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S Ferré

Publications and source records attributed to S Ferré.

At least 73 records · Page 4Linked to original sources
PubMed1993

Noradrenergic modulation of midbrain dopamine cell firing elicited by stimulation of the locus coeruleus in the rat.

Electrical stimulation techniques were employed in the chloral hydrate anaesthetized male rat to evaluate if the pontine noradrenergic nucleus locus coeruleus can influence the activity of midbrain dopamine neurons in the ventral tegmental area and zona compacta, substantia nigra. Single-pulse locus coeruleus stimulation evoked an excitation, followed by an inhibition, of the electrical activity of single midbrain dopamine neurons. Neither of these responses were observed in animals pretreated with reserpine, implicating noradrenaline as a mediator. The alpha 1-adrenoceptor antagonist prazosin decreased the excitation, while other adrenoceptor antagonists were without general effect. Burst-type stimulation produced only a more long-lasting inhibition. The influence from the locus coeruleus on midbrain dopamine neurons could be important in behavioural situations involving novelty and reward, and might also be of importance for the actions of psychotropic drugs.

Animals↗
PubMed1993

Dopamine D2 receptor-mediated regulation of serotonin extracellular concentration in the dorsal raphe nucleus of freely moving rats.

Morphological and pharmacological data suggest the existence of a reciprocal interaction between the mesencephalic dopamine (DA) system and the serotonin (5-HT) system originating in the dorsal raphe nucleus (DRN). In the present work, a DA D2 receptor-mediated regulation of 5-HT extracellular concentrations in the DRN is described, by using brain microdialysis in freely moving rats. Local infusion of the nonselective DA agonist apomorphine produced a dose-dependent increase in the extracellular concentration of 5-HT in the DRN, which was prevented by previous infusion of the specific D2 antagonist raclopride but not of the D1 antagonist SCH-23390. Furthermore, local infusion of the selective D2 agonist LY-171,555 increased extracellular 5-HT levels in the DRN, and this effect was also prevented by the previous infusion of raclopride. It is postulated that DA, either from projections from the substantia nigra or the ventral tegmental area or from the DA-containing neurons of the DRN, may increase 5-HT release in the DRN, which, through autoreceptor stimulation, can profoundly influence the activity of ascending serotoninergic neurons.

Animals↗
PubMed1993

The striopallidal neuron: a main locus for adenosine-dopamine interactions in the brain.

Recent pharmacological data suggest that a receptor-receptor interaction between adenosine A2 and dopamine D2 receptors in the brain underlies the behavioral effects of adenosine agonists and adenosine antagonists, such as caffeine and theophylline. According to this interaction, stimulation of A2 receptors inhibits and their blockade potentiates the effects of D2 receptor stimulation. Furthermore, both A2 and D2 receptors are selectively colocalized on GABAergic striopallidal neurons. In this microdialysis investigation the effect of intrastriatal infusion of adenosine and dopamine agonists and antagonists alone or in combination was studied on the release of GABA from the terminals of the striopallidal neuron in awake, freely moving rats. We report that the GABAergic striopallidal neuron, which is a key component of the indirect striatal efferent pathway, is a main locus for A2-D2 interactions in the brain and possibly a main target for the central actions of adenosine agonists and antagonists.

Animals↗
PubMed1992

Dopamine denervation leads to an increase in the intramembrane interaction between adenosine A2 and dopamine D2 receptors in the neostriatum.

We have previously found, in striatal membrane preparations from young (2 months old) rats, that stimulation of adenosine A2 receptors (with the selective adenosine A2 agonist CGS 21680) increases the dissociation constants of high- (Kh) and low-affinity (Kl) dopamine D2 binding sites (labelled with the selective dopamine D2 antagonist [3H]raclopride) without changing the proportion of high affinity binding sites (Rh). In the present study in striatal preparations from adult (6 months old) rats, it was found that in addition to the increase in both Kh and Kl values, stimulation of adenosine A2 receptors is associated with an increase in Rh. These results suggest that, in the adult rat, adenosine A2 stimulation may inhibit the behavioural effects induced by dopamine D2 stimulation both by decreasing the affinity and the transduction of dopamine D2 receptors. We have also studied the intramembrane A2-D2 receptor interaction in an experimental model of Parkinson's disease, namely in rats with a unilateral 6-OH-dopamine-induced lesion of the nigro-striatal dopamine pathway. It was found that a unilateral dopamine denervation is associated with a higher density of striatal dopamine D2 receptors in the order of 20%, without any change in their affinity compared with the unlesioned neostriatum. Furthermore, the density (Bmax values) of dopamine D2 receptors in the contralateral neostriatum was significantly higher (about 20%) than in the striatum from naive animals. This finding suggests that an unilateral dopamine denervation also induces compensatory long-lasting changes of dopamine D2 receptors in the contralateral neostriatum.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1991

Stimulation of adenosine A2 receptors induces catalepsy.

