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F Vives

Publications and source records attributed to F Vives.

At least 37 records · Page 2Linked to original sources

Melatonin-dopamine interaction in the striatal projection area of sensorimotor cortex in the rat.

The excitatory response to motor cortex stimulation of 201 striatal neurones was recorded electrophysiologically to test the effects of melatonin (aMT) and/or D1 and D2 antagonists. Iontophoresis of aMT attenuated the excitatory response in 68.5% of neurones, with a latency of 2-4 min and enhanced the excitatory response in 11.9% of the neurones; 19.6% showed no change in response. Iontophoresis of sulpiride (D2 antagonist) produced an immediate increase in the excitatory response in 62.8% of neurones, an attenuation in 2.3% and no change in the response of 34.9%. The ejection of sulpiride counteracted the aMT-dependent inhibition of the excitatory response of striatal neurones. SCH-23390 (D1 antagonist) iontophoresis had no significant effect. The results show that the same striatal units may be driven by aMT and D2 receptors. However, the significant difference in the latency of the responses suggests that the effects of these two substances are mediated by different receptor/intracellular messengers.

Animals↗

Age-related changes of neuronal responsiveness to melatonin in the striatum of sham-operated and pinealectomized rats.

The age-related changes and the acute effects of intravenous melatonin on the activity of striatal neurons of 1-, 3-, 6-, 12-, and 18-month-old sham-operated and pinealectomized rats were investigated. There was a decline in responsiveness from 3- to 18-months of age, although in sham-pinealectomized rats the responses were similar at 12 and 18 months; in pinealectomized rats, the neuronal responses were quite stable at early ages. In all age groups of sham-pinealectomized rats, neuronal firing decreased in most cells, and increased in only a small percentage of cells after intravenous melatonin injection (100 ng/kg). However, in pinealectomized rats, the injection of melatonin at the same doses significantly increased the firing rate of most neurons compared to that in sham-operated animals at all age-groups, while the number of neurons showing an inhibitory response decreased. These results indicate that melatonin may be involved in the modulation of the activity of striatal neurons and demonstrates an age-dependent reduction in striatal sensitivity to melatonin. They also suggest that other compounds of pineal origin may modulate the activity of motor control centers.

Aging↗

Electrophysiological study of the response of medial prefrontal cortex neurons to stimulation of the basolateral nucleus of the amygdala in the rat.

The neural connections from the basolateral nucleus of the amygdala (BLA) to the medial prefrontal cortex (MPC) in urethane-anesthetized rats were investigated. Extracellular recordings were made from 200 neurons with spontaneous firing in the MPC, and the BLA was electrically stimulated. The most frequent response to BLA stimulation was inhibition (63.5%). Excitatory responses were found in 17 units (8.5%), while 56 neurons (28%) did not change their spontaneous firing after BLA stimulation. Inhibitory responses showed a wide range of latencies, suggesting the coexistence of mono- and polysynaptic pathways. On the contrary, the excitatory responses seem to be mediated by a monosynaptic pathway. BLA projections to the MPC play a predominantly inhibitory role in the spontaneous activity of prefrontal neurons. This inhibition may modulate central motor systems and motivated behaviors.

Action Potentials↗

Plasma and CSF levels of immunoreactive beta-endorphin in algic peaks of patients with herniated intervertebral discs.

Plasma and CSF levels of beta-Endorphin (beta-End) were measured by radioimmunoassay in three groups of human subjects. The first group consisted of healthy adults, and only plasma beta-End was determined. The second group consisted of patients showing non-painful neurological diseases. The third group consisted of patients suffering from acute pain due to herniated intervertebral discs. In the last two groups, beta-End levels were measured in plasma and CSF. The results showed that plasma levels of beta-End were similar in the first two groups of patients. In contrast, patients with acute pain showed significantly increased levels of beta-End in plasma. CSF levels of beta-End did not show significant differences among the groups. The results suggest that the increase in plasma levels of beta-End was a consequence of the stress produced by acute pain.

Humans↗

Beta-endorphin and ACTH in plasma: effects of physical and psychological stress.

