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G C Andrioli

Publications and source records attributed to G C Andrioli.

At least 19 recordsLinked to original sources
PubMed1992

5-Hydroxytryptamine3 receptors sited on cholinergic axon terminals of human cerebral cortex mediate inhibition of acetylcholine release.

Synaptosomes prepared from freshly obtained human cerebral cortex and labeled with [3H]choline have been used to investigate the modulation of [3H]acetylcholine ([3H]ACh) release by 5-hydroxytryptamine (5-HT). The Ca(2+)-dependent release of [3H]-ACh occurring when synaptosomes were exposed in superfusion to 15 mM KCl was inhibited by 5-HT (0.01-1 microM) in a concentration-dependent manner. The effect of 5-HT was mimicked by 1-phenylbiguanide, a 5-HT3 receptor agonist, but not by 8-hydroxy-2-(di-n-propylamino)tetralin, a 5-HT1A receptor agonist. The 5-HT3 receptor antagonists tropisetron and ondansetron blocked the effect of 5-HT, whereas spiperone and ketanserin were ineffective. It is suggested that cholinergic axon terminals in the human cerebral cortex possess 5-HT receptors that mediate inhibition of ACh release and appear to belong to the 5-HT3 type.

Acetylcholine↗
PubMed1992

Subclassification of release-regulating alpha 2-autoreceptors in human brain cortex.

1. Release-regulating alpha 2-autoreceptors in human brain were characterized pharmacologically in cortical slices from patients undergoing neurosurgery to remove subcortical tumours; the slices were prelabelled with [3H]-noradrenaline ([3H]-NA) and stimulated electrically (3 Hz, 2 ms, 24 mA) under superfusion conditions. 2. The stimulus-evoked tritium overflow was almost totally Ca(2+)-dependent and tetrodotoxin-sensitive. 3. Clonidine and oxymetazoline 0.01 to 1 microM inhibited in a concentration-dependent manner the evoked overflow of tritium. The two drugs were equipotent (EC50 = 0.03 microM) and their maximal effect was approx. 45%. Phenylephrine and methoxamine, up to 1 microM, did not affect tritium overflow. 4. Yohimbine (0.01-0.1 microM) shifted the concentration-response curve of clonidine to the right. The calculated pA2 value was 8.29. 5. Prazosin and 2-[2-[4-(o-methoxyphenyl)piperazine-1-yl]ethyl]-4,4- dimethyl-1,3(2H,4H)-isoquinolinedione (AR-C 239), tested at 0.3 microM, did not modify the concentration-response curve of clonidine. 6. The effect of clonidine was antagonized by (+)-mianserin (pA2 = 7.74), but not by up to 0.3 microM of the (-)-enantiomer. The concentration-response curve of clonidine was shifted to the right by the novel alpha 2-adrenoceptor antagonist, 5-chloro-4-(1-butyl-1,2,5,6-tetrahydropyridin-3-yl)-thiazole-2-ami ne (Z)-2-butenedioate (1:1) salt (ORG 20350) (pA2 = 7.55). 7. Yohimbine, (+)-mianserin and ORG 20350, but not prazosin and (-)-mianserin, increased the electrically-evoked tritium overflow, suggesting that autoreceptors may be tonically activated by endogenous NA. 8. Desipramine (1 microM) increased evoked tritium overflow from human cortex slices. The effect of clonidine (0.01- 1 g1M) on the evoked overflow of tritium was reduced in presence of 1 muM desipramine.9. It is proposed that autoregulation of NA release can occur in human cerebral cortex. The process involves activation of alpha 2-adrenoceptors which may be either the alpha2X or the alpha2D subtype.

Adrenergic alpha-Agonists↗
PubMed1991

Cholinergic nerve terminals of human cerebral cortex possess a GABA transporter whose activation induces release of acetylcholine.

The effect of gamma-aminobutyric acid (GABA) on the release of [3H]acetylcholine [( 3H]ACh) from human cerebral cortex nerve terminals was investigated using synaptosomes prepared from neurosurgical specimens (which had to be removed to reach deeply located tumors) prelabeled with [3H]choline and exposed in superfusion to varying concentrations of GABA. The amino acid (3-100 microM) increased in a concentration-dependent manner (maximal effect: 40%; EC50 = 14.7 microM) the release of [3H]ACh but not that of [3H]choline. The GABAA receptor agonist muscimol (up to 100 microM) did not increase significantly the release of [3H]ACh. Accordingly, the effect of GABA was insensitive to the GABAA receptor antagonist bicuculline. The release of [3H]ACh was not affected by the GABAB receptor agonist (-)-baclofen (100-300 microM). The GABA-induced [3H]ACh release was counteracted by two inhibitors of GABA uptake, N-(4,4-diphenyl-3-butenyl)nipecotic acid (SKF 89976A) and nipecotic acid. Moreover, the enhancing effect of GABA on [3H]ACh release was clearly Na+-dependent and was reduced by almost 90% in presence of 23 mM NaCl. The data indicate that, similarly to what had been observed in the rat, cholinergic nerve terminals in the human cerebral cortex possess a GABA transporter. Activation of this carrier brings about release of newly synthesized ACh. GABA and ACh might co-exist in some cerebrocortical nerve endings in the vertebrate brain, including man.

