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Biomedical subjects

E Scarnati

Publications and source records attributed to E Scarnati.

At least 55 records · Page 3Linked to original sources
PubMed1982

Neuronal responses to iontophoretically applied dopamine, glutamate, and GABA of identified dopaminergic cells in the rat substantia nigra after kainic acid-induced destruction of the striatum.

Kainic acid (KA 1.2-1.5 micrograms) was injected unilaterally into the rat striatum (ST). Fifteen to 30 days later neurons of the substantia nigra (SN) were identified by antidromic stimulation from the ST or medial forebrain bundle (MFB). The projecting axons had conduction velocity similar to that recorded in unlesioned animals. REsponses to iontophoretically applied dopamine (DA), glutamate (GLU), and GABA (5-100 nA) were recorded from neurons of the dopaminergic pars compacta-striatal projection. Control experiments were performed in intact rats. GABA and DA inhibited neurons tested in controls while GLU had an excitatory effect. Changes in firing rate induced by GABA and GLU developed 1-5 s after the beginning of their ejection while the action of DA appeared after a delay of 20-40 s. Neurons in lesioned animals showed a net decrease in sensitivity to all three neurotransmitters. The highest current tested gave responses 50-70% lower than in controls. The data suggest that destruction of striatal efferents with KA does not induce hypersensitivity in the pars compacta of the SN.

Action Potentials↗
PubMed1981

Neuroexcitatory properties of kainic acid. II) Neuronal damages following intracerebreal microinjections in behavioural rats.

Microinjection of low doses of kainic acid, a neurotoxic analogue of glutammate, in different brain areas (striatum, hippocampus, substantia reticularis pontis) induces neuronal damages in injected and distant areas. Particularly severe neuronal damages have been observed in striatum and CA3 hippocampal area; neuronal degeneration has also been observed in substantia nigra following kainic acid infusion into the substantia reticularis pontis.

Animals↗
PubMed1980

[Possible use of stable tracers in hematological research. Preliminary note].

The aim of the paper was to verify the possible use in blood cells labeling both of stable K analogue elements and of stable compounds employed in nuclear medicine. The technique of analysis by XRF has been utilized. The paper presents some data obtained labeling red cells with Rb. The results indicate that in vitro red cells labeling with stable elements is a valid tool in the field of haematology.

Animals↗
PubMed1980

Dopaminergic and non-dopaminergic neurons in substantia nigra: differential response to bromocriptine.

Bromocriptine reduces the spontaneous firing rate of neurons in the pars compacta of the substantia nigra but does not change the electrical activity of the neurons located in the pars reticulata. On the other hand, bromocriptine induces contralateral circling behaviour in rats with unilateral 6-hydroxydopamine nigral lesion. This increased motor activity follows an initial period of hypomotility. The decrease of the neuronal firing rate in the pars compacta of the substantia nigra coincides with the hypomotility observed in the lesioned rats.

Animals↗
PubMed1980

Striatal cholinergic receptors and dyskinetic motor activity in the rat.

An injection of D-tubocurarine into the rat striatum produces a complex motor syndrome resembling in part that induced by picrotoxin. The destruction of the dopaminergic terminals by 6-hydroxydopamine does not prevent these effects of D-tubocurarine on motor activity. Hence neither dopamine release nor the presynaptic acetylcholine receptors are responsible for the D-tubocurarine-induced movements. On the other hand, lesion of the striatum by kainic acid abolishes the motor abnormalities due to D-tubocurarine but not those due to picrotoxin injection. Therefore, the effects of picrotoxin might be attributable to an action on GABA receptors still present in the kainic acid-treated striatum, whereas the effects of D-tubocurarine might be due to its action on striatal postsynaptic acetylcholine receptors.

Animals↗
PubMed1979

Sleep induced by low doses of apomorphine in rats.

The effect of apomorphine on the EEG of freely moving rats was studied. Apomorphine at the dose of 1 mg/kg caused stereotypy and a marked reduction of total sleep. On the contrary, acute subcutaneous administration of apomorphine at the dose of 100 microgram/kg, or less, markedly increased the amount of total sleep (corresponding mostly to synchronized sleep). Moreover, the infusion of apomorphine (80 microgram/kg/h) for 4 h doubled the duration of slow and REM sleep. The hypnotic effect of apomorphine was prevented by neuroleptics, such as pimozide, benzperidol and L-sulpiride, at doses which, per se, did not modify the EEG of the animals. These results suggest the existence in the CNS of DA receptors mediating sleep.

Animals↗