The effects of the expectancy of an official race (22000 m) and the performance of this last event on plasma levels of beta-Endorphin (B-End) and ACTH have been assessed. In a group of nine athletes, samples were obtained first in basal conditions; second in the day of the run before the warming up period and third after running. B-End immunoactivity was increased from 15.7 +/- 2.0 pg/ml to 23.4 +/- 2.5 pg/ml before the run and up to 30.6 +/- 2.9 pg/ml after the trial. ACTH levels were increased from 8.4 +/- 1.2 pg/ml to 17.9 +/- 2.3 pg/ml before running and up to 36.2 +/- 3.9 pg/ml after running. The results suggest that psychological and physical stress act synergically to increase the levels of B-End and ACTH during the practice of physical exercise.

Adrenocorticotropic Hormone↗

Lesions of connections of the medial prefrontal cortex in rats: differential effects on self-stimulation and spontaneous motor activity.

The effects of lesions of the mediodorsal nucleus of the thalamus (MD) and the nucleus caudate putamen (CP) on self-stimulation (SS) of the medial prefrontal cortex (MPC) were investigated. After bilateral electrolytic lesions of the MD or the anteromedial segment of the CP, SS rate and spontaneous motor activity (SMA) were measured. Both MD and CP lesions induced a significant decrease in SS. After 8 days post-lesion, SS rate recovered to pre-lesion levels. SMA did not change significantly after MD lesion. However, SMA showed a significant decrease the 1st and the 5th days after lesioning the CP. The results suggest that the MD and possibly the CP are associated with SS, although it appears that they do not have an essential but rather a modulatory role. The recovery of SS occurs within a few days, presumably due to the compensatory effect of other pathways and structures. The results are also discussed in relation to the effect found after electrolytic lesion of ventrotegmental area and locus coeruleus.

Animals↗

Effects of agonists and antagonists of cholinergic receptors on self-stimulation of the medial prefrontal cortex of the rat.

The effects of agonists and antagonists of muscarinic and nicotinic receptors on self-stimulation (SS) of the medial prefrontal cortex (MPC) were investigated. Rats, implanted chronically with monopolar electrodes in the MPC, received subcutaneous injections of nicotine (0.2, 0.4 and 0.8 mg/kg), mecamylamine (2.0, 4.0 and 8.0 mg/kg), pilocarpine (0.5, 1.0, 2.0 and 4.0 mg/kg), scopolamine (0.05, 0.1, 0.2, 0.4 and 0.8 mg/kg) and physostigmine (0.1, 0.2 and 0.4 mg/kg). In order to assess the possible non-specific effects of drugs such as sedation or motor dysfunction, spontaneous locomotor activity (SLA) was used as control. In those groups of rats in which the drugs produced an effect on SS, an operant behaviour for drinking (DB) on an FR-10 schedule was also used as control. Nicotine and mecamylamine had no effect on SS. Both pilocarpine and physostigmine produced a decrease in SS, SLA and DB. Scopolamine, on the contrary, produced a dose-related decrease on SS rate, which was accompanied by a facilitatory effect on SLA and DB. These results suggest that only muscarinic receptors could play a specific role on SS of the MPC.

Acetylcholine↗

Electrophysiological study of the effects of D1 and D2 dopamine antagonists on the interaction of converging inputs from the sensory-motor cortex and substantia nigra neurons in the rat.

The interaction of stimulation of the cerebral cortex and of the substantia nigra on the activity of neostriatal neurons was investigated in urethane-anesthetized rats. Neurons of the dorsal striatum were activated by single pulse stimulation of the sensory-motor cortex. The effects of nigral conditioning stimulation on this excitatory response of striatal neurons to cortical stimulation were studied in a series of parametric experiments in which the length of the train of pulses and the intensity of the nigral stimulation were varied. One and five pulses of nigral conditioning stimulation had little or no effect. Ten pulses of nigral conditioning stimulation reduced the excitatory response, the magnitude of the reduction being greater with higher current intensities. In another series of experiments, the effects of dopaminergic receptor antagonists on the interaction of cortical and nigral inputs to striatal neurons were studied. Sulpiride, a D2 antagonist, reversed the attenuating effects of nigral conditioning stimulation on the excitatory response of striatal neurons to cortical stimulation, whereas SCH 23390 a D1 antagonist, had no effect. The present findings support the hypothesis that the nigrostriatal dopaminergic pathway modulates the excitatory response of striatal neurons to cortical stimulation by means of dopamine D2 receptors.