Acetylcholine↗
PubMed1990

Pirenzepine-insensitive muscarinic autoreceptors regulate acetylcholine release in human neocortex.

The release of [3H]acetylcholine ([3H]ACh) and its modulation mediated by autoreceptors were investigated in synaptosomes prepared from fresh human cerebral cortex prelabelled with [3H]choline ([3H]Ch) and depolarized in superfusion with 15 mM KCl. The K(+)-evoked release of tritium was almost totally accounted for by unmetabolized [3H]ACh and was largely calcium-dependent. Exogenous ACh decreased the depolarization-evoked release of [3H]ACh in a concentration-dependent manner (EC50 = 1.5 microM). The inhibitory effect of ACh on [3H]ACh release was counteracted by the non-selective muscarinic antagonist atropine. In contrast, the selective M1 receptor antagonist pirenzepine was ineffective. It is concluded that muscarinic autoreceptors regulating the release of ACh are present on cholinergic nerve terminals of human cerebral cortex and appear to belong to a pirenzepine-insensitive subtype.

Acetylcholine↗
PubMed1990

Modulation of 5-hydroxytryptamine release by presynaptic inhibitory alpha 2-adrenoceptors in the human cerebral cortex.

Slices and synaptosomes from human cerebral cortex (which had to be removed to reach deeply located tumours) and, for comparison, synaptosomes from guinea-pig and rat cerebral cortex were preincubated with [3H]5-hydroxytryptamine and superfused with physiological salt solution containing an inhibitor of 5-hydroxytryptamine uptake. The effects of alpha-adrenoceptor agonists and antagonists on the electrically (slices) or potassium-evoked (synaptosomes) tritium overflow were studied. In human cerebral cortical slices, the electrically-evoked [3H] overflow was inhibited by noradrenaline (pIC25 value: 6.35); the non-selective alpha-adrenoceptor antagonist phentolamine, at a concentration of 0.32 mumol/l, strongly antagonized the inhibitory effect of noradrenaline (apparent pA2 value: 8.19) but did not affect the evoked overflow by itself. In synaptosomes from humans, guinea-pigs and rats, noradrenaline also inhibited the K(+)-evoked [3H] overflow in a concentration dependent manner; the alpha 2-adrenoceptor clonidine (1 mumol/l), but not the alpha 1-adrenoceptor agonist methoxamine (1 mumol/l), mimicked the effects of noradrenaline; the effect of noradrenaline (0.3 mumol/l) was abolished by the alpha 2-adrenoceptor antagonist idazoxan (0.5 mumol/l), but not by the alpha 1-adrenoceptor antagonist prazosin (1 mumol/l). It is concluded that release-inhibiting adrenoceptors of the alpha 2-subtype exist on 5-hydroxytryptamine terminals innervating the cerebral cortex in human and guinea-pig brain.

Adrenergic alpha-Agonists↗
PubMed1989

Release-regulating autoreceptors of the GABAB-type in human cerebral cortex.

1. The depolarization-evoked release of gamma-aminobutyric acid (GABA) and its modulation mediated by autoreceptors were investigated in superfused synaptosomes prepared from fresh human cerebral cortex. 2. The release of [3H]-GABA provoked by 15 mM K+ from human cortex nerve endings was almost totally (85%) calcium-dependent. 3. In the presence of the GABA uptake inhibitor SK&F 89976A (N-(4,4-diphenyl-3-butenyl)-nipecotic acid), added to prevent carrier-mediated homoexchange, GABA (1-10 microM) decreased in a concentration-dependent manner the K+-evoked release of [3H]-GABA. The effect of GABA was mimicked by the GABAB receptor agonist (-)-baclofen (1-100 microM) but not by the GABAA receptor agonist muscimol (1-100 microM). Moreover, the GABA-induced inhibition of [3H]-GABA release was not affected by two GABAA receptor antagonists, bicuculline or SR 95531 (2-(3'-carbethoxy-2'-propenyl)-3-amino-6-paramethoxy-phenyl-pyr idazinium bromide). 4. (-)-Baclofen also inhibited the depolarization-evoked release of endogenous GABA from human cortical synaptosomes. 5. It is concluded that GABA autoreceptors regulating the release of both newly taken up and endogenous GABA are present in human brain and appear to belong to the GABAB subtype.

Aged↗
PubMed1988

Electrical stimulation of the motor tracts in cervical spondylosis.

Motor action potentials evoked by percutaneous electrical stimulation of the scalp and of the cervical (or lumbar) vertebral region were recorded from the biceps, thenar and tibialis anterior muscles in 30 patients with cervical spondylosis. Twelve normal controls were matched for age and height. Abnormalities of central motor conduction (absence or increased central delay of cortical responses) for at least one muscle were observed in all (but one) the patients with myelopathy alone or combined with radiculopathy. An increase in latency of the responses evoked by cervical stimulation occurred in 40% of patients with radiculopathy or myelo-radiculopathy. Changes of motor conduction occurred even in the absence of abnormalities of somatosensory evoked potentials, while the opposite was never observed. Direct stimulation of the motor tracts may be of value in the functional assessment of the motor pathways in cervical spondylosis.

