The Role of a Global Mechanism in Developmental Change in Speed of Processing

Author(s):  
Robert Kail
Author(s):  
Leo Sher

Abstract Adolescent suicide research has mostly focused on demographic risk factors. Such studies focus on who is at risk, but do not explain why certain adolescents are at risk for suicide. Studies of the neurobiology of adolescent suicide could clarify why some youths are more suicidal than others and help to find biological markers of suicidal behavior in teenagers. Over the past decade the role of brain-derived neurotrophic factor (BDNF) in the pathophysiology of suicidal behavior has attracted significant attention of scientists. BDNF is involved in the pathophysiology of many psychiatric disorders associated with suicidal behavior including depression, post-traumatic stress disorder, schizophrenia, and obsessive-compulsive disorder. BDNF dysregulation could be associated with increased suicidality independently of psychiatric diagnoses. BDNF plays an important role in the regulation and growth of neurons during childhood and adolescence. Prominent among the brain regions undergoing developmental change during adolescence are stressor-sensitive areas. The serotonin dysfunction found in adolescent and adult suicidal behavior could be related to the low level of BDNF, which impedes the normal development of serotonin neurons during brain development. BDNF dysfunction could play a more significant role in the pathophysiology of psychiatric disorders and suicidal behavior in adolescents than in adults. Treatment-induced enhancement in the BDNF function could reduce suicidal behavior secondary to the improvement in psychiatric pathology or independently of improvement in psychiatric disorders. It is interesting to hypothesize that BDNF could be a biological marker of suicidal behavior in adolescents or in certain adolescent populations.


2010 ◽  
Vol 365 (1541) ◽  
pp. 819-830 ◽  
Author(s):  
Jan A. K. W. Kiel

Cells need a constant supply of precursors to enable the production of macromolecules to sustain growth and survival. Unlike metazoans, unicellular eukaryotes depend exclusively on the extracellular medium for this supply. When environmental nutrients become depleted, existing cytoplasmic components will be catabolized by (macro)autophagy in order to re-use building blocks and to support ATP production. In many cases, autophagy takes care of cellular housekeeping to sustain cellular viability. Autophagy encompasses a multitude of related and often highly specific processes that are implicated in both biogenetic and catabolic processes. Recent data indicate that in some unicellular eukaryotes that undergo profound differentiation during their life cycle (e.g. kinetoplastid parasites and amoebes), autophagy is essential for the developmental change that allows the cell to adapt to a new host or form spores. This review summarizes the knowledge on the molecular mechanisms of autophagy as well as the cytoplasm-to-vacuole-targeting pathway, pexophagy, mitophagy, ER-phagy, ribophagy and piecemeal microautophagy of the nucleus, all highly selective forms of autophagy that have first been uncovered in yeast species. Additionally, a detailed analysis will be presented on the state of knowledge on autophagy in non-yeast unicellular eukaryotes with emphasis on the role of this process in differentiation.


2013 ◽  
pp. n/a-n/a ◽  
Author(s):  
Stephan A. Verschoor ◽  
Michiel Spapé ◽  
Szilvia Biro ◽  
Bernhard Hommel

1997 ◽  
Vol 272 (3) ◽  
pp. C894-C900 ◽  
Author(s):  
K. S. Shin ◽  
J. Y. Park ◽  
H. Kwon ◽  
C. H. Chung ◽  
M. S. Kang

We examined the developmental change of inwardly rectifying K+ channels (IRK) and its possible role in myogenesis. Northern blot analysis revealed an increase in the level of IRK mRNA during myogenesis. Accordingly, IRK current was not detectable in replicating myoblasts but first appeared in aligned myoblasts that were competent for fusion and gradually increased thereafter. The time course change of IRK activity was closely related to the increase in resting membrane potential during myogenesis. Application of 0.5 mM Ba2+ to the bath depolarized the membrane and blocked IRK currents dramatically but not outwardly rectifying K+ currents. Myoblasts devoid of IRK had low resting K+ permeability, whereas myotubes that possess IRK had high resting K+ permeability. In some aligned myoblasts, anomalous hyperpolarization was elicited by increasing extracellular K+ concentration, which may be attributable to the increased conductance of IRK. Noteworthy was the fact that maximal fusion was obtained at this range of K+ concentration. These findings imply that IRK is responsible for the change in the K+ permeability during chick myogenesis, which may provide a larger driving force for Ca2+ influx that is a prerequisite for myoblast fusion.


2003 ◽  
Vol 53 (1) ◽  
pp. 165-202 ◽  
Author(s):  
Rob Schoonen ◽  
Amos van Gelderen ◽  
Kees de Glopper ◽  
Jan Hulstijn ◽  
Annegien Simis ◽  
...  

2002 ◽  
Vol 35 (6) ◽  
pp. 510-525 ◽  
Author(s):  
Hugh W. Catts ◽  
Matthew Gillispie ◽  
Laurence B. Leonard ◽  
Robert V. Kail ◽  
Carol A. Miller

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