Seasonal Neuroendocrine Rhythms in the Male Siberian Hamster Persist After Monosodium Glutamate-Induced Lesions of the Arcuate Nucleus in the Neonatal Period

• Published in: Journal of neuroendocrinology Vol. 10; no. 9; pp. 701 - 712
• Main Authors: Ebling, Francis P., Arthurs, Owen J., Turney, Ben W., Cronin, Anna S.
• Format: Journal Article
• Language: English
• Published: Oxford, UK Blackwell Science Ltd 01.09.1998; Wiley Subscription Services, Inc
• Subjects: Adipose Tissue - pathology; Aging - physiology; Animals; Animals, Newborn - physiology; Arcuate Nucleus of Hypothalamus - drug effects; Arcuate Nucleus of Hypothalamus - growth & development; Body Weight - physiology; Brain Diseases - chemically induced; Brain Diseases - physiopathology; Cricetinae; Epididymis - pathology; Luteinizing Hormone - metabolism; Male; Molting - physiology; Neurosecretory Systems - physiopathology; Organ Size - physiology; Periodicity; Phodopus - physiology; Photoperiod; Reproduction - drug effects; Reproduction - radiation effects; Seasons; Sodium Glutamate - pharmacology
• ISSN: 0953-8194; 1365-2826
• DOI: 10.1046/j.1365-2826.1998.00253.x

The aim of these experiments was to examine the role of the arcuate nucleus in the control of seasonal cycles of body weight, feed intake, moulting and reproduction in the Siberian hamster. The arcuate nucleus has previously been implicated as a central site where systemic feedback signals (e.g. leptin) might act to regulate feed intake and body weight, so it was predicted that hamsters with lesions of this structure would be unable to display the inhibitory effects of short days on these parameters. In the first series of studies, lesions that destroyed approximately 80% of the cells in the arcuate nucleus were produced by treating hamsters neonatally with monosodium glutamate (MSG; 4 mg/g body weight sc), and vehicle‐ and MSG‐treated males were raised from birth in long days (LD) or short days (SD). In hamsters raised in LD, the initial gain in body weight and testicular growth were significantly reduced by MSG treatment, however, growth rate and testis weight were still significantly greater than in vehicle‐ or MSG‐treated hamsters raised in SD. In the second study, hamsters treated neonatally with vehicle or MSG were raised in LD for 8 weeks and, subsequently, approximately half in each group were transferred to SD for 18 weeks. As expected, vehicle‐treated hamsters showed a characteristic decline in body weight when exposed to SD, while those remaining in LD continued to increase body weight. Feed intake decreased in parallel with the decline in body weight in SD, a complete moult to the white winter pelage occurred by 16 weeks in SD, and testicular regression occurred. Responses to SD also occurred in the MSG‐treated hamsters: body weight decreased in SD but increased in their lesioned litter mates remaining in LD, and feed intake paralleled body weight changes in these groups. The moult to winter pelage was significantly retarded in MSG‐treated hamsters transferred to SD. The testes were completely regressed in sham‐ and MSG‐treated hamsters exposed to SD, whereas testes weights in MSG‐treated hamsters maintained in LD were intermediate between those in vehicle‐treated hamsters in SD and LD. Thus, despite initial effects on growth, the MSG‐treated hamsters bearing substantial lesions of the arcuate nucleus were able to show appropriate responses to photoperiod, although not always of the same magnitude as the unlesioned controls. We conclude that feedback mechanisms operating via the arcuate nucleus are not the major regulators of seasonal cycles of body weight, feed intake, pelage and reproduction.