PubMed Health⌕ Search

Biomedical subjects

M Morelli

Publications and source records attributed to M Morelli.

At least 163 records · Page 9Linked to original sources
PubMed1980

Lesions of substantia nigra by kainic acid: effects on apomorphine-induced stereotyped behaviour.

Fifteen days after bilateral lesions of the substantia nigra by local infusion of kainic acid (0.75 microgram) or after intranigral injection of vehicle, rats were administered 0.1, 0.25, 1.0 and 2.5 mg/kg s.c. of apomorphine and the stereotyped items (locomotion, sniffing and gnawing) were recorded on an event-recorder and motility was measured by a photocell apparatus. After low doses of apomorphine (0.1, 0.2 mg/kg), rats lesioned in the substantia nigra with kainic acid showed a degree of stimulation of motility and of sniffing similar to controls; on the other hand, in rats lesioned with kainic acid in the nigra, a dramatic reduction of gnawing and its replacement by sniffing was observed after administration of higher doses of apomorphine (1.0, 2.5 mg/kg). Bilateral infusion of kainic acid (0.75 microgram) into the reticular information, 2.0 mm dorsal to the substantia nigra, had no effect on apomorphine-induced stereotyped behaviour. These results are in agreement with the concept that the substantia nigra, through non-DA pars reticulata neurons, mediates motor and behavioural syndromes of striatal origin.

Animals↗
PubMed1980

Effect of discrete kainic acid-induced lesions of corpus caudatus and globus pallidus on glutamic acid decarboxylase of rat substantia nigra.

Locally applied kainic acid was used in order to destroy pallidal perikarya without damaging axons en passage, in an effort to clarify the role of the globus pallidus as a source of nigral GABAergic terminals. Rats were microinjected unilaterally with kainic acid in the globus pallidus, head, body and tail of the caudate and were sacrificed 7 days later. The forebrain of each rat was examined histologically in order to establish the extent of the lesion and nigral glutamate decarboxylase (GAD) was assayed as a marker of GABAergic terminals. Kainic acid produced in the globus pallidus loss of neuronal perikarya and reactive gliosis. Large multipolar neurons of the globus pallidus were characteristically absent on the lesioned-side. Lesions of the pallidum resulted in a non-significant (5.5%) reduction of nigral GAD. Kainate lesions restricted to the head of the caudate resulted in a significant (19%) drop of nigral GAD, while lesions of the caudate body provided the largest reductions of nigral GAD (53%). Lesions of the caudate tail were without effect. The results indicate that nigral GAD arises mostly from the body and, in part, also from the head of the caudate but not from the globus pallidus or from the tail of the caudate.

Animals↗
PubMed1980

Cytokinetic evaluation in human head and neck cancer by autoradiography and DNA cytofluorometry.

As part of a comprehensive research program on cell proliferation characteristics of squamous cell carcinoma in humans and the relation of these characteristics to treatment, 4 untreated cases of head and neck cancer and 2 recurrences were studied. Previously, cell kinetics following the percent labelled mitoses method were done and the same carcinomas now studied by measuring microfluorometrically the time distribution of the nuclear DNA content. Two cases were characterized by a homogeneous cell population, whereas in 2 other cases, two cycling subpopulations distinguished by their DNA content were encountered. The clinical response was not related to the occurrence of single- or multiple-cell populations. In all cases, a great variability in the mitotic index (MI) and in the proportion of cells in the different cycle phases was found. The heterogencity in the proliferative structure of these tumors stresses the need for a greater accuracy in performing cell kinetics studies in vivo and could account for the difficulties in devising a therapeutic regimen based on cycle or phase-specific agents.

Autoradiography↗
PubMed1980

Loss of striatal neurons after local microinjection of colchicine.

Intrastriatal injections of colchicine (4 micrograms) produced irreversible striatal damage characterized 30 days later by loss of intrinsic striatal neurons, gliosis and shrinkage but no apparent damage to myelinated bundles of the internal capsule. This neuronal loss was associated with a dramatic reduction of striatal and nigral glutamate-decarboxylase (GAD), the marker of GABA-ergic synapses and of striatal choline-acetyltransferase (CAT), the marker of cholinergic synapses. The levels of dopamine (DA) and serotonin (5HT) in the striatum as well as those of their metabolites were also reduced, indicating that colchicine exerts toxic effects also on terminals of striatal afferent neurons.

