Dendritic pruning of the medial amygdala during pubertal development of the male Syrian hamster.
The medial amygdala (Me), a brain region essential for mating behavior, changes in size during puberty. In pre-, mid-, and late pubertal (21, 35, and 49 days of age) male Syrian hamsters, we examined neuronal structure in Me and protein levels of spinophilin and synaptophysin in the amygdaloid complex for evidence of synaptic plasticity coincident with behavioral and physiological development. Body weight, testes weight, and testosterone levels increased during puberty. Mounting behavior, including ectopic, nonintromittive, and intromittive mounts, also increased. Neuronal structure in the posterodorsal medial amygdala (MePD) was assessed in Golgi-impregnated neurons. Pruning occurred during puberty in the number of dendrites emanating from the cell body and in terminal dendritic spine densities. Approximately half of all MePD neurons analyzed had an axon emanating from a dendrite rather than the cell body. However, prepubertal males were more likely to have the axon emanating from a higher order dendritic segment (secondary or tertiary) than were mid- and late pubertal males. Finally, protein levels in the amygdaloid complex varied with pubertal age. Spinophilin decreased, while synaptophysin and GAPDH protein levels increased. These results suggest that puberty is a period of dramatic synaptic plasticity in Me. Specifically, pruning of dendrites and spines, in combination with axonal changes, is likely to modify the afferent influences and electrophysiological properties of Me neurons. Because the Me is an integral component of a social behavior neural network, these changes may be related not only to sexual behavior, but also to other behaviors that mature during puberty, including aggressive, risk-taking, fear-related, and parental behaviors.
Neuroscience Program, Michigan State University, East Lansing, MI 48824, USA. zehrj@msu.edu
Julia L
JL
Zehr
Brigitte J
BJ
Todd
Kalynn M
KM
Schulz
Margaret M
MM
McCarthy
Cheryl L
CL
Sisk
D000375:Aging / Q000502:physiology; D000679:Amygdala / Q000254:growth & development* / Q000378:metabolism / Q000648:ultrastructure; D000818:Animals; D002454:Cell Differentiation / Q000502:physiology*; D048430:Cell Shape / Q000502:physiology; D006224:Cricetinae; D003712:Dendrites / Q000378:metabolism* / Q000648:ultrastructure; D049229:Dendritic Spines / Q000378:metabolism / Q000648:ultrastructure; D005987:Glyceraldehyde-3-Phosphate Dehydrogenases / Q000378:metabolism; D008297:Male; D008647:Mesocricetus / Q000033:anatomy & histology / Q000254:growth & development*; D008840:Microfilament Proteins / Q000378:metabolism; D009419:Nerve Tissue Proteins / Q000378:metabolism; D009473:Neuronal Plasticity / Q000502:physiology*; D009929:Organ Size / Q000502:physiology; D012733:Sex Differentiation / Q000502:physiology; D012726:Sexual Behavior, Animal / Q000502:physiology; D016622:Silver Staining; D013569:Synapses / Q000378:metabolism / Q000648:ultrastructure; D009435:Synaptic Transmission / Q000502:physiology; D016708:Synaptophysin / Q000378:metabolism; D013737:Testis / Q000254:growth & development; D013739:Testosterone / Q000097:blood; D015854:Up-Regulation / Q000502:physiology; D000099273:Neurabins
D005987:Glyceraldehyde-3-Phosphate Dehydrogenases; D008840:Microfilament Proteins; D009419:Nerve Tissue Proteins; D016708:Synaptophysin; D013739:Testosterone; D000099273:Neurabins