messenger metabolism, Rats, Rats, Sprague-Dawley, Self Administration, Up-Regulation drug effects, Brain drug effects, Cocaine pharmacology, Fibroblast Growth Factor 2 biosynthesis
- Abstract
Rationale: During adolescence, the brain is maturing and more sensitive to drugs of abuse that can influence its developmental trajectory. Recently, attention has been focused on basic fibroblast growth factor (FGF-2) given that its administration early in life enhances the acquisition of cocaine self-administration and sensitization at adulthood (Turner et al. (Pharmacol Biochem Behav 92:100-4, 2009), Clinton et al. (Pharmacol Biochem Behav103:6-17, 2012)). Additionally, we found that abstinence from adolescent cocaine exposure long lastingly dysregulates FGF-2 transcription (Giannotti et al. (Psychopharmacology (Berl) 225:553-60, 2013 )., Objectives: The objectives of the study are to evaluate if (1) a single injection of cocaine (20 mg/kg) at postnatal day 35 alters FGF-2 messenger RNA (mRNA) levels and (2) the first injection influences the trophic response to a second injection (10 mg/kg) provided 24 h or 7 days later., Results: We found regional differences in the FGF-2 expression pattern as either the first or the second injection of cocaine by themselves upregulated FGF-2 mRNA in the medial prefrontal cortex and nucleus accumbens while downregulating it in the hippocampus. The first injection influences the trophic response of the second. Of note, 24 h after the first injection, accumbal and hippocampal FGF-2 changes produced by cocaine in saline-pretreated rats were prevented in cocaine-pretreated rats. Conversely, in the medial prefrontal cortex and hippocampus 7 days after the first injection, the cocaine-induced FGF-2 changes were modified by the subsequent exposure to the psychostimulant., Conclusions: These findings show that a single cocaine injection is sufficient to produce enduring changes in the adolescent brain and indicate that early cocaine priming alters the mechanisms regulating the trophic response in a brain region-specific fashion. more...
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- 2015
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9. Dynamic modulation of basic Fibroblast Growth Factor (FGF-2) expression in the rat brain following repeated exposure to cocaine during adolescence.
- Author
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Giannotti G, Caffino L, Calabrese F, Racagni G, and Fumagalli F
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- Aging metabolism, Aging psychology, Analysis of Variance, Animals, Brain growth & development, Brain metabolism, Cocaine administration & dosage, Data Interpretation, Statistical, Dose-Response Relationship, Drug, Male, Nucleus Accumbens drug effects, Nucleus Accumbens growth & development, Nucleus Accumbens metabolism, Prefrontal Cortex drug effects, Prefrontal Cortex growth & development, Prefrontal Cortex metabolism, Rats, Rats, Sprague-Dawley, Real-Time Polymerase Chain Reaction, Aging drug effects, Brain drug effects, Cocaine pharmacology, Fibroblast Growth Factor 2 biosynthesis, Stress, Psychological metabolism
- Abstract
Rationale: Our study stems from four related lines of evidence: (1) FGF-2 is expressed in the developing brain; (2) psychostimulants modulate FGF-2 expression; (3) stress alters FGF-2 expression; and (4) exogenous administration of FGF-2 long-lastingly alters cocaine acquisition of self-administration., Objectives: This research aims to study the effects of adolescent cocaine exposure on FGF-2 mRNA levels and its influence on the response to stress., Materials and Methods: Rats were treated subcutaneously with saline or cocaine from postnatal day (PND) 28 to PND 42, a period that roughly approximates adolescence in humans. At PND 45 and PND 90, rats were exposed to an acute stress. Real-time PCRs were performed on total RNA extracted from the prefrontal cortex, hippocampus, nucleus accumbens and striatum., Results: In the prefrontal cortex, repeated cocaine treatment during adolescence increased FGF-2 mRNA levels in PND 90 rats and altered its response to an acute stress in both PND 45 and PND 90 rats. In the hippocampus of PND 45 rats, we found an increase of FGF-2 mRNA levels following repeated cocaine administration. No changes in the trophic factor gene expression were found in the striatum and nucleus accumbens., Conclusions: Our data show that cocaine exposure during adolescence alters FGF-2 mRNA levels throughout life in rat prefrontal cortex and modulates its response to an adverse event. These results point to FGF-2 as a potential molecular target through which exposure to cocaine early in life may dynamically and persistently alter brain homeostasis. more...
