Hot and Steady: Elevated Temperatures Do Not Enhance Muscle Disuse Atrophy During Prolonged Aestivation in the Ectotherm Cyclorana Alboguttata.

Hot and steady: Elevated temperatures do not enhance muscle disuse atrophy during prolonged aestivation in the ectotherm Cyclorana alboguttata.

Filed under: Depression Treatment

J Morphol. 2012 Sep 20;
Young KM, Cramp RL, Franklin CE

Animals that undergo prolonged dormancy experience minimal muscle disuse atrophy (MDA) compared to animals subjected to artificial immobilisation over shorter timeframes. An association between oxidative stress and MDA suggests that metabolic depression presumably affords dormant animals some protection against muscle disuse. Because aerobic metabolism is temperature sensitive, we proposed that MDA in dormant (aestivating) ectotherms would be enhanced at elevated temperatures. In the green-striped burrowing frog, Cyclorana alboguttata, the thermal sensitivity of skeletal muscle metabolic rate is muscle-specific. We proposed that the degree of atrophy experienced during aestivation would correlate with the thermal sensitivity of muscle metabolic rate such that muscles with a relatively high metabolic rate at high temperatures would experience more disuse atrophy. To test this hypothesis, we examined the effect of temperature and aestivation on the extent of MDA in two functionally different muscles: the M. gastrocnemius (jumping muscle) and M. iliofibularis (non-jumping muscle), in C. alboguttata aestivating at 24 or 30°C for 6 months. We compared a range of morphological parameters from muscle cross-sections stained with succinic dehydrogenase to show that muscle-specific patterns of disuse atrophy were consistent with the relative rates of oxygen consumption of those muscle types. However, despite muscle-specific differences in thermal sensitivity of metabolic rate, aestivation temperature did not influence the extent of atrophy in either muscle. Our results suggest that the muscles of frogs aestivating at high temperatures are defended against additional atrophy ensuring protection of muscle function during long periods of immobilisation. J. Morphol., 2012. © 2012 Wiley Periodicals, Inc.
HubMed – depression


Differences between Depression and Paranoia: The Role of Emotional Memories, Shame and Subordination.

Filed under: Depression Treatment

Clin Psychol Psychother. 2012 Sep 20;
Pinto-Gouveia J, Matos M, Castilho P, Xavier A

The present study explores how emotional memories, shame and submissive behaviour in adulthood are differently related to depression and paranoia, in a sample of 255 subjects from the general community population. Results show that emotional memories (especially, shame traumatic memory) are significantly correlated with external and internal shame. Emotional memories are significantly associated with submissive behaviour. Both types of shame are correlated with submissive behaviour, particularly internal shame. Emotional memories, external and internal shame are linked to depressive symptoms. Emotional memories, external and internal shame, and submissive behaviour are significantly related to paranoia. Path analysis results suggested that (1) shame traumatic memory and recall of threat and submissiveness in childhood predicted depressive symptoms through external and internal shame; (2) early emotional memories of shame, threat and submissiveness predicted paranoid ideation both directly and indirectly, through external shame; and (3) emotional memories impact on paranoid ideation both through their effect upon external shame and also through their indirect effect upon submission, which in turn fully mediates the effect of internal shame upon paranoid ideation. These findings highlight the differences between depression and paranoia. In depression, it is the internalization of early experiences of shame, threat and submissiveness that heighten the vulnerability to depressive states. In paranoia, not only shame traumas and recollections of threat and submissiveness directly influence paranoid beliefs but also these memories promote external and internal shame thoughts and feelings and submissive defenses, which in turn increase paranoid ideation. Copyright © 2012 John Wiley & Sons, Ltd. KEY PRACTITIONER MESSAGE: Individuals with shame traumas, threat and submissiveness experiences in childhood and high levels of external and internal shame report more depressive symptoms. High levels of paranoid beliefs are associated with high negative emotional memories, external and internal shame thoughts and feelings, and submissive behaviour defenses. Therapy for depression needs to incorporate strategies that help individuals develop skills to deal with shame experiences and its outputs. Treatment for paranoid ideation must address external and internal shame, as well as emotional memories of shame, threat and submissiveness in childhood and development of assertive skills.
HubMed – depression


?-Amyloid induced effects on cholinergic, serotonergic, and dopaminergic neurons is differentially counteracted by anti-inflammatory drugs.

Filed under: Depression Treatment

J Neurosci Res. 2012 Sep 20;
Hochstrasser T, Hohsfield LA, Sperner-Unterweger B, Humpel C

?-Amyloid (A?) is a small peptide that plays a potent role in synaptic plasticity as well as forms amyloid plaques in Alzheimer’s disease (AD). Recent studies suggest that A? deposition is deleterious not only in AD, but also in Parkinson’s disease (PD) and depression. This A? effect is associated with inflammatory processes. However, further evaluation is needed to understand how A? and inflammation interact and contribute to the regulation of the cholinergic, serotonergic, and dopaminergic neuronal populations. The aim of the present study was to investigate the effects of A?(1-42) on cholinergic neurons of the nucleus basalis of Meynert (which degenerate in AD), on serotonergic neurons of the dorsal raphe nucleus (which play a role in depression), and on dopaminergic neurons of the ventral mesencephalon (which degenerate in PD) in rat organotypic brain slices. Furthermore, we investigated whether anti-inflammatory drugs (celecoxib, citalopram, cyclooxygenase-2 inhibitor, ibuprofen, indomethacin, piclamilast) modulate or counteract A?-induced effects. Two-week-old organotypic brain slices of the nucleus basalis of Meynert, dorsal raphe nucleus, and ventral mesencephalon were incubated with 50 ng/ml A?(1-42) with or without anti-inflammatory agents for 3 days. Our results reveal that A? significantly decreased the number of choline acetyltransferase-positive cholinergic, tryptophan hydroxylase-positive serotonergic, and tyrosine hydroxylase-positive dopaminergic neurons and that anti-inflammatory drugs partially counteracted the A?-induced neuronal decline. This decline was not due to apoptotic processes (as evaluated by TUNEL, propidium iodide, caspase), oxidative stress (as measured by nitrite, catalase, or superoxide dismutase-2), or inflammation, but was most likely caused by a downregulation of these key enzymes. © 2012 Wiley Periodicals, Inc.
HubMed – depression


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