Adult↗
PubMed1986

Is computed tomography really effective in the early detection of brain tumors? A cooperative study.

A cooperative study based on 1,112 patients was undertaken in order to ascertain whether computed tomography (CT) allows earlier diagnosis of brain tumors or not. The patients were divided into 2 groups. In the first group (pre-CT period; 552 patients) diagnosis was made without CT, in the second (CT period; 560 patients) with CT. Duration of symptoms, assumed as the interval between onset and definite diagnosis, was the main parameter considered. The most relevant results were: a) during the CT period a significant decrease in duration of symptoms before diagnosis was observed for meningiomas (from 21 to 13 months) and low-grade gliomas (from 16 to 9 months), while no significant change was recorded for high-grade tumors (from 4.6 to 3.5 months); b) during the CT period the figure for benign tumors operated upon rose to 44 per cent (pre-CT: 25%) balanced by a marked decrease in surgery for malignancies (from 43% to 23%); c) better indications for surgery were associated with a significant reduction in cases operated upon during the CT period (72% versus 79%, p less than 0.01).

Brain Neoplasms↗
PubMed1985

Severe head injury in children: early prognosis and outcome.

The outcome is reported in 62 children with severe head injuries following a road traffic accident. All patients were comatose for at least 6 h; all patients were graded using the Glasgow Coma Score (GCS) or the Children Coma Score (CCS). Fifty-four patients were comatose immediately after injury, 8 after a lucid interval. Thirty patients had isolated head injuries and 32 had associated injuries, either long bone fractures or rupture of an abdominal organ. Additional information concerning main brainstem reflexes, posture and respiration was included in the study. The overall mortality was 32%. The goal of the study was to identify those clinical features available soon after injury which are important indicators of treatment and outcome.

Accidents, Traffic↗
PubMed1983

Traumatic primary brain stem haemorrhage. A clinical and experimental study.

We report 36 cases of post-traumatic "primary brain stem haemorrhage" visualized by the CT scan and confirmed at autopsy. Clinical experience shows that many technical factors influence the inability to visualize brain stem haemorrhages. Experimental injection of fresh blood into the pons and midbrain of cadavers shows that lesions as small as 0.25 ml in volume may be visualized. The volume and the anatomical configuration of traumatic lesions of the brain stem extended over a rostro-caudal direction, and their proximity to bony structures at the base of the skull are obstacles to the visualization of brain stem haemorrhages.

Adolescent↗
PubMed1983

[Epidural hematomas in the infant].

A report is given on eight cases of epidural haematoma in children aged 0 to 2 (11 per cent of a total of 70 epidural haematomas found in children). The individual clinical phenomena and courses of the disease are shown on the basis of our own patients. The prognosis of epidural haemorrhages is more favourable for such children than for older children and adults.

Brain Injuries↗
PubMed1982

Traumatic posterior fossa haemorrhage in children.

We report ten cases of post-traumatic posterior fossa haemorrhage occurring in children. All patients were studied by CT scan. Five had an intracerebellar haemorrhage, three a brain stem haemorrhage, and two an extradural haematoma. In four cases we have found the coexistence of supratentorial and infratentorial haemorrhagic lesions. The incidence of posterior fossa haemorrhage in children, the importance of linear occipital fracture, the clinical course, the conservative or surgical treatment, and the prognosis are discussed.

Brain Injuries↗
PubMed1981

Concurrent primary intracranial tumours of different histogenesis.

The occurrence of intracranial tumours of diverse histogenesis can be considered occasional. In a careful survey of the literature we have encountered 63 cases of concurrent intracranial tumours: we report five personal observations, too. This review raises the question as to whether the conjoint occurrence of two intracranial tumours is purely coincidental. The statistical analysis of the cases of concurrent intracranial tumours, and the comparison between the frequency found for each different tumour when it is solitary and when it is coincident in a same patient, suggests that a casual connection can be found between tumours of diverse histogenesis.

Astrocytoma↗
PubMed1981

Multiple meningiomas.

The authors discuss the criteria of differential diagnosis for a correct use of the term "multiple meningiomas". Reviewing a series of 934 meningiomas, of which 834 were intracranial and 100 were spinal, they found 14 cases of multiple meningiomas, i.e. an incidence of 1.5%. The study shows that multiple meningiomas are quite similar to solitary meningiomas in all their biological characteristics. Furthermore, the possible presence of more than one meningioma must always be kept in mind in the clinical and radiological evaluation of a patient. The aetiology of multiple separate meningiomas is discussed: the hypothesis which suggests their origin from multicentric neoplastic foci activated by a supposed "tumour-producing factor" appears to be the most reliable.

Adult↗