Action Potentials↗

Electrophysiological evidence that the mediodorsal nucleus of the thalamus is a relay between the ventral pallidum and the medial prefrontal cortex in the rat.

The neural connections from the ventral pallidum (VP) through the mediodorsal nucleus of the thalamus (MD) to the medial prefrontal cortex (MPC) were investigated. Extracellular recordings were made from 219 neurons in the medial and lateral portions of the MD and the VP and the MPC were stimulated. The most frequent response to VP stimulation was inhibition and inhibition preceded by excitation. Also, the most frequent response of MD units to MPC stimulation was inhibition and inhibition preceded by excitation. Nineteen of 26 MD units, activated antidromically by MPC stimulation, responded orthodromically to VP stimulation. The most frequent orthodromic response of these MD output neurons was inhibition and inhibition preceded by excitation. GABA iontophorized onto MD neurons reduced their rate of discharge. GABA and picrotoxin iontophorized onto MD neurons did not influence the inhibitory or excitatory responses to VP stimulation. These electrophysiological results support previous anatomical findings of connections between the VP and the MPC by way of the MD. MD output neurons to the MPC receive mostly inhibitory inputs from VP afferents. A high proportion of MD neurons respond orthodromically to both VP and MPC stimulation, suggesting the convergence of synaptic inputs from these structures to the same MD units.

Animals↗

Opioid peptides and self-stimulation of the medial prefrontal cortex in the rat.

The possible involvement of opioid peptides as part of the neurochemical substrates of self-stimulation (SS) in the medial prefrontal cortex (MPC) of the rat was investigated in two different groups of rats bilaterally implanted with monopolar electrodes in the MPC. In the first group, morphine (5, 10, and 20 micrograms) and an enkephalin analogue (BW 180) (5, 10, 20 and 40 micrograms) were injected through cannulae implanted into the lateral ventricles (IV). In the second group, naloxone (0.04, 0.4, and 1.6 micrograms) and morphine (5, 10 and 20 micrograms) were injected through cannulae implanted into the MPC, 1.5 mm above the tip of the stimulating electrodes. In the first group, spontaneous motor activity (SMA) was measured as a control for non-specific effects (sedation or motor dysfunction). In the second group SS, contralateral to the microinjected side, served as control. SS and SMA were were measured 1 and 2 h postinjection. One hour after IV injection of morphine SS was not affected, although SMA was decreased. Two hours postinjection, on the contrary, SS was increased while SMA remained decreased. Similar effects were found with IV microinjections of BW 180. Naloxone, intraperitoneally injected, reversed all these effects. Naloxone or morphine injected intracerebrally (MPC) produced no changes in SS either in the injected or in the contralateral side, which served as control. The present results suggest that the effects found with IV injections of opioids on SS of the MPC are indirect (through activation of other brain areas) and not mediated by a direct action on the neurochemical substrates underlying this behaviour in the MPC.

Animals↗

Effects of agonists and antagonists of D1 and D2 dopamine receptors on self-stimulation of the medial prefrontal cortex in the rat.

The possible participation of D1 versus D2 dopamine receptors in mediating dopaminergic neurotransmission of self-stimulation (SS) in the medial prefrontal cortex (MPC) of the rat was studied neuropharmacologically. Intracerebral as well as intraperitoneal injections of agonists and antagonists of dopamine receptors were used in this study. In all experiments performed with systemic injections, spontaneous motor activity (SM) was measured parallel to self-stimulation behavior as control for non specific effects of the drugs. Intracranial injections were done unilaterally serving SS of the contralateral side (not injected or injected with 0.9% NaCl) as control in the same animals. Spiroperidol and pimozide were used as D1-D2 dopamine antagonists, while sulpiride was used as a specific D2 antagonist. Apomorphine was used as D1-D2 agonist, while bromocriptine and lergotrile were used at doses in which these ergot drugs are considered predominantly D2 agonists. Sulpiride, intraperitoneally or intracerebrally injected at the same locus at which the stimulating electrode was located produced no effect on SS. On the contrary, the D1-D2 antagonists, spiroperidol and pimozide intraperitoneally or intracerebrally injected produced a dose-dependent decrease on SS. On the basis of these data it is suggested, that the dopamine neurotransmission involved in SS of the MPC is mediated via D1 dopamine receptors. This suggestion is further emphasized by the results obtained with the agonists, apomorphine, bromocriptine and lergotrile. Apomorphine produced a dose-related decrease on SS and a decrease at lower doses and an increase at higher doses on SM. Bromocriptine and lergotrile had, on the contrary, no effect on SS and a dose-related decrease on SM.

