Effects of social deprivation in prepubescent rhesus monkeys: immunohistochemical analysis of the neurofilament protein triplet in the hippocampal formation.
Social deprivation during early postnatal life has profound and long-lasting effects on the behavior of primates, including prolonged and exaggerated responses to stress as well as impaired performance on a variety of learning tasks. Although the cellular changes that underlie such alterations in behavior are unknown, environmentally induced psychopathology may involve morphologic or biochemical changes in select neuronal populations. The hippocampal formation of both socially deprived and socially reared prepubescent rhesus monkeys was selected for immunocytochemical investigation because of its association with the behavioral stress response and learning. Immunocytochemical analysis using antibodies specific for the neurofilament protein triplet was performed since these proteins are modified within degenerating neurons in a variety of neurodegenerative disorders. Results from optical density measurements indicate an increase in the intensity of non-phosphorylated neurofilament protein immunoreactivity in the dentate gyrus granule cell layer of socially deprived monkeys in comparison with that of socially reared animals, suggesting that early social deprivation may result in an increase in the amount of non-phosphorylated neurofilament protein in these cells. This phenotypic difference in dentate granule cells between differentially reared monkeys supports the notion that specific subpopulations of neurons in brain regions that subserve complex behaviors may undergo long-term modifications induced by environmental conditions. Furthermore, the data suggest that constitutive chemical components related to structural integrity may be as susceptible to early environmental manipulations as the more traditionally viewed measures of cellular perturbations, such as neurotransmitter dynamics, cell density and the establishment of connectivity. The observed modifications may serve as an anatomical substrate for behavioral abnormalities that persist in later life.
Fishberg Research Center for Neurobiology, Mount Sinai School of Medicine, New York, NY 10029.
S J
SJ
Siegel
S D
SD
Ginsberg
P R
PR
Hof
S L
SL
Foote
W G
WG
Young
G W
GW
Kraemer
W T
WT
McKinney
J H
JH
Morrison
D000818:Animals; D000911:Antibodies, Monoclonal; D006624:Hippocampus / Q000166:cytology / Q000502:physiology*; D007150:Immunohistochemistry; D008253:Macaca mulatta; D016900:Neurofilament Proteins / Q000032:analysis / Q000378:metabolism*; D009474:Neurons / Q000166:cytology / Q000502:physiology*; D011712:Pyramidal Tracts / Q000166:cytology / Q000502:physiology*; D012741:Sexual Maturation; D012934:Social Isolation
D000911:Antibodies, Monoclonal; D016900:Neurofilament Proteins