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Biomedical subjects

M Morra

Publications and source records attributed to M Morra.

At least 19 recordsLinked to original sources
PubMed1992

Platelet catecholamines in cluster headache.

Platelet tyrosine and catecholamine (CA) content was measured in cluster headache sufferers during the different phases of the illness. Compared with controls, cluster headache sufferers had lower platelet levels of norepinephrine (NE) and epinephrine (E) in all phases of the syndrome. Tyrosine levels were increased significantly during the cluster headache attack. We suggest that these results provide biochemical evidence of sympathetic nervous system (SNS) hypofunction in cluster headache.

Adult↗
PubMed1992

Characterization of dopamine receptors associated with steroid secretion in frog adrenocortical cells.

We investigated the type of receptors involved in the mechanism of action of dopamine on corticosteroid secretion from the frog interrenal (adrenal) gland, using the in-vitro perifusion technique. Exposure of dispersed interrenal cells to 50 microM dopamine for 20 min had a biphasic effect on corticosterone and aldosterone secretion, i.e. a transient stimulation followed by an inhibitory phase. Repeated administration of equimolar pulses of dopamine, given at 150-min intervals, resulted in an enhancement of corticosteroid secretion followed by a subsequent blockade of the stimulatory phase of the response. In contrast, the dopamine-evoked inhibition of corticosteroid release did not show any sensitization or desensitization phenomena. Infusion of repeated pulses of the D1 receptor agonist SKF38393 (32 microM) stimulated corticosteroid release and mimicked the sensitization-desensitization phenomenon induced by dopamine. Repeated administration of the D2 receptor agonist LY171555 (50 microM) resulted in a reproducible inhibition of corticosterone and aldosterone secretion. These results suggested the presence of two different receptors for dopamine, i.e. D1 and D2, on frog adrenocortical cells, responsible respectively for the stimulatory and inhibitory effects of dopamine on steroid secretion. However, bromocriptine (50 microM) and CV205-502 (50 microM), two other D2 receptor agonists, had no effect on corticosteroid release. In addition, several classical D2 receptor antagonists failed to block the effect of dopamine on steroidogenesis. It was also observed that (-)sulpiride, a specific D2 antagonist, did not alter dopamine-induced inhibition of inositol phosphate formation. On the other hand, dopamine and the selective D1 and D2 antagonists SKF38393 and LY171555 did not affect the formation of cyclic AMP by interrenal tissue. Taken together, these data indicate that dopamine directly regulates corticosteroid secretion from frog adrenocortical cells. The effect of dopamine is not coupled to adenylate cyclase activity but is probably mediated through the phosphoinositide-turnover pathway. The pharmacological characteristics of the receptors involved in the mechanism of action of dopamine clearly differ from those of the D1 and D2 subtypes previously described in mammals.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗
PubMed1991

Platelet glycine, glutamate and aspartate in primary headache.

Platelet levels of glutamic and aspartic acid and glycine were measured in patients with migraine with aura, migraine without aura, tension headache and cluster headache. High levels of these amino acids were found in patients with migraine with aura compared to normal subjects and other headache groups. During headache, glutamate levels further increased in migraine with aura patients. These findings may have relevance to the neurological symptoms of migraine with aura.

Aspartic Acid↗
PubMed1991

Dopamine inhibits inositol phosphate production, arachidonic acid formation, and corticosteroid release by frog adrenal gland through a pertussis toxin-sensitive G-protein.

We have previously shown that dopamine-evoked inhibition of corticosteroid production from adrenocortical cells is mediated through a decrease in prostaglandin biosynthesis. Since the catecholamine did not alter the stimulatory effect of arachidonic acid, it was proposed that dopamine may inhibit the formation of arachidonate from glycerophospholipids. To test this hypothesis, the effect of dopamine on phosphoinositol lipid metabolism was investigated in frog interrenal (adrenal) tissue. In [3H]myo-inositol-prelabeled frog interrenal slices, a short pulse of dopamine (50 microM) induced a biphasic effect on inositol phosphate production: a transient (1-min) increase, followed by a sustained inhibition. Concurrently, dopamine induced a transient reduction followed by a sustained increase in polyphosphoinositides. A 10-min pulse of the D2 dopamine receptor agonist apomorphine (50 microM) elicited a significant inhibition of basal levels of inositol phosphates (tris-, bis-, and mono-), and an increase in plasma membrane phosphoinositol lipid contents. The inhibitory effect of dopamine on inositol phosphate formation and corticosteroid release was abolished by a 24-h incubation of interrenal slices with pertussis toxin. In [3H]arachidonic acid-prelabeled interrenal slices, dopamine also decreased diacylglycerol (DG) and arachidonic acid (AA) concentrations. A delay of 1 min was observed between inhibition of DG and arachidonate, suggesting that AA is probably generated from DG. We conclude that in the adrenal cortex, activation of dopamine D2 receptors is coupled to a phosphoinositide-specific phospholipase-C mediated via a pertussis toxin-sensitive G-protein. Taken together, our data indicate that inhibition of inositol phosphate and AA formation is one of the mechanisms by which dopamine controls corticosteroid production by adrenocortical cells.

Adrenal Cortex Hormones↗
PubMed1990

Dopamine inhibits corticosteroid secretion from frog adrenal gland, in vitro.

