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M Marchi

Publications and source records attributed to M Marchi.

At least 109 records · Page 6Linked to original sources
PubMed1984

Is there a functional linkage between neurotransmitter uptake mechanisms and presynaptic receptors?

The possibility of interaction between neurotransmitter uptake mechanisms and presynaptic receptors regulating transmitter release was investigated using rat brain synaptosomes in superfusion. Various conditions were considered including: absence of substrate for the uptake with uptake potentially operative; absence of substrate and presence of uptake inhibitors; and uptake activated by added substrate, with or without uptake inhibitors. The release of [3H]-5-hydroxytryptamine ([3H]-5-HT) evoked by 15 mM KCl from cerebral cortex synaptosomes was inhibited by lysergic acid diethylamide. The 5-HT uptake inhibitors citalopram and chlorimipramine did not affect the inhibitory action of lysergic acid diethylamide. Clonidine decreased both the K+-evoked release of [3H]norepinephrine and that of [3H]-5-HT in cortical synaptosomes through the activation of presynaptic alpha-2 adrenoceptors. In superfusion conditions, the action of clonidine on [3H]norepinephrine release was not antagonized by the norepinephrine uptake inhibitors desipramine or cocaine; similarly, the inhibition of [3H]-5-HT release was unaffected when 5-HT uptake was blocked. The K+-evoked release of [3H]dopamine from striatal nerve terminals was potentiated by acetylcholine (ACh) through the activation of muscarinic presynaptic receptors. The action of ACh was not modified by the presence of nomifensine, a dopamine uptake inhibitor. Finally, in superfused cortical synaptosomes, the block of the high-affinity uptake of choline by hemicholinium-3 had no effect on the muscarinic autoreceptor-mediated inhibition of [3H]ACh release by ACh. Altogether the present results do not support the previously proposed idea that in nerve terminals a functional coupling may exist between uptake mechanisms and presynaptic receptors.

Acetylcholine↗
PubMed1983

Is acetylcholine release from striatal nerve endings regulated by muscarinic autoreceptors?

The presence in cholinergic nerve endings of muscarinic autoreceptors regulating the release of acetylcholine elicited by depolarizing stimuli was investigated in different areas of the rat brain. Synaptosomes prepared from cerebral cortex, hippocampus or corpus striatum were prelabeled with [3H]choline and the inhibitory effect of exogenous acetylcholine on the Ca2+-dependent release of [3H]acetylcholine evoked by 15 mM KCl was analyzed by superfusion. While acetylcholine was equally active in reducing its own release in hippocampus and cortex, it was much less effective in striatal synaptosomes. In contrast the values of several presynaptic cholinergic parameters ([3H]choline uptake, [3H]acetylcholine synthesis and release) were the highest in the striatum. Since experiments with slices showed that autoregulation of acetylcholine release through muscarinic receptors appeared to occur as efficiently in the striatum as in the two other areas, the present results suggest that in the striatum the autoregulation of acetylcholine release may not necessarily require the activation of autoreceptors located on cholinergic nerve terminals.

Acetylcholine↗
PubMed1983

Calcium-dependent [3H]acetylcholine release and muscarinic autoreceptors in rat cortical synaptosomes during development.

A number of presynaptic cholinergic parameters (high affinity [3H]choline uptake, [3H]acetylcholine synthesis, [3H]acetylcholine release, and autoinhibition of [3H]acetylcholine release mediated by muscarinic autoreceptors) were comparatively analyzed in rat brain cortex synaptosomes during postnatal development. These various functions showed a differential time course during development. At 10 days of age the release of [3H]acetylcholine evoked by 15 mM KCl from superfused synaptosomes was Ca2+-dependent but insensitive to the inhibitory action of extrasynaptosomal acetylcholine. The muscarinic autoreceptors regulating acetylcholine release were clearly detectable only at 14 days, indicating that their appearance may represent a criterion of synaptic maturation more valuable than the onset of a Ca2+-dependent release.

Acetylcholine↗
PubMed1983

Increased uptake of [3H]choline by rat superior cervical ganglion: an effect of dexamethasone.

The high affinity uptake of [3H]choline by the superior cervical ganglion, isolated from the rat, was found to be increased by dexamethasone. Maximal increase (60-65% above control values) occurred at the steroid concentration of 5 X 10(-5) M. Other glucocorticoids (triamcinolone, corticosterone and hydrocortisone) were without an effect on the [3H]choline uptake. Following administration of dexamethasone (25 mg/kg, i.p.), there was a marked increase in the level of choline in the ganglion. The increase was 3-fold at 1 hr and 10-fold at 6 hr, and by 24 hr the choline levels still remained higher in the steroid-treated animals than in the controls. Levels of acetylcholine in the ganglion were also increased, beginning at 1 hr after the injection of steroid. The increase was 85% by 3 hr and 60% by 6 hr. Triamcinolone, a glucocorticoid that was without an effect on [3H]choline uptake in vitro, was also ineffective in altering the levels of choline and acetylcholine in vivo. It seems probable that the increase of choline uptake in the ganglion induced by dexamethasone may, at least in part, occur in the preganglionic cholinergic terminals, leading to increased synthesis of acetylcholine. Such an effect of dexamethasone provides another case of a selective steroid acting directly on nerve terminals by altering a transport mechanism.

