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Biomedical subjects

L Pulvirenti

Publications and source records attributed to L Pulvirenti.

45 records · Page 3Linked to original sources
PubMed1985

Repeated treatment with amitriptyline reduces immobility in the behavioural 'despair' test in rats by activating dopaminergic and beta-adrenergic mechanisms.

Seven days of treatment with amitriptyline 10 mg kg-1 day-1, reduced the immobility time in the behavioural 'despair' test in rats. 0.5, but not 0.25 mg kg-1 haloperidol significantly counteracted the reduction of immobility caused by amitriptyline. Its anti-immobility effect was reduced by 50 and 100 mg kg-1 sulpiride, another blocker of dopamine receptors, and 5 mg kg-1 (+/-)-propranolol, a beta-adrenolytic drug. Prazosin, 3 mg kg-1, an antagonist of post-synaptic alpha-adrenoceptors, had no effect. It is suggested that dopaminergic and beta-adrenoceptors mediate the anti-immobility effect of repeated amitriptyline treatment in rats.

Amitriptyline↗
PubMedDate not supplied

SDZ-205,152, a novel dopamine receptor agonist, reduces oral ethanol self-administration in rats.

The effects of SDZ-205,152, a synthetic mixed D1/D2 dopamine receptor agonist, was investigated in rats trained to orally self-administer ethanol (10% w/v) in a free-choice, two-lever operant task. Pretreatment with SDZ-205,152, at doses of 0.5-5.0 mg/kg subcutaneously 30 min prior to limited access to 10% ethanol and water, selectively reduced ethanol-reinforced responding without affecting responses for water. These results demonstrate that ethanol-reinforced responding was attenuated by SDZ-205,152 and suggests that dopamine neural systems may mediate, in part, the reinforcing properties associated with voluntary ethanol self-administration.

Animals↗
PubMedDate not supplied

Corticotropin-releasing factor microinfused into the locus coeruleus produces electrocortical desynchronization and immunosuppression.

In freely moving rats with cannulae chronically implanted into the locus coeruleus (LC), the effects of corticotropin-releasing factor (CRF) on electrocortical (ECoG) spectrum power activity and on immune mechanisms (splenocyte mitotic response to concanavalin A, Con A, and lipopolysaccharide, LPS, natural killer cell, NK, activity) were assessed. CRF (100-300 ng) microinfused into the LC produced marked ECoG desynchronization characterized by a significant decrease in total voltage power as well as in power of frequency bands of 0.25-3 and 3-6 Hz. These effects lasted 30-60 min according to the dose. A prior administration of alpha-helical CRF(9-41) (200 ng into the LC 15 min before) prevented ECoG desynchronization induced by CRF (100 ng). In addition, CRF (100 ng) given into the LC produced a significant decrease 45 min later in the splenocyte proliferative response to Con A and LPS and a significant fall of NK activity. These effects were prevented by prior microinfusion into the same site of alpha-helical CRF (200 ng). In conclusion, the present experiments show that CRF given into the LC produces an intense state of ECoG desynchronization accompanied by marked immunodepression and suggest that LC is an important site in the brain through which CRF exerts its immunosuppressive activity.

Animals↗
PubMedDate not supplied

Evidence for an involvement of dopamine D1 receptors in the limbic system in the control of immune mechanisms.

Indirect evidence suggests that dopamine within the brain may participate in the regulation of immune responses both in humans and in rodents. The aim of the present study was to investigate the possible modulatory role played by specific dopamine D1 receptor subtypes within discrete sites of the brain dopaminergic pathways. Mitogen responsiveness of splenocytes and natural killer (NK) cell activity were measured in rats following microinfusion of SKF 38393, a specific dopamine D1 receptor agonist, into the ventral tegmental area, the amygdala, the nucleus accumbens and the CA1 area of the hippocampus. We report here that microinfusion of SKF 38393 (100 nmol) within the central amygdala increased the proliferative response of splenocytes to concanavalin A (ConA) while it did not modify the proliferative response of splenocytes to lipopolysaccharide (LPS) or NK cell activity. On the contrary, microinfusion of SKF 38393 into the nucleus accumbens decreased the proliferative response of splenocytes to ConA and LPS, while NK cell activity remained unchanged. Similarly, microinfusion of SKF 38393 into the CA1 area of the hippocampus decreased the proliferative response of splenocytes to LPS, but not to ConA and did not affect NK cell activity. Finally, microinfusion of SKF 38393 into the ventral tegmental area did not significantly modify the proliferative response of splenocytes to either ConA or LPS and did not affect NK cell activity. All immunological changes evoked through the different areas of the brain following microinfusion of SKF 38393 were prevented by systemic administration of SCH 23390, a specific D1 receptor antagonist.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗
PubMedDate not supplied

Physiological significance of long-term potentiation.

Long-term potentiation (LTP) is a form of synaptic plasticity that follows repetitive, high frequency stimulation of excitatory presynaptic fibers. It produces a long-lasting enhancement of synaptic strength that is usually revealed as an increased size of excitatory postsynaptic potentials. It is most prominent in the hippocampus, although it may be evoked in other brain regions. Use-dependent modifications in synaptic function are probably the basis of learning and memory, thus the study of LTP may represent a useful model for investigating the physiological mechanisms underlying the process of information storage.

Animals↗
PubMedDate not supplied

Neural plasticity and memory: towards an integrated view.

The search for the neural determinants of learning and memory has recently focused on phenomena of neural plasticity. The present paper will try to review and relate the functional significance of such specific plastic changes within neural elements to the process of learning in several species and cell types. Pioneer work proposed in simple organisms and recent emerging evidence on the role of the NMDA receptor complex and calcium-related events will be analyzed in the light of experimental findings suggesting that common biochemical events may underlie different forms of experience-dependent neural adaptation.

Animals↗
PubMedDate not supplied

Functional neurotoxicity of drugs of abuse.

The epidemic growth of the use of controlled substances has brought their toxic effects to clinical attention. Several drugs of abuse are known to induce nerve cell toxicity after acute and chronic administration. In addition, it has been suggested that the three main classes of abused substances, namely psychostimulants, ethanol and opiates, also induce changes in the function of discrete neural pathways. These alterations may eventually be responsible for the loss of behavioral control often observed during the natural history of the addiction process. Therefore, biochemical and behavioral toxicity deserve equal attention. A complex neural network within the forebrain limbic system which has been characterized over the past few years seems to mediate drug-seeking behavior and maintain drug self-administration in rodents. A striking similarity has been observed between this circuit and the neural substrates of motivated behavior. This review focuses on the possibility that drugs of abuse may acquire significance as reinforcers by usurping the physiological role of this circuit which normally operates to ensure survival of the individual. This may represent a subtle mechanism through which drugs of abuse may induce behavioral toxicity even in the absence of nerve cell loss.

Animals↗
PubMedDate not supplied

Evidence that CRH microinfused into the locus coeruleus decreases cell-mediated immune response in rats.

Rat/human-corticotropin-releasing hormone (CRH) microinfused unilaterally into the locus coeruleus (LC) of awake, chronically cannulated rats produced intense behavioral stimulation accompanied by a marked decrease of the proliferative response of splenocytes to Con A and LPS and natural killer activity. These effects were specifically prevented by prior administration into the same site of the CRH antagonist (alpha-helical CRH [9-41]). The present results confirm that a strict relationship exists between the CNS and cell-mediated immunity; in addition, they also indicate that CRH produces its behavioral and immune changes by an interaction with specific receptors and that one of the main sites through which CRH exerts these effects is represented by the LC.

Animals↗