Long term effects of vincristine on the peripheral nervous system

1993 ◽  
Vol 15 (1) ◽  
pp. 23-27 ◽  
Author(s):  
T. J. Postma ◽  
B. A. Benard ◽  
P. C. Huijgens ◽  
G. J. Ossenkoppele ◽  
J. J. Heimans

1987 ◽  
Vol 7 (1) ◽  
pp. 29-37 ◽  
Author(s):  
Sergio Barbieri ◽  
Carlo Pirovano ◽  
Guglielmo Scarlato ◽  
Paolo Tarchini ◽  
Alessandro Zappa ◽  
...  


1992 ◽  
Vol 94 (1) ◽  
pp. 80
Author(s):  
T.J. Postma ◽  
B.A. Benard ◽  
P.C. Huijgens ◽  
G.J. Ossenkoppele ◽  
J.J. Heimans


2014 ◽  
Vol 72 (8) ◽  
pp. 648-648
Author(s):  
Joseph B.B. Brooks ◽  
Luisa F. Rocha ◽  
Yara Dadalti Fragoso


1991 ◽  
Vol 9 (2) ◽  
pp. 479-495 ◽  
Author(s):  
Patricia K. Duffner ◽  
Michael E. Cohen


2011 ◽  
Vol 27 (2) ◽  
pp. 229-233
Author(s):  
Katrin Sabine Blum ◽  
Christian Hagel ◽  
Eva Neuen-Jacob ◽  
Peter Herkenrath ◽  
Jens Fiehler ◽  
...  


Nutrients ◽  
2018 ◽  
Vol 11 (1) ◽  
pp. 7 ◽  
Author(s):  
Gitalee Sarker ◽  
Daria Peleg-Raibstein

Ample evidence from epidemiological studies has linked maternal obesity with metabolic disorders such as obesity, cardiovascular disease, and diabetes in the next generation. Recently, it was also shown that maternal obesity has long-term effects on the progeny’s central nervous system. However, very little is known regarding how maternal overnutrition may affect, in particular, the cognitive abilities of the offspring. We reported that first-generation offspring exposed to a maternal high-fat diet (MHFD) displayed age-dependent cognitive deficits. These deficits were associated with attenuations of amino acid levels in the medial prefrontal cortex and the hippocampus regions of MHFD offspring. Here, we tested the hypothesis that MHFD in mice may induce long-term cognitive impairments and neurochemical dysfunctions in the second and third generations. We found that MHFD led to cognitive disabilities and an altered response to a noncompetitive receptor antagonist of the N-Methyl-D-aspartic acid (NMDA) receptor in adult MHFD offspring in both second and third generations in a sex-specific manner. Our results suggest that maternal overnutrition leads to an increased risk of developing obesity in subsequent generations as well as to cognitive impairments, affecting learning and memory processes in adulthood. Furthermore, MHFD exposure may facilitate pathological brain aging which is not a consequence of obesity. Our findings shed light on the long-term effects of maternal overnutrition on the development of the central nervous system and the underlying mechanisms which these traits relate to disease predisposition.



1980 ◽  
Vol 39 (3) ◽  
pp. 368 ◽  
Author(s):  
Y. Kress ◽  
F. Gaskin ◽  
C. Brosnan ◽  
S. Levine


2004 ◽  
Vol 77 (5) ◽  
pp. 662-669 ◽  
Author(s):  
Ravi J. Tolwani ◽  
Jos� M. Cosgaya ◽  
Sushama Varma ◽  
Reza Jacob ◽  
Lydia E. Kuo ◽  
...  


Author(s):  
Orla Moriarty ◽  
Suellen M. Walker

Nociceptive pathways are functional following birth, and acute responses to noxious stimuli have been documented from early in development in clinical and laboratory studies. The ability of noxious afferent input to alter the level of sensitivity of nociceptive pathways in the adult nervous system, with, for example, the development of central sensitization, is well established. However, the developing nervous system has additional susceptibilities to alterations in neural activity, and pain in early life may produce effects not seen following the same input at older ages. As a result, early tissue injury may lead to persistent changes in somatosensory processing and altered sensitivity to future noxious stimuli. Furthermore, there is increasing evidence that neonatal pain can result in long-term changes in cognitive and affective behavior. Effects of pain in early life are superimposed on a highly plastic developing system, and long-term outcomes vary depending on the type and severity of the injury, and on the evaluation methods used. Laboratory studies allow evaluation of different injuries, potential confounding factors, underlying mechanisms, and potential analgesic modulation.



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