Animals↗

Afferent pathways to points of self-stimulation in the medial prefrontal cortex of the rat as revealed by the horseradish peroxidase technique.

Afferent projections to points of self-stimulation (SS) in the medial prefrontal cortex (MPC) of the rat were studied using the horseradish peroxidase (HRP) technique. Intracranial microinjections of HRP (30%) were delivered at the same stereotaxic points at which the electrodes eliciting SS were located. Retrogradely transported HRP labeled neurons in different thalamic, hypothalamic, mesencephalic and pontine areas. In the thalamus, labeled neurons were found in the dorsomedial, anteromedial, anteroventral, ventral, ventromedial, posteromedial, paratenial, parafascicular nuclei and n. reuniens. Labeled neurons in mesencephalic areas were found in the n. interpeduncularis, ventral tegmental area (AVT) and substantia nigra (SN). In the pons, labeled neurons were found in the locus coeruleus and in the periaqueductal gray. Other nuclei in which labeled neurons were also found were: lateral hypothalamus (LH), periventricular gray and zona incerta (ZI). Theoretically it is possible that all these afferent areas contribute to SS of MPC. This assumption is discussed and criticized in connection with previous literature on SS. It is suggested that only specific areas and their projections are good candidates for the neural mechanisms involved in the reward produced by electrical stimulation of the prefrontal cortex.

Afferent Pathways↗

Monoamines and self-stimulation of the medial prefrontal cortex in the rat.

The participation of noradrenaline (NE) and serotonine (5-HT) in self-stimulation (SS) of the medial prefrontal cortex (MPC) in the rat has been studied. Three groups of rats with bilateral electrodes implanted into the MPC were used in these experiments. In one of the groups, electrodes were also implanted into the locus coeruleus. In the first group, the rats received systemic injections of the following drugs: clonidine (alpha-agonist), phenoxybenzamine (alpha-antagonist), isoproterenol (beta-agonist) and propranolol (beta-antagonist). In the second group, p-chlorophenylalanine (a 5-HT synthesis inhibitor) was administered intragastrically and SS measured during the following 16 days. In these two groups of rats and previous to every SS session, spontaneous motor activity (SM) was measured as control for non specific effects of the drugs. In a third group of rats, lesions of the locus coeruleus were performed unilaterally and SS measured in both prefrontal cortex during the following 16 days post-lesion. SS contralateral to the lesioned side served as control for non-specific effects of the lesions. After all these treatments, SS of the MPC was not specifically affected. Our results suggest the non participation of NE and 5-HT terminals in the neural substrates underlying SS of the MPC.

Adrenergic alpha-Antagonists↗

Effect of insulin on acetate metabolism in chicken adipocytes.

The effects of insulin on the metabolism of acetate-U-14C in isolated chicken adipocytes have been investigated. Insulin added in vitro at physiological concentrations did not stimulate the incorporation of acetate-U-14C into triglycerides or CO2 when the acetate was present alone. In the presence of glucose 11m M, however, insulin stimulated significantly lipogenesis from acetate. This is an indirect action mediated by glucose.

Acetates↗

Evidence for an involvement of acetylcholine in self-stimulation of the prefrontal cortex in the rat.

The effects of injections of antagonists of muscarinic and nicotinic receptors on self-stimulation of the prefrontal cortex in the rat were studied. The results of this investigation suggest that acetylcholine is involved in self-stimulation of the prefrontal cortex through activation of muscarinic receptors, and also suggest a possible interaction between acetylcholine and dopamine in mediating self-stimulation of this area of the brain.

Acetylcholine↗