Biomedical subjects

M Bahro

Publications and source records attributed to M Bahro.

41 records · Page 3Linked to original sources

PubMed1987

Short-term inhibition of cellular autophagy by isoproterenol in the submandibular gland.

The present study examines the short-term (i.e. 10 min after injection) influence of isoproterenol on cellular autophagy in the rat submandibular gland. The volume fraction of autophagic vacuoles was significantly reduced, suggesting that an anticatabolic reaction, namely inhibition of cellular autophagy, is an early and significant event in the growth of the submandibular gland which is known to occur with long-term isoproterenol treatment.

Animals↗

PubMed1987

Short-term stimulation by propranolol and verapamil of cardiac cellular autophagy.

The influence of propranolol and verapamil, i.e. two cardiodepressant drugs differing in their pharmacological actions, on cellular autophagy in the left ventricular myocardium of the rat was investigated. In the first experimental series 10 animals were given propranolol subcutaneously (3 mg/kg body weight). Ten controls received physiological saline. In the second series 8 animals were treated with verapamil subcutaneously (9 mg/kg body weight) and 8 controls with physiological saline. Two to 4 h after the injections in the first series and 1 3/4 to 3 h in the second series retrograde perfusion fixation was carried out via the abdominal aorta with a paraformaldehyde-glutaraldehyde mixture. Myocardial tissue from the left anterior wall was processed for electron microscopy and was morphometrically evaluated for volume fraction and numerical density of early stages of autophagic vacuoles (AVs). Propranolol and verapamil significantly increased the AV volume fraction 4.3- and 2.7-fold, respectively. The numerical density was increased by the two drugs, although to a lesser degree (2.3-fold, and 1.7-fold, respectively). As verapamil affects neither the beta-adrenoreceptors nor the intracellular levels of the second messenger cAMP, the only common denominator for the stimulation of cellular autophagy seems to be the cardiodepressive effect of the two drugs. The data suggest that the rise in cellular autophagy is an early regulatory step in the adaptation of heart muscle mass to reduced work load.

Animals↗

PubMedDate not supplied

The value of REM sleep parameters in differentiating Alzheimer's disease from old-age depression and normal aging.

Pseudodementia as a common trait in elderly depressives presents a major problem in gerontopsychiatry, especially for the differential diagnosis between Old-Age Depression (OAD) and Dementia of the Alzheimer Type (DAT). The present polysomnographic study examined parameters of sleep continuity, sleep architecture, and REM sleep to differentiate DAT from OAD. The investigation was based on the theoretical framework of the cholinergic-aminergic imbalance model of depression, the cholinergic deficit hypothesis of Alzheimer's disease and the reciprocal interaction model of Non-REM/REM sleep regulation, according to which REM sleep parameters should have high discriminative value to differentiate OAD and DAT. We investigated 35 DAT patients, 39 OAD patients and 42 healthy controls for two consecutive nights in the sleep laboratory. The DAT patients were in relatively early/mild stages of the disease, the severity of depression in the OAD group was moderate to severe. Depressed patients showed characteristic 'depression-like' EEG sleep alterations, i.e. a lower sleep efficiency, a higher amount of nocturnal awakenings and decreased sleep stage 2. Sleep continuity and architecture in DAT was less disturbed. Nearly all REM sleep measures differentiated significantly between the diagnostic groups. OAD patients showed a shortened REM latency, increased REM density and a high rate of Sleep Onset REM periods (SOREM), whereas in DAT REM density was decreased in comparison to control subjects. REM latency in DAT was not prolonged as expected. To assess the discriminative power of REM sleep variables a series of discriminant analyses were conducted. Overall, 86% of patients were correctly classified, using REM density and REM latency measures. Our findings suggest that REM density as an indicator of phasic activity appears to be more sensitive as a biological marker for the differential diagnosis of OAD and DAT than REM latency. The results support the role of central cholinergic neurotransmission in REM sleep regulation and the pathogenesis of DAT and OAD.

Aged↗

PubMedDate not supplied

Interactions of prefrontal cortex during eyeblink conditioning as a function of age.

Changes in regional cerebral blood flow (rCBF) in eleven elderly subjects during pairings of tone and air puff were compared to rCBF changes during pairings in young subjects. Although all subjects reported being aware of the relationship between tone and air puff, elderly subjects did not condition as well as young subjects and their rCBF measures were attenuated. Covarying the performance differences between young and old subjects did not change this conclusion suggesting that differences in neural activation during learning are related to binding of CS-US information prior to the impact of the association on performance. Both groups showed learning-specific rCBF changes in cerebellum, inferior right prefrontal cortex and posterior cingulate. However, only in young subjects were there learning-specific changes in rCBF in left temporal cortex, midbrain, caudate, and inferior left prefrontal cortex. Analysis of learning-dependent patterns of functional connectivity of inferior left prefrontal cortex showed only young subjects had a strong left prefrontal functional connectivity with cerebellum, hippocampus, thalamus and temporal cortex. Thus, beyond changes in regional activity, these data also suggest that age may alter the operations of functional networks underlying learning and memory.

Adolescent↗

PubMedDate not supplied

Involvement of autophagic degradation in ACTH-induced skeletal muscle atrophy.

Intracellular autophagic breakdown was investigated in skeletal myocytes undergoing atrophy under the influence of ACTH. Adult male Sprague-Dawley rats received s.c. injections of ACTH (12.5 U/kg body wt) or physiological saline as control twice daily. 5 experimental and 5 control animals were sacrificed by perfusion fixation after 6, 9, and 12 days of treatment. While the weight of the left pectoralis minor muscle decreased significantly in the ACTH-treated animals compared with controls, the volume fraction of autophagic vacuoles, as determined by quantitative electron microscopy, increased significantly after 9 days (2.6-fold) and 12 days (2.9-fold) in the atrophying skeletal myocytes of experimental animals compared with controls. Only non-myofibrillar components were detected as contents of autophagic vacuoles. Since, however, the ratio of myofibrils to other cytoplasmic components remained constant, the degradation of myofibrils seems to occur via a non-lysosomal pathway. The data suggest that the breakdown of cytoplasmic components by cellular autophagy is important for the development of skeletal muscle atrophy as observed following long-term ACTH treatment or in Cushing's syndrome.

Adrenocorticotropic Hormone↗