- Published
- 2013
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10. Stress and cocaine interact to modulate Arc/Arg3.1 expression in rat brain.
- Author
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Caffino L, Racagni G, and Fumagalli F
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- Animals, Cocaine-Related Disorders genetics, Corpus Striatum drug effects, Corpus Striatum metabolism, Cytoskeletal Proteins drug effects, Hippocampus drug effects, Hippocampus metabolism, Injections, Intraperitoneal, Male, Nerve Tissue Proteins drug effects, Neurons drug effects, Neurons metabolism, Prefrontal Cortex drug effects, Prefrontal Cortex metabolism, RNA, Messenger metabolism, Rats, Rats, Sprague-Dawley, Cocaine pharmacology, Cytoskeletal Proteins genetics, Gene Expression Regulation drug effects, Nerve Tissue Proteins genetics, Stress, Psychological genetics
- Abstract
Rationale: The interaction between stress and drugs of abuse is a critical component of drug addiction, but the underlying molecular mechanisms remain elusive. Arc/Arg3.1 is an effector immediate early gene that may represent a bridge connecting short- and long-term neuronal modifications associated with exposure to stress and drugs of abuse., Objectives: This research aims to study the modulation of Arc/Arg3.1 expression as a marker of neuronal changes associated with exposure to stress and cocaine., Materials and Methods: Rats exposed to either single or repeated stress sessions were subjected to a single intraperitoneal injection of cocaine hydrochloride (10 mg/kg) and sacrificed 2 h later. RNase protection assay was used to determine changes in Arc/Arg3.1 gene expression in different brain regions., Results: We found significant stress-cocaine interactions in the prefrontal cortex (p < 0.001) and hypothalamus (p < 0.05). In the prefrontal cortex, acute stress potentiated cocaine-induced Arc/Arg3.1 mRNA elevation, whereas prolonged stress attenuated the response to cocaine. In the hypothalamus, although markedly reduced by acute stress, Arc/Arg3.1 gene expression was still increased by cocaine. No interaction was observed following repeated stress. Notably, cocaine-induced Arc/Arg3.1 mRNA levels were not influenced by stress in striatum and hippocampus., Conclusions: In our experimental model, stress interacted with cocaine to alter Arc/Arg3.1 expression in a regionally selective fashion and in a way that depended on whether stress was acute or repeated. These results point to Arc/Arg3.1 as a potential molecular target modulated by stress to alter cellular sensitivity to cocaine. more...
- Published
- 2011
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11. ELAV-GAP43 pathway activation following combined exposure to cocaine and stress.
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Pascale A, Amadio M, Caffino L, Racagni G, Govoni S, and Fumagalli F
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- Animals, Blotting, Western, Cocaine-Related Disorders genetics, ELAV Proteins genetics, GAP-43 Protein genetics, Gene Expression Regulation drug effects, Hippocampus drug effects, Hippocampus metabolism, Injections, Subcutaneous, Male, Neurons metabolism, Polymerase Chain Reaction, Protein Kinase C-alpha metabolism, Rats, Rats, Sprague-Dawley, Cocaine pharmacology, ELAV Proteins metabolism, GAP-43 Protein metabolism, Stress, Psychological
- Abstract
Rationale: An increasing body of evidence suggests that drug addiction engages circuits also associated with memory processes. In particular, in the hippocampus, a substantial similarity seems to exist between the changes yielded by drugs of abuse and those induced by hippocampal-dependent learning., Objectives: Considering the key involvement of neuronal Embryonic Lethal Abnormal Vision (nELAV) proteins in memory processes occurring within the hippocampus and the critical role of stress for compulsive drug use and relapse, we investigated the effect of cocaine and stress challenges on the activation of the nELAV cascade., Materials and Methods: Rats were treated subcutaneously with vehicle or cocaine hydrochloride (20 mg/kg, once a day for 2 weeks). Three days later, half of them were also subjected to a single stress exposure. Western blotting and real-time polymerase chain reaction (PCR) experiments were performed on the hippocampi., Results: Our results show that the combination of repeated exposure to cocaine and acute stress significantly enhances nELAV expression and phosphorylation in the hippocampus with a concomitant increase of GAP43 expression (a specific nELAV target), an effect that seems to involve, upstream, protein kinase C alpha (PKCα). The activation of this pathway occurs independently from widespread neuronal activation since no alterations were observed in the expression of the immediate early gene Arc (a widely established index of neuronal activity), suggesting that the activation of the nELAV-GAP43 cascade reflects a targeting of specific processes rather than a global interference with hippocampal homeostasis., Conclusions: Based on our results, we speculate that cocaine and stress may recruit such a pathway, crucial for physiological learning, potentially contributing to the aberrant engagement of learning mechanisms observed in drug addiction behavior. more...