Acetylcholine↗
PubMed1982

Presynaptic muscarinic receptors increase striatal dopamine release evoked by "quashi-physiological" depolarization.

The effects of acetylcholine on the release of [3H]dopamine was studied in superfused rat striatal synaptosomes prelabeled with the radioactive amine. The results confirm the presence of muscarinic presynaptic receptors mediating potentiation of the spontaneous release of the catecholamine. However, under depolarizing conditions, the release of dopamine evoked by 15 mM KC1 was increased by the activation of muscarinic receptors and not decreased, as previously found in striatal synaptosomes or slices depolarized with higher (50-60 mM) KC1 concentrations.

Acetylcholine↗
PubMed1982

Multiple sclerosis among shoe and leather workers: an epidemiological survey in Florence.

The observation of many multiple sclerosis (MS) cases among shoe and leather workers prompted a survey of the risk of MS in this working population. Eighty-one patients with definite or probable MS alive in Florence on May 1st 1976 were interviewed regarding their occupation at onset of the disease. Five of the 41 patients working at the time had worked in shoe a leather factories. The relative risk for these workers was 4.87 compared to the general populations and 4.91 compared to the active population, both results being significantly different from one. This survey indicates an increased risk of MS among shoe and leather workers. Organic solvents, contained in large quantities in the glues used, may be involved in the pathogenic mechanism through a possible interference with the immune system.

Adhesives↗
PubMed1981

3H-thymidine long survival autoradiography as a method for dating the time of neuronal origin in the chick embryo: the locus coeruleus and cerebellar Purkinje cells.

Contrary to previous assumptions, we have found that a single dose of 3H-thymidine (25 muCi), injected into the yolk sac of White Leghorn chick eggs on 2 days of incubation (d.i.) only remains available for DNA-synthesizing (proliferating) cells for 48 hours following the time of injection. This finding now makes it possible to date the time of neuronal origin in the avian embryo using a single injection of isotope and a long survival time (30 days posthatch) as in mammalian studies where 3H-thymidine is only available as a short "pulse." Using this method, we have determined that neurons in the chick locus coeruleus (LC) cease proliferation on 2-6 d.i. with a peak of neuronal genesis on 3-5 d.i. In addition, neuronal genesis is not homogeneous throughout the LC cell population, but occurs in a predominantly caudorostral gradient. Conversely, the cerebellar Purkinje cells cease division on 3-8 d.i. with a peak of heavy labeling on 4-6 d.i., 1 day later than that observed in the LC.

Animals↗
PubMed1981

Autoregulation of acetylcholine release in isolated hippocampal nerve endings.

The existence of presynaptic autoreceptors modulating acetylcholine release from central cholinergic nerve endings was investigated by using rat hippocampal synaptosomes in a superfusion system. The presence of exogenous acetylcholine, carbachol or oxotremorine in the superfusion fluid produced a dose-dependent inhibition of the release of [3H]acetylcholine elicited by 15 mM KCl in synaptosomes prelabeled with tritiated choline. The inhibition was counteracted by atropine. Another well known muscarinic agonist, bethanechol, had no effect on [3H]acetylcholine release. Our results indicate that central cholinergic nerve terminals possess autoreceptors of the muscarinic type for the control of acetylcholine release. Moreover, differences seem to exist between pre-and postsynaptic muscarinic receptors in the central nervous system.

Acetylcholine↗
PubMed1981

Development and aging of noradrenergic cell bodies and axon terminals in the chicken.