Animals↗
PubMed1980

[Control of arterial pressure in aortic coarctation surgery].

After reporting personal experience in the pharmacological control of intraoperative hypertension in 14 patients with aortic coarctation, 7 of them treated with trimetaphan (TMF) and 2 with nitroprussiate of sodium (NPS), stress is laid on the advantages of NPS in comparison with TMF, namely as regards speed of induction, prompt reversibility of action and lesser interference with the haemodynamics of the renal and coronary circulations. Attention is also called to the collateral effects, such as reflex cardiostimulation, which may require the use of beta-blocking drugs, and cyanide-induced toxicity which demands dose limitation (0.5 mg/kg/h). NPS is considered the drug of choice in those situations which require emergency pressure control and in controlled hypotension, for which TMF was used in the past.

Adolescent↗
PubMed1979

Evidence for a GABAergic projection from the substantia nigra to the ventromedial thalamus and to the superior colliculus of the rat.

Unilateral intranigral infusion of kainic acid (1.5 microgram) produced neuronal loss in the lateral two-thirds of the nigra while sparing axons en passage. Fink-Heimer silver impregnation revealed dense terminal degeneration in the nigra itself (both in the compacta and in the reticulata) and in areas of non-dopaminergic nigral projection such as the ventromedial (VM) nucleus of the thalamus, the superior colliculus and the reticular formation; only spare terminal degeneration was found in areas of dopaminergic projection such as the caudate and septum. In order to clarify the nature of the transmitter of the nigrothalamic and nigrocollicular neurons, the activity of glutamic decarboxylase (GAD), the marker of cholinergic neurons, was measured in the VM and ventrobasal (VB) thalamus and in the nigra of each side, 7 days after unilateral intranigral injection of kainic acid. GAD activity was reduced significantly in the VM-thalamus (-33%), in the superior colliculus (-40%) and in the substantia nigra (-18%) but not in the VB-thalamus of the lesioned side. CAT remained unchanged in these areas. Similar results were obtained in the thalamus and in the superior colliculus after electrocoagulative lesions of the nigra. The results indicate the existence of a nigrothalamic and of a nigrocollicular GABAergic pathway. This projection might play an important role in motor coordination and gaze control.

Animals↗
PubMed1979

Substantia nigra as an out-put station for striatal dopaminergic responses: role of a GABA-mediated inhibition of pars reticulata neurons.

Intranigral administration of kainic acid results in loss of pars reticulata neurons without damage to axons traversing or terminating within the nigra. Unilateral nigral lesions with kainic acid result in an ipsilateral turning upon administration of apomorphine, a dopamine (DA)-receptor agonist and in contralateral turning upon administration of haloperidol, a DA-receptor blocker. Destruction of post-synaptic structures in the striatum of the side contralateral to that injected with kainic acid results in a drastic reduction, abolition or even reversal of the turning effects elicited by apomorphine and haloperidol. Unilateral intranigral microinjection of nanogram amounts of the GABA-receptor antagonists picrotoxin and bicuculline elicits ipsilateral circling upon apomorphine administration. Kainic-induced lesion or microinjection of picrotoxin or bicuculline in the nigra ipsilateral to a 6-OHDA-lesion of nigro-striatal DA-neurons results in reduction, abolition or reversal of the contralateral circling produced by apomorphine. The results indicate that the nigra pars reticulata is a station for dopaminergic impulses originating from the striatum and suggest that the turning behavior in response to striatal DA-receptor stimulation is due to a GABA-mediated inhibition of ipsiversive pars reticulata neurons.

Animals↗
PubMed1979

Opposite turning effects of dainic and ibotenic acid injected in the rat substantia nigra.

Unilateral intranigral administration of kainic and ibotenic acid, two putative stimulants of glutamatergic mechanisms, elicited turning behaviour starting from doses of 10 ng. While the turning produced by kainic acid was ipsilateral, that produced by ibotenic acid was contralateral to the injected side. Previous destruction of dopaminergic neurons on the side of the intranigral injection failed to reduce the turning behaviour. Peripheral treatment with picrotoxin did not reduce the turning in response to ibotenic acid. The results might suggest the existence of excitatory and inhibitory glutamate receptors which control nigral non-dopaminergic neurons mediating turning-behaviour.

Animals↗