Selective blockade of mGlu5 metabotropic glutamate receptors is protective against methamphetamine neurotoxicity.

Methamphetamine (MA), a widely used drug of abuse, produces oxidative damage of nigrostriatal dopaminergic terminals. We examined the effect of subtype-selective ligands of metabotropic glutamate (mGlu) receptors on MA neurotoxicity in mice. MA (5 mg/kg, i.

A new GABA-A receptor subtype coupled with Ca++/Cl- synporter modulates aminergic release from rat brain neuron terminals.

The aim of the present study was to give a better characterization of GABA receptors that modulate aminergic release. GABA or muscimol (15 microM) increased basal noradrenaline (3H-NA) release but reduced the following K+-evoked 3H-NA release in the synaptosomes from rat cerebellar cortex. Bicuculline and picrotoxin counteracted these two effects.

An immunohistochemical analysis of nm23 gene product expression in uveal melanoma.

Uveal melanoma is characterized by an unpredictable clinical course, during which metastatic disease may occur after a prolonged and, at present, undefinable disease-free interval. Because of its relative rarity and the dispersion of cases, the possible genetic alterations implicated in the invasive and metastatic behaviour of this ocular neoplasm have not yet been characterized. The aim of this immunohistochemical retrospective study was to assess the expression of nm23 gene product, proposed to be a metastasis-suppressor gene, in uveal melanoma and to analyse its prognostic significance in relation to the various conventional histopathological parameters, currently considered the major prognostic indicators in this intra-ocular neoplasm.

Influence of prelimbic and sensorimotor cortices on striatal neurons in the rat: electrophysiological evidence for converging inputs and the effects of 6-OHDA-induced degeneration of the substantia nigra.

These studies were designed to investigate whether there are convergent prelimbic and sensorimotor cortical inputs onto striatal neurons in the rat and whether dopaminergic (DA) nigrostriatal fibers regulate these inputs. The influence of the nigrostriatal DA system was assessed in rats with either small or large 6-hydroxydopamine-induced lesions of the substantia nigra. In normal rats 39 out of 74 neurons (52.

Age-related changes in rat brain monoamines release: peculiarity of dopamine release.

Our aim has been to investigate the ability of the rat brain to retain its level of neurotransmitter release over life. We have investigated the neurotransmitter release from the rat brain synaptosomes prelabeled with 3H-DA, 3H-NA, or 3H-5HT, and perfused with Krebs-Ringer medium alone (basal release) or containing a high K+, calcium ionophore, tyramine or amphetamine (evoked release). Brain areas have been dissected of animals 45 days and 4, 6, and 11 months old.

5HT2-receptors and serotonin release: their role in human platelet aggregation.

Involvement of 5HT2 receptors in human platelet aggregation was assessed by studying the effect of ADP, epinephrine and thrombin on 3H-5HT release from platelets. The release experiments were made with a perfusion method to preserve any compound, released or formed by platelet, from interacting with platelet itself. In these conditions, aggregation does not occur, as confirmed by Scanning Electron Microscopy.

Rat brain alpha 2-pre- and postsynaptic receptors are different or differently modulated?

In order to get better characterization of alpha 2-pre- and postsynaptic noradrenergic receptors in the rat brain, we investigated the alpha 2-receptor changes which take place during a 12-day treatment with the alpha 2-antagonists yohimbine (4 mg/kg) and mianserin (10 mg/kg). These treatments caused a significant increase in the sensitivity of hypothalamic synaptosomes to the inhibitory action of the noradrenergic agonist clonidine on the 3H-noradrenaline release elicited by K depolarization. Frontal cortex alpha 2-autoreceptors were not affected by drug treatments.

Long-term treatment with clonidine and alpha-receptors in the brain of normotensive rats.

The aim of the present study was to investigate whether or not changes in rat brain alpha-adrenoceptors take place during chronic treatment with a low dose of clonidine. Male Wistar normotensive rats were treated with clonidine (0.1 mg/kg)i.

Etomidate inhibits prolactin release but not through a dopaminergic mechanism.

A short-acting non-barbiturate intravenous general anaesthetic, etomidate, when administered i.v. lowered serum prolactin levels in the rat.

Effects of naloxone on the secretion of prolactin and corticosterone induced by 5-hydroxytryptophan and a serotonergic agonist, mCPP.

The effects of naloxone, an opiate "pure" receptor antagonist, on the release of prolactin and corticosterone in the rat were studied following the administration of the serotonin precursor 5-hydroxytryptophan or the serotonin receptor agonist (-) -m-chlorophenylpiperazine. Naloxone clearly antagonizes the release of prolactin induced by 5-hydroxytryptophan administered alone at a dosage of 50 mg/Kg/b.wt.

Dopamine biosynthesis is regulated by the amine newly recaptured by dopaminergic nerve endings.

The synthesis of dopamine from labeled tyrosine (but not from labeled DOPA) in rat striatal synaptosomes was effectively inhibited by exogenous dopamine only when the amine was allowed to enter the nerve endings. In the presence of the uptake blocker nomifensine, extracellular dopamine was almost inactive. The evolution of 14CO2 from [14C]tyrosine was consistently higher when synaptosomes were 'incubated' in the presence of nomifensine than in its absence.

Evidence for a similar compartmentation of recaptured and endogenously synthesized dopamine in striatal synaptosomes.

The aim of the present study was to compare the release pattern of [3H]dopamine ([(3H]DA) originated from [3H]tyrosine or by uptake in striatal synaptosomes. Synaptosomes prelabeled either with [3H]DA or with [3H]tyrosine were superfused in three conditions stimulating DA release by different mechanisms: (1) depolarization with high K+ (2) inversion of the NA+ gradient across the plasma membrane; (3) exposure to d-amphetamine. Since DA contained in different pools may exit from nerve endings by different processes, DA release was analyzed in the presence or in the absence of nomifensine which allows discrimination between carrier-mediated and carrier-independent processes.

Serotonin release is modulated by presynaptic autoreceptors.

The existence of presynaptic autoreceptors controlling the release of 5-hydroxytryptamine (5HT) from serotonergic nerve endings was investigated utilizing superfused hypothalamic synaptosomes. Extracellular 5HT reduced the high K+-induced release of previously accumulated 3H-5HT. The central 5HT receptor blocker methiothepin counteracted the inhibitory effect of 5HT.