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- 2011
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12. Modulation of neuroplastic molecules in selected brain regions after chronic administration of the novel antidepressant agomelatine.
- Author
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Calabrese F, Molteni R, Gabriel C, Mocaer E, Racagni G, and Riva MA
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- Animals, Brain anatomy & histology, Brain-Derived Neurotrophic Factor genetics, Brain-Derived Neurotrophic Factor metabolism, Cyclohexanols pharmacology, Cytosol drug effects, Cytosol metabolism, Fibroblast Growth Factor 2 genetics, Fibroblast Growth Factor 2 metabolism, Neuronal Plasticity genetics, Rats, Rats, Sprague-Dawley, Synaptosomes drug effects, Synaptosomes metabolism, Time Factors, Venlafaxine Hydrochloride, Acetamides pharmacology, Antidepressive Agents pharmacology, Brain drug effects, Gene Expression Regulation drug effects, Neuronal Plasticity drug effects
- Abstract
Rationale: Neuronal plasticity is associated with depression, probably as a result of modified expression of proteins important for cellular resiliency. It is therefore important to establish if and how antidepressant drugs may be able to regulate these mechanisms in order to achieve relevant clinical effects., Objective: We investigated the effects of chronic treatment with agomelatine (an MT(1)/MT(2) receptor agonist and 5-HT(2C) receptor antagonist) on the brain-derived neurotrophic factor (BDNF), fibroblast growth factor (FGF-2), and activity-regulated cytoskeleton-associated protein (Arc)., Methods: Animals were treated for 21 days with agomelatine, venlafaxine, or a vehicle and sacrificed 1 h (6 p.m.) or 16 h after the last injection (9 a.m.) to evaluate the messenger RNA (mRNA) and protein expression of these neuroplastic markers in the hippocampus and prefrontal cortex., Results: Agomelatine, but not venlafaxine, produced major transcriptional changes in the hippocampus, where significant up-regulations of BDNF and FGF-2 were observed. Both drugs up-regulated the Arc transcription levels. No effects were observed in the prefrontal cortex. Instead, the levels of BDNF protein were elevated by agomelatine in both regions: the effects of the drug on mRNA levels in the hippocampus and cortex are different, while the effects on the protein seem to have the same cumulative result, suggesting different modulatory mechanisms in the two regions., Conclusions: Our data provide new information regarding the molecular mechanisms that contribute to the chronic effects of the new antidepressant agomelatine on brain function. The ability of agomelatine to modulate the expression of these neuroplastic molecules, which follows a circadian rhythm, may contribute to its antidepressant action. more...
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- 2011
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13. Basal and stress-induced modulation of activity-regulated cytoskeletal associated protein (Arc) in the rat brain following duloxetine treatment.
- Author
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Molteni R, Calabrese F, Mancini M, Racagni G, and Riva MA
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- Animals, Antidepressive Agents pharmacology, Antidepressive Agents therapeutic use, Cytoskeletal Proteins genetics, Cytoskeletal Proteins metabolism, Duloxetine Hydrochloride, Entorhinal Cortex drug effects, Entorhinal Cortex metabolism, Gene Expression, Male, Mesencephalon drug effects, Mesencephalon metabolism, Motor Cortex drug effects, Motor Cortex metabolism, Nerve Tissue Proteins genetics, Nerve Tissue Proteins metabolism, Physical Exertion, RNA, Messenger genetics, RNA, Messenger isolation & purification, Rats, Rats, Sprague-Dawley, Swimming, Thiophenes pharmacology, Time Factors, Up-Regulation, Cytoskeletal Proteins antagonists & inhibitors, Nerve Tissue Proteins antagonists & inhibitors, Stress, Psychological drug therapy, Stress, Psychological etiology, Thiophenes therapeutic use
- Abstract
Rationale: Therapeutic efficacy of antidepressant drugs appears to be related to their ability in producing neuroadaptive changes that restore normal brain function. Activity-regulated cytoskeletal associated protein (Arc) is an effector immediate early gene that plays a fundamental role in activity-dependent neural plasticity in corticolimbic brain regions and has been implicated in the modulation of several functions known to be profoundly perturbed in depressive states., Objective: In the present study, we investigated transcriptional and translational changes of Arc in response to acute or chronic treatment with the novel antidepressant duloxetine., Results: Although a limited increase of Arc messenger RNA (mRNA) levels was found in some structures after acute antidepressant administration, a marked up-regulation of its gene expression was found after chronic treatment, primarily at the level of frontal cortex. The changes observed after prolonged duloxetine administration strongly correlates with those previously reported on brain-derived neurotrophic factor mRNA levels Calabrese et al. (Neuropsychopharmacol 32:2351-2359, 2007). In addition, we found an anatomical-specific influence of chronic duloxetine on stress-dependent Arc modulation, which was limited to the frontal cortex., Conclusions: We suggest that these neuroadaptive changes, among others, might contribute to the normalization of neuroplastic defects associated with mood disorders. more...