The central administration of the adenosine A2 agonist CGS 21680 induced catalepsy in the rat. This effect was counteracted by the previous systemic administration of the adenosine antagonist theophylline or the D2 agonist BHT-920. These results are in agreement with the view that adenosine A2 receptors regulate central dopamine D2 transmission and underline the potential antipsychotic activity of A2 agonists.

Adenosine↗
PubMed1991

Postsynaptic dopamine/adenosine interaction: I. Adenosine analogues inhibit dopamine D2-mediated behaviour in short-term reserpinized mice.

Mice pretreated with reserpine 5 mg/kg (4 h prior to the start of motor activity recording) showed locomotor activation after the administration of the D-2 agonist bromocriptine (5 mg/kg). This bromocriptine-induced locomotor activity was dose dependently inhibited by the co-administration of a D-2 antagonist (sulpiride) and dose dependently potentiated by a D-1 agonist (CY 208-243). The potentiating effect of the D-1 agonist could be inhibited by either a D-1 or a D-2 antagonist (SCH 23390 1 mg/kg or sulpiride 100 mg/kg, respectively). The bromocriptine-induced locomotor activity was not altered by either blockade of D-1 dopaminergic receptors (SCH 23390 1 mg/kg) or by co-administration of a greater dose of reserpine (10 mg/kg) plus the dopamine synthesis inhibitor, alpha-methyl-p-tyrosine (200 mg/kg). The adenosine agonists, L-PIA (a preferentially A-1 adenosine agonist) and NECA (an A-1 and A-2 adenosine agonist with above 10-fold greater affinity for A-2 than L-PIA) inhibited in a dose-dependent manner the effect of bromocriptine, NECA being above ten times more potent than L-PIA. The findings show that bromocriptine stimulates postsynaptic D-2 receptors in dopamine-depleted mice and that this effect can be inhibited by adenosine stimulation. The existence of a postsynaptic D-2/A-2 interaction is suggested, the stimulation of A-2 receptors causing an inhibition of responses elicited by postsynaptic D-2 stimulation.

Adenosine↗
PubMed1991

Postsynaptic dopamine/adenosine interaction: II. Postsynaptic dopamine agonism and adenosine antagonism of methylxanthines in short-term reserpinized mice.

Caffeine and its first-stage metabolites (paraxanthine, theophylline and theobromine) caused a significant potentiation of the locomotor activity induced by bromocriptine, 5 mg/kg, in mice pretreated with reserpine, 5 mg/kg (4h prior to the start of motor activity recordings). None of these substances significantly enhanced locomotor activity in reserpinized mice when administered alone. The rank order of potency was caffeine greater than paraxanthine greater than theophylline greater than theobromine. A high dose of a D-2 antagonist (sulpiride 100 mg/kg) caused a marked inhibition of the locomotor activity induced by bromocriptine, 5 mg/kg, plus 25 mg/kg of caffeine, paraxanthine or theophylline. However, a high dose of a D-1 antagonist (SCH-23390 1 mg/kg) caused a significant decrease of the locomotor activity induced by bromocriptine 5 mg/kg, plus 25 mg/kg of caffeine or paraxanthine, but did not change the locomotor activity caused by bromocriptine, 5 mg/kg, plus theophylline 25 mg/kg. The inhibitory effect of 5'-(N-ethyl)carboxamido-adenosine (NECA), 0.025 mg/kg, on bromocriptine-induced locomotor activation in reserpinized mice was reversed by the simultaneous administration of 10, 25 and 50 mg/kg of caffeine, paraxanthine or theophylline. The rank order of potency for reversal was theophylline greater than paraxanthine = caffeine. We suggest that methylxanthines act postsynaptically by potentiating the effects of D-2 stimulation and that this potentiation can be produced by D-1 agonism (paraxanthine or caffeine) and by adenosine antagonism (theophylline, paraxanthine or caffeine), most probably involving A-2 receptors.

Adenosine↗
PubMed1990

Paraxanthine displaces the binding of [3H]SCH 23390 from rat striatal membranes.

We present evidence showing that paraxanthine (1,7-dimethylxanthine), the main metabolite of caffeine in man, displaces the binding of [3H]SCH 23390, a radioligand which selectively labels dopamine D-1 receptors when used at low concentrations, from striatal membranes of the rat. The displacement was competitive and indicated the existence of two affinity states (Hill coefficient = 0.49; K(high) = 0.15 microM; K(low) = 95.9 microM, %R(high) = 32.4). When the stable GTP analog Gpp(NH)p was included, the displacement curve indicated the presence of only the low-affinity state (Hill coefficient = 1.16; Ki = 72.1 microM). However, paraxanthine did not displace the specific binding of [3H]spiperone. After injection of 30 mg/kg s.c. of caffeine, a maximum of 10 microM of paraxanthine was found in striatal homogenates, which could be sufficient to occupy dopamine D-1 receptors. Our results suggest that a dopaminergic action of paraxanthine could be involved in the behavioural stimulation produced by caffeine.