Tyrosine hydroxylase activity was measured in the region of locus coeruleus, cerebellum, cervical spinal cord, lumbar sympathetic ganglia, and iris throughout most of the life span of the chicken (8 days of incubation to 5 years) to compare developmental trends in tyrosine hydroxylase activity in noradrenergic cell bodies and in axon terminals in both the central and peripheral nervous system. Fluorescence histochemistry and retrograde transport of horseradish peroxidase were used to characterize further the coeruleo-cerebellar projections. Tyrosine hydroxylase activity was detected in the cerebellum as early as 8 days of incubation, which is the earliest stage so far reported. The greatest increase in total tyrosine hydroxylase activity in the region of the locus coeruleus and cerebellum occurred during the embryonic period. There was a more pronounced increase in the cerebellum than in the locus coeruleus region. This is in contrast to the cervical spinal cord where tyrosine hydroxylase activity increased at approximately the same rate during the embryonic and post-hatching periods. Moreover, the cerebellum and cervical spinal cord, two locus coeruleus target sites, displayed different trends in tyrosine hydroxylase activity throughout development and aging. In both structures examined in the peripheral nervous system, the greatest increase in total tyrosine hydroxylase activity occurred during the post-hatching period, with a greater rise in the cell bodies of the lumbar sympathetic ganglia than in the noradrenergic terminals of the iris. In both the central and peripheral nervous system, total tyrosine hydroxylase activity continued to increase in noradrenergic terminals long after hatching reaching the highest levels at 7 months when the chicken is considered fully mature. During aging, 16 months to 5 years, there was a greater decrease in total tyrosine hydroxylase activity in the terminals of noradrenergic neurons than in the cell bodies in both the central and peripheral nervous system, a phenomenon that was more marked in the peripheral nervous system than in the brain.

Aging↗
PubMed1981

Development and aging of cholinergic synapses. V. Changes in nicotinic cholinergic receptor binding in ciliary ganglia and irises of the chicken.

In order to study possible age-dependent changes in the number of cholinergic binding sites, we have examined alpha-bungarotoxin (ABTX) binding in the ciliary ganglion and iris of the chicken from 3 months after hatching (a.h.) to 5 years of age and have compared it to acetylcholinesterase (AChE) activity and acetylcholine (AChE) levels. In ciliary ganglia the amount of ABTX binding per ganglion increases 16-fold between 3 and 7 months, after which it returns almost to the 3-month level, at 1.3 years. It then remains virtually unchanged to 5 years. A similar pattern is observed in the amount of binding per protein. ACh levels and AChE activity show a different pattern than ABTX binding. In the iris the amount of ABTX binding remains constant between 3 months and 1.3 years and then it increases 1.6-fold up to 3 years. This period is followed by a decrease to 5 years. The amount of ABTX binding per protein which has increased continuously in the iris from the period following hatching up to 7 months, decreases continuously from 7 months to 5 years. In the iris, both ACh levels and AChE activity per protein follow a pattern which is similar to ABTX binding, decreasing from 3 months to 2 years and then remaining relatvely unvaried between 2 and 6-7 years. Our results suggest that a decrease in receptor number begins during early adulthood in the ganglia, whereas this event occurs at a later stage in the iris. However, the total amount of ABTX binding is still relatively high at late stages. These results support our view that the presynaptic component is more affected by the aging process than the postsynaptic component.

Acetylcholine↗
PubMed1980

Age dependent changes in choline uptake of the chick iris.

The kinetics of the uptake of choline, the rate-limiting substrate in the in vivo synthesis of acetylcholine, were studied during the period 1--7 years in the iris of the chick. These changes were correlated to the endogenous levels of acetylcholine and choline in the same organ. Vmax values per iris decrease significantly at 5 years and continue to decrease at 7 years, to 64% and 37% of the one year value, respectively. If the variation in Vmax is calculaed per protein the decline is 34% between 1 and 5 years. Km does not change significantly during the period 1--7 years. Total acetylcholine and choline levels follow a similar trend, decreasing progressively from 1 to 7 years. Sensitivity to hemicholinium (5.5 X 10(-5) M) decreases significantly between 5 days of incubation (d.i.) and 5 years. Inhibition by ouabain (10(-4) M) shows an opposite trend, increasing significantly from 20% at 5 d.i. to 52% at 3 months. At 5 years sensitivity to ouabain is the same as at 3 months. Nardependence decreases significantly between 5 d.i. and 5 years but no significant changes are seen between 5 d.i. and 3 months. Uptake at 27 degrees C decreases from 59% of control at 5 d.i. to 45% at 3 months, and is not changed at 5 years. Our observations suggest that the effect of aging on peripheral cholinergic neurons is not generalized, but is specifically directed toward the neuronal periphery (terminals) as opposed to cell bodies.

Acetylcholine↗
PubMed1980

Norepinephrine uptake in aging adrenergic nerve terminals.

Norepinephrine (NE) uptake has been studied in the adult (3-6 months) and aging (5 yr) chick iris, in which there is a discrete population of norepinephrine containing nerve terminals. although total accumulation of 3H-NE in the iris does not change with age, there is a decline in Na+-dependence, temperature-sensitivity, ouabain-and inhibitor -sensitivity of uptake. The results indicate either a loss of active, carrier-mediated NE uptake during aging, or a change in the biochemical and pharmacological characteristics of this uptake. changes in the composition of the organ and in the sites of accumulation of NE are considered.

Aging↗