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Biomedical subjects

M Orsetti

Publications and source records attributed to M Orsetti.

48 records · Page 3Linked to original sources
PubMed1983

Behavioral interferences modify the acceleration in memory decay caused by diazepam.

A staircase maze has been used to test the modification induced by a chronic administration of different doses of diazepam in the decay of the rat performance caused by an interruption of 20 days in the daily training. The possibility that behavioral interferences modify the diazepam effect has been examined by testing the rat in an open field or in a Y maze during the interruption of the training in the staircase maze. The diazepam effect on the rat behavior in the staircase maze increased linearly with the doses; an intercalated training in the open field increased the diazepam effect, while an intercalated training in a Y maze completely abolished the increase of forgetting caused by diazepam.

Animals↗
PubMed1983

Drug antagonism studied on frog flexor reflex and on mouse motility.

This study concerns the effects of strychnine and caffeine on ethanol, pentobarbital and atropine-induced depression of mouse motility and of frog spinal reflex. Competitive antagonism was found for the interaction between caffeine and ethanol, caffeine and pentobarbital, strychnine and atropine and strychnine and pentobarbital. The same kind of interaction was found in the mouse motility and in the frog spinal reflex. An attempt is made to interpret the biochemical basis of the competitive antagonisms. The antagonism between strychnine and atropine may be explained taking into account the presynaptic action of atropine and the antagonism between strychnine and pentobarbital is in agreement with a GABAergic action of the barbiturates.

Animals↗
PubMed1982

The associations acetylcholine-eserine and acetylcholine-morphine studied on the frog rectus abdominis muscle.

The interaction of morphine and eserine with acetylcholine (Ach) on frog rectus abdominis muscle was studied. Both eserine and morphine potentiate the effects of exogenous Ach and this effect is certainly not due to the anticholinesterase action of the two drugs. Morphine is less effective than eserine in potentiating the response of the muscle to the Ach introduced in the organ-bath. The synergisms Ach-eserine and Ach-morphine are synergisms with potentiation: it is concluded that eserine and morphine in amphibian muscle interact with specific receptors. These binding sites are different from both the esterase and the ACh binding sites of the cholinergic receptor but appear to influence its function.

Abdominal Muscles↗
PubMed1982

Modification of the synergism acetylcholine-eserine induced by morphine in amphibian muscle.

The modification of the synergism acetylcholine-eserine induced by two different concentrations of morphine (0.2 and 8 microgram/ml) was studied on the frog rectus abdominis muscle. Morphine increases the Ach-potentiating action of low concentrations of eserine (from 3 to 40 ng/ml). On the contrary at higher eserine concentrations (from 0.1 to 1.0 microgram/ml), morphine reduces the potentiation of Ach effects caused by eserine. It is concluded that in amphibian muscle eserine and morphine potentiate the effects of exogenous Ach by acting on the same population of receptors.

Abdominal Muscles↗
PubMed1979

The synergism acetylcholine-eserine in the epinephrine induced ventricular automaticity.

Heart ventricular strips of the rat in Krebs solution were used to test the synergism acetylcholine-eserine. Ventricular automaticity induced by epinephrine 1 10(-6) is inhibited by acetylcholine (a 50% reduction of the automatism is observed with acetylcholine 1,23 10(-8) while four different concentrations of eserine cause an evident potentiation of the effect of acetylcholine (with eserine a 10(-5) the ED50 of acetylcholine is 2,57 10(-14)). It is concluded that the synergism eserine-acetylcholine is a synergism with potentiation and the acetylcholine introduced in the Krebs solution interacts with receptors different from those activated by the acetylcholine which accumulates when cholinesterase is inhibited by eserine.

Acetylcholine↗
PubMed1979

Acetylcholine distribution in the spinal cord of the rat.

Spinal cord of male albino rats is cut in four parts: the cervical enlargement (C2-C8) the thoracic cord (T1-T10) the lumbar enlargement (T11-L3) and the sacral extremity (L4-S4). A considerable increase in the acetylcholine levels from the cervical (0,80 g/g +/- 0,15 st.err.) to the sacral section (2,67 g/g +/- 0,48 st.err.) has been observed. It is concluded that the increase of acetylcholine levels in the lower part of spinal cord is the consequence of the relative increase of gray matter at this level.

Acetylcholine↗
PubMed1979

The "grasping reflex" in rats with altered thyroid activity.

The "grasping reflex" test was performed in adult rats with altered thyroid function. Any modification of the thyroid activity (hyper or hypothyroidism) caused a prolongation of the grasping time. Our data indicate that the condition of hypo or hyperthyroidism induces behavioural modifications in the adult rats.

Animals↗
PubMedDate not supplied

Action of diisopropylfluorophosphate and of diacetylmonoxime on acetylcholine levels and on cholinesterase activity in the central nervous system.

The modification of the acetylcholinesterase (AChE) activity and of the acetylcholine (ACh) levels caused by diisopropylfluorophosphate (DFP) alone and in association with 300 mg/kg of diacetylmonoxime (DAM) have been studied in the olfactory brain, in the cortex and in the medulla-pons of the rat. DFP caused a reduction of the levels of ACh at 0.25 and 0.5 mg/kg. An increase of the levels of ACh was observed at 4.0 mg/kg of DFP only in the olfactory brain and in the cortex. A dose-dependent reduction of the AChE activity was observed after DFP. DAM reactivated the AChE activity to the levels of the controls after 0.25 and 0.5 mg/kg of DFP. In this experimental situation, the ACh levels returned to the control levels after 0.25 mg/kg of DFP and, in the medulla-pons, also after 0.5 mg/kg of DFP. DAM caused a partial recovery of the AChE activity but no modification of the ACh levels at 1.0, 2.0 and 4.0 mg/kg of DFP.

Acetylcholine↗