Animals↗
PubMed1990

T-maze performance in rats following chronic neuroleptic treatment.

The effects of chronic haloperidol treatment (0.5 mg/kg/day for 21 days) on maze learning in the rat were studied. There were no differences between haloperidol- and saline-treated groups in percentage of correct responses, but the latency to respond was longer and extinction was faster in the haloperidol-treated group. We speculated that differences between both groups were due to a decrease of appetitive motivation in haloperidol-treated animals, probably caused by a decrease of dopaminergic neurotransmission.

Animals↗
PubMed1990

Is experimental catalepsy properly measured?

Following logarithmic transformation (ln) of total duration of haloperidol-induced catalepsy in the rat, measured by means of the bar test, a normalization of the results is achieved. With the help of this transformation we have been able to study what are probably the most important variables involved in the measuring of experimental catalepsy and to establish some criteria for a better use of such measures: 1) repeated measures of catalepsy have to be taken in order to avoid the stress-induced inhibition of catalepsy caused by the new experimental situation, 2) the dose of neuroleptic used has to be sufficiently low to permit the measurement of total or real duration of catalepsy between two determinations, and 3) the dose of neuroleptic has to be sufficiently high to prevent the development of a learned "pseudocatalepsy."

Adrenal Glands↗
PubMed1989

Relationship between rotational behaviour induced by apomorphine and caffeine in rats with unilateral lesion of the nigrostriatal pathway.

The contralateral rotational behaviour produced by apomorphine and caffeine has been studied in 100 rats with unilateral lesion of the nigrostriatal pathway induced with 6-OHDA. Rats with a two-peak rotational pattern induced by apomorphine, showed a greater number of contralateral turns, induced by apomorphine and caffeine, than rats which did not show this rotational pattern. A correlation was observed between the number of rotations induced by apomorphine and those induced by caffeine. A relationship between the two-peak rotational pattern induced by apomorphine and the initial-peak pattern induced by caffeine was also observed.

Animals↗
PubMed1989

Rotational behaviour induced by theophylline in 6-OHDA nigrostriatal denervated rats is dependent on the supersensitivity of striatal dopaminergic receptors.

We studied apomorphine- and theophylline-induced rotational behaviour in rats with a unilateral 6-hydroxydopamine lesion of the dopaminergic nigrostriatal pathway. It was seen that there was a direct correlation between the number of apomorphine- and theophylline-induced contralateral turns. These data suggest the existence of a relationship between theophylline-induced rotational behaviour and the degree of supersensitivity of the striatal dopaminergic receptors. Because the rotational behaviour induced by theophylline is in the same direction as dopaminergic agonists, contralateral to the nigrostriatal pathway lesion, these results suggest the possibility of a direct dopaminergic agonism of methylxanthines.

Animals↗
PubMed1988

Comparison between apomorphine and amphetamine-induced rotational behaviour in rats with a unilateral nigrostriatal pathway lesion.

Apomorphine and amphetamine-induced rotational behaviour in 310 rats with a unilateral 6-OHDA nigrostriatal pathway lesion has been studied. Animals presenting an apomorphine-induced contralateral rotation with a "two-peak" pattern, showed a greater number of contralateral turns induced by apomorphine and fewer ipsilateral turns induced by amphetamine than rats without this pattern. In addition, we have not found any correlation between apomorphine and amphetamine-induced turning behaviour.

Amphetamine↗
PubMedDate not supplied

Receptor-receptor interactions as an integrative mechanism in nerve cells.

Several lines of evidence indicate that interactions among transmission lines can take place at the level of the cell membrane via interactions among macromolecules, integral or associated to the cell membrane, involved in signal recognition and transduction. The present view will focus on this last subject, i.e., on the interactions between receptors for chemical signals at the level of the neuronal membrane (receptor-receptor interaction). By receptor-receptor interaction we mean that a neurotransmitter or modulator, by binding to its receptor, modifies the characteristics of the receptor for another transmitter or modulator. Four types of interactions among transmission lines may be considered, but mainly intramembrane receptor-receptor interactions have been dealt with in this article, exemplified by the heteroregulation of D2 receptors via neuropeptide receptors and A2 receptors. The role of receptor-receptor interactions in the integration of signals is discussed, especially in terms of filtration of incoming signals, of integration of coincident signals, and of neuronal plasticity.

Animals↗