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T Antonelli

Publications and source records attributed to T Antonelli.

61 records · Page 4Linked to original sources
PubMed1983

Modulation of cortical acetylcholine and gamma-aminobutyric acid release in freely moving guinea pigs: effects of clonidine and other adrenergic drugs.

The effects of various doses of clonidine and norepinephrine (NE) on the release of acetylcholine (ACh) and gamma-aminobutyric acid (GABA) from the brain surface of freely moving guinea pigs have been investigated in order to study the role of alpha adrenoceptors on the function of cortical cholinergic and GABAergic neurons. Clonidine administration at doses of 7.5 and 18.7 nmol/kg inhibits by 40% the release of ACh; larger doses (112 nmol/kg) are inactive. On the other hand, the largest dose of clonidine used in this study (112 nmol/kg) increases the release of GABA by 45%, whereas lower doses are inactive. Norepinephrine (0.9 mumol i.c.v.) decreases by 40% the release of ACh and increases by 80% that of GABA. The inhibitory effects of clonidine and of NE on cortical ACh output are completely antagonized by yohimbine (0.28 mumol/kg), a selective alpha-2 antagonist, thus suggesting an involvement of the alpha-2 adrenoceptors in the neurochemical action of the drug. However, yohimbine releases GABA and does not prevent the action of clonidine or of NE on the cortical GABA system. On the other hand, prazosin (35.8 nmol/kg), a selective alpha-1 antagonist, completely antagonizes the stimulating effects of clonidine and of NE on the release of GABA, suggesting that alpha-1 receptors modulate this release. The present experiments indicate that the neurochemical and neuropharmacological profile of activity of clonidine is strictly dependent upon the dose of the drug. In addition, they support the concept that cortical alpha adrenoceptors modulate the function of neurons releasing ACh or GABA.

Acetylcholine↗
PubMed1982

[Stimulation of cholinergic receptors and changes in cyclic nucleotide levels in the cerebral cortex of the guinea pig].

The effect of Atropine and Physostigmine on 3'5' AMP and 3'5' GMP content was investigated in slices of guinea-pig cerebral cortex maintained at rest or electrically-stimulated. Atropine and Physostigmine did not modify either the basal content or the electrically-evoked increase of 3'5' AMP and 3'5' GMP. On the contrary, Betanechol 25 micro M significantly increased 3'5' GMP and 3'5' AMP content in slices kept at rest. The effect was abolished by Atropine 1,5 x 10(-7) M and d-tubocurarine 7 x 10(-6) M, respectively.

Animals↗
PubMed1981

Changes in synaptosomal high affinity choline uptake following electrical stimulation of guinea-pig cortical slices: effect of atropine and physostigmine.

1 Superfused guinea-pig cortical slices were electrically stimulated at different frequencies and the changes in acetylcholine (ACh) content measured. Synaptosomes were prepared at the end of the stimulation period and high affinity choline uptake (HACU) rate was measured. 2 The effect of increasing KC1 concentrations was compared on ACh content of the slices and on synaptosomal HACU. 3 Electrical stimulation (2, 5, 10, 20 Hz) elicited a frequency-dependent linear increase in synaptosomal HACU rate and a decrease in ACh content of the slices. 4 The addition of atropine (1.5 x 10(-8) M) to the slices enhanced and that of physostigmine (3 x 10(-5) M) reduced the frequency-dependent increase in HACU rate. Atropine (1.5 x 10(-6) M) not only antagonized the effect of physostigmine, but the HACU rate measured after treatment with both drugs was larger than that found after atropine alone. 5 These results indicate that in the cortical cholinergic nerve endings, depolarization caused by electrical stimulation is coupled with an increase in choline transport which can be modulated by the addition of atropine or physostigmine. Furthermore, within given experimental conditions a linear relationship exists between the reciprocal of ACh content in the slices and synaptosomal HACU.

Acetylcholine↗
PubMedDate not supplied

Effect of alpha-adrenoreceptors in the control of spontaneous motility and morphine withdrawal syndrome.

The effects of different alpha-2 agonists on the spontaneous motility in naive and morphine tolerant mice were studied. Clonidine caused a reduction at the lower (1-3 micrograms Kg-1 i.p.) and higher (100 micrograms Kg-1 i.p.) doses and no effect at 10-30 micrograms Kg-1 i.p. in naive mice, while an increase was found at the intermediate doses (10-30 micrograms Kg-1 i.p.) in morphine tolerant mice. The clonidine-induced inhibition on spontaneous motility at the lower and higher doses was prevented both in naive and tolerant mice by idazoxan pretreatment. In morphine-treated animals the increase induced by clonidine was antagonized by prazosin. The action of guanabenz and guanfacine on locomotion differed from clonidine, by producing inhibition only at higher doses (100-300 micrograms Kg-1 i.p.). Clonidine, but not guanfacine or guanabenz, prevented the withdrawal syndrome precipitated by naloxone. Thus the only alpha-2 agonistic properties do not appear sufficient to explain the prevention of morphine abstinence by clonidine in mice, which can represent a single model to screen anti-withdrawal drugs.

Adrenergic alpha-Agonists↗