The effect of dopamine on corticosteroid secretion from frog interrenal (adrenal) tissue was investigated in vitro using a perifusion system technique. Administration of graded concentrations of dopamine (5 X 10(-8) M to 10(-3) M) to interrenal slices induced a dose-dependent inhibition of steroid secretion. The half-maximal effective dose of dopamine was 7 X 10(-6) M for corticosterone and 4 X 10(-6) M for aldosterone. Noradrenaline and adrenaline were also able to elicit a dose-related inhibition of steroid release, but these catecholamines were approximately 100 and 2000 times less potent than dopamine in our model. Administration of repeated pulses of dopamine (5 X 10(-5) M), at 150-min intervals, led to a reproducible inhibition of corticosteroid secretion without any desensitization phenomenon. Similarly, prolonged infusion of dopamine (5 X 10(-6) M) caused a sustained inhibition of steroidogenesis. The inhibitory action of dopamine was also observed using enzymatically dispersed adrenal cells, indicating that dopamine exerts a direct effect on adrenocortical cells. After the second pulse, dopamine also induced a transient stimulation of steroid secretion from acutely dispersed cells. Administration of short pulses of apomorphine (5 X 10(-5) M) induced a transient inhibition of corticosteroid secretion, and the kinetics of the response were very similar to that observed with dopamine. During prolonged administration of dopamine, the steroidogenic actions of ACTH (10(-9) M) and serotonin (5 X 10(-6) M) were not altered. In contrast, dopamine induced a marked inhibition of angiotensin II-evoked corticosteroid secretion. Taken together, these results show that the neurotransmitter dopamine exerts a direct inhibitory effect on steroid secretion from frog adrenocortical cells. Our results also indicate that dopamine and angiotensin II likely act through a common intracellular pathway. These data suggest that dopamine, released by chromaffin cells during neurogenic stress, may modulate the response of adrenocortical cells through a paracrine mode of communication.

Adrenal Cortex Hormones↗
PubMed1989

Dopamine inhibits corticosteroid secretion in frog adrenocortical cells: evidence for the involvement of prostaglandins in the mechanism of action of dopamine.

We have investigated the possible involvement of arachidonic acid metabolites in dopamine-induced inhibition of adrenocortical steroidogenesis. Administration of dopamine (5 x 10(-5) M) for 20 min to perifused frog adrenal slices caused a marked reduction of the release of both prostaglandin E2 (PGE2) and 6-keto-PGF1 alpha, the stable metabolite of prostacyclin (PGI2). Dopamine also induced a significant inhibition of corticosterone and aldosterone secretion. A lag period of 20 min was observed between inhibition of prostanoid and corticosteroid releases. Prolonged dopamine infusion did not prevent the stimulatory effect of PGE1, PGE2 or arachidonic acid on corticosteroid secretion. These observations indicate that activation of dopaminergic receptors in adrenocortical cells is linked to an inhibition of arachidonic acid metabolism. Our data also suggest that the inhibitory effect of dopamine occurs at a step preceding arachidonic acid formation.

Adrenal Cortex↗
PubMed1988

Immunohistochemical and biochemical evidence for the presence of serotonin in amphibian adrenal chromaffin cells.

The presence of serotonin (5-HT) in chromaffin cells of the frog adrenal (inter-renal) gland has been demonstrated both by immunocytochemical and biochemical techniques. Using antisera against 5-HT and tyrosine hydroxylase (TH) on consecutive sections, we found by means of the indirect immunofluorescence technique that a majority of chromaffin cells were also immunopositive for 5-HT. When antibodies to 5-HT and phenylethanolamine-N-methyltransferase (PNMT) were applied on consecutive sections, 5-HT-like immunoreactivity was observed in almost all epinephrine-producing cells which represented about 90% of the total chromaffin cells. No 5-HT-containing fibres could be detected. At the ultrastructural level, using a pre-embedding procedure associated with gold-silver intensification of the immunoperoxidase reaction, 5-HT-immunoreactivity was visualized in secretory vesicles essentially located in the periphery of epinephrine cells. Combination of high performance liquid chromatography and electrochemical detection showed the presence of both 5-HT and its metabolite 5-hydroxyindolacetic acid (5-HIAA) in frog adrenal extracts. Transection of the splanchnic nerve enhanced 5-HT immunoreactivity and augmented the amount of 5-HT in adrenal extracts. Taken together, these results indicate that epinephrine-producing cells of the frog adrenal contain significant amounts of serotonin. The observation of the storage of 5-HT in secretory vesicles of epinephrine cells suggests that serotonin may be released with catecholamines under stress conditions.

Adrenal Medulla↗
PubMedDate not supplied

Platelet as a model to test autonomic function in migraine.

In order to evaluate the role of the sympathetic autonomic nervous system (SANS) in common migraine we measured platelet catecholamine levels in a group of patients and in control subjects after 1 and 30 min of supine rest. Common migraine patients showed, at 1 min of supine rest, higher platelet norepinephrine (NE) content in comparison with the controls. This result may reflect a decreased release of platelet dense bodies in migraineurs. The same patients showed after 30' of supine rest a hardly significant increase of platelet NE levels in contrast to the clearly significant increase found in controls. These findings support the hypothesis of sympathetic hypofunction in migraine.

Adult↗