Effect of limbic system lesions on acetylcholine release from the cerebral cortex of the rat

The effect of electrocoagulative lesions placed in the septum, fornix and fimbria, fimbria and hippocampus on ACh release from the cerebral cortex was investigated in rats under urethane anaesthesia. At least 2 weeks elapsed between the stereotactic placement of the lesions and the determination of ACh output. ACh was determined by bioassay on the dorsal muscle of the leech. No lesion affected the spontaneous release of ACh. The increase in ACh output induced by i.p. administration of amphetamine was abolished by the septal lesion only. On the other hand, the increase in ACh output induced by i.p. administration of scopolamine was strongly reduced by lesions of the septum, of the fornix and fimbria and to a lesser extent of the fimbria. The administration of amphetamine and scopolamine discloses therefore a specific functional impairment of the cerebral cholinergic mechanisms in rats with limbic lesions.This research was supported by Grant No. 71.00870.04 of the Consiglio Nazionale delle Ricerche.     

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 μg) 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 μg) 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.     

FcRIII (CD16) expression on neutrophils from chronic myeloid leukemia. A flow cytometric study

FcRIII (CD16) expression an neutrophils from 17 patients with chronic myeloid leukemia (CML) was studied by flow cytometry using monoclonal antibodies. A variable proportion of CD16-negative neutrophils were found both in CML patients in chronic phase (3 out of 8 patients) and in CML patients in hematological remission (3 out of 9 patients). Neutrophils with reduced FcR111 expression showed more defective chemiluminescence and phagocytosis than neutrophils with normal FcRIII expression. Circulating myeloid cells from three patients in chronic phase, showing a normal percentage of CD16-positive neutrophils, were isolated and fractionated by discontinuous Percoll gradients. This study showed that CD16 appears at the stage of metamyelocyte, that band cells and segmented neutrophils display an identical pattern of membrane FcRIII, and that the fluorescence intensity shown by metamyelocytes is different from that displayed by more mature cells. The association between low FcRIII expression and function abnormality could be suggestive of a defect in CML neutrophil maturation.     

Evaluation of the cardiomyopathy in becker muscular dystrophy

To evaluate the features and the course of cardiomyopathy in Becker muscular dystrophy, 68 patients–identified by clinical assessment and by reduced dystrophin labeling and/or DNA analysis–were followed in the years 1976–1993, for periods ranging from 3 to 18 years (mean 8). Patients periodically underwent clinical, electrocardiographic, echocardiographic, nuclear, and radiological assessments. Preclinical cardiac involvement was found in 67.4% of patients under 16 years of age, decreasing to 30% in patients older than 40. Clinically evident cardiomyopathy was found in 15% of patients under 16 years of age, increasing to 73% in patients older than 40. A real, dilated cardiomyopathy is the most frequent type of myocardial involvement after the age of 20. Results show that the severity of cardiac involvement can be unrelated to the severity of skeletal muscle damage and confirm that cardiac dysfunction is a primary feature of Becker muscular dystrophy.© 1995 John Wiley &Sons, Inc.     

The effect of pirenzepine (LS 519), a specific antimuscarinic drug,on cortisol levels in man

The authors investigated the effect of a single 75-mg oral dose of pirenzepine, a drug which selectively blocks the muscarinic receptors and does not cross the blood-brain barrier, on the function of the HPA axis. A significant decrease in basal cortisol values following the administration of the drug was observed in comparison with a placebo test. Moreover, the adrenal response to exogenous adrenocorticotropin (ACTH) administration was unchanged following a 5-day course of the drug, ruling out direct action of pirenzepine at the adrenal level. These data suggest that cholinergic muscarinic hypothalamic and/or pituitary systems may be involved in the regulation of ACTH-cortisol secretion.     

Prospective study of X-linked progressive muscular dystrophy in campania

Within the Campania region of southern Italy a prospective study on X-linked progressive muscular dystrophy was conducted over a period of 12 years from 1969 to 1980, inclusive. The mean incidence rate was 21.7 per 100,000 male livebirths for Duchenne muscular dystrophy (DMD) cases and 3.2 per 100,000 male livebirths for Becker muscular dystrophy (BMD) cases. The familial cases were 38.5% among the DMD patients and 50% among the BMD patients. Myocardial involvement appeared in DMD patients at about 6 years of age in a high percentage of cases and increased progressively until the last years of life, when cardiac damage occurred in 95% of cases. The percentage of myocardial involvement in BMD patients was very low before 13 years of age, but increased progressively until 20 years, when cardiac damage occurred in 80% of cases studied; severe cardiomyopathy did not occur before the age of 21. The data reported also include the effects of age on physical performance, serum creatine kinase activity and serum myoglobin levels, the types of cardiac damage, and the causes of death.