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- 2008
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14. Stress and cocaine interact to modulate basic fibroblast growth factor (FGF-2) expression in rat brain.
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Fumagalli F, Di Pasquale L, Caffino L, Racagni G, and Riva MA
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- Animals, Corpus Striatum drug effects, Corpus Striatum metabolism, Fibroblast Growth Factor 2 genetics, Hippocampus drug effects, Hippocampus metabolism, Male, Prefrontal Cortex drug effects, Prefrontal Cortex metabolism, RNA, Messenger metabolism, Rats, Rats, Sprague-Dawley, Cocaine pharmacology, Dopamine Uptake Inhibitors pharmacology, Fibroblast Growth Factor 2 drug effects, Gene Expression Regulation drug effects, Stress, Psychological
- Abstract
Rationale: Our laboratory has previously demonstrated that the expression of basic fibroblast growth factor (FGF-2), a protein involved in survival and maintenance of several cell phenotypes as well as in synaptic plasticity, is modulated by stress (Molteni et al., Brain Res Rev 37:249-258, 2001; Fumagalli et al., Neurobiol Dis 20:731-737, 2005) and cocaine (Fumagalli et al., J Neurochem 96:996-1004, 2006)., Objectives: Since it is widely recognized that stress influences drug seeking, we decided to investigate whether stress, acute or repeated, could influence the changes in FGF-2 gene expression brought about by cocaine., Results: Our data demonstrate that stress and cocaine interact to produce significant changes on FGF-2 expression in rat prefrontal cortex and striatum. In prefrontal cortex, our experiments demonstrated that a single exposure to stress potentiated cocaine-induced FGF-2 elevation, whereas prolonged stress prevented the modulation of the trophic factor in response to cocaine. In striatum, the magnitude of cocaine-induced FGF-2 response is enhanced by repeated stress, whereas no interaction was observed when acute stress and single exposure to cocaine were combined., Conclusions: Our findings demonstrate that stress interacts with cocaine to alter the pattern of FGF-2 expression in a way that depends on whether stress is acute or chronic and in a regionally selective fashion. These results identify a potential molecular target through which stress alters cellular sensitivity to cocaine and might prove useful in understanding the mechanisms underlying brain vulnerability to stress. more...
- Published
- 2008
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15. Differential effects of lithium on platelet protein phosphorylation in bipolar patients and healthy subjects.
- Author
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Zanardi R, Racagni G, Smeraldi E, and Perez J
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- Adult, Blood Platelets metabolism, Cyclic AMP pharmacology, Humans, Male, Phosphorus Radioisotopes, Phosphorylation drug effects, Antimanic Agents pharmacology, Bipolar Disorder blood, Blood Platelets drug effects, Lithium pharmacology
- Abstract
In the present study we have investigated the cAMP-dependent phosphorylation system in platelets of euthymic bipolar patients and healthy volunteers before and after 15 days of lithium treatment. The results showed that 15 days of lithium treatment enhanced the basal and the cAMP-stimulated 32P incorporation in the 22 and 38 kDa phosphoproteins in bipolar patients, but not in healthy subjects. Moreover, we provided further evidence of increased phosphorylation in the 22 kDa platelet phosphoprotein in untreated euthymic bipolar patients when compared with controls. Overall, these findings suggest an implication of protein phosphorylation in the biochemical action of lithium and in the pathophysiology of bipolar disorder. more...
- Published
- 1997
- Full Text
- View/download PDF
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