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This Article Full Text Full Text (PDF) All Versions of this Article: JOE-09-0323v1 204/1/31    most recent Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Nieves-Martinez, E Articles by Nicolle, M M Search for Related Content PubMed PubMed Citation Articles by Nieves-Martinez, E Articles by Nicolle, M M

¹ Neuroscience Program
² Physiology and Pharmacology
³ , Neurobiology and Anatomy
⁴ Department of Internal Medicine, Section of Gerontology, Wake Forest University Health Sciences, Medical Center Boulevard, Winston-Salem, North Carolina 27157-1083, USA
⁵ Reynolds Oklahoma Center on Aging, Oklahoma University Health Sciences Center, Oklahoma City, Oklahoma 73104, USA

(Correspondence should be addressed to M M Nicolle; Email: mnicolle{at}wfubmc.edu)

^* (E Nieves-Martinez and W E Sonntag contributed equally to this work)

GH levels increase to high concentrations immediately before puberty then progressively decline with age. GH deficiency (GHD) originating in childhood is treated with GH supplementation to foster somatic development during adolescence. It is not clear if or how early GH replacement affects memory in adulthood, or whether it can prevent the cognitive deficits commonly observed in adults with childhood-onset GHD. Rats homozygous for the Dw-4 mutation (dwarf) do not exhibit the normal increase in GH at 4 weeks of age when GH levels normally rise and are used to model childhood or early-onset GHD (EOGHD). One group of these rats was injected with GH from 4 to 14 weeks of age to model GH supplementation during adolescence with GHD beginning in adulthood (adult-onset GHD; AOGHD). Another group received GH from 4 weeks throughout the lifespan to model normal lifespan GH (GH-replete). Age-matched, Dw-4 heterozygous rats (HZ) do not express the dwarf phenotype and were used as controls. At 8 and 18 months of age, spatial learning in the water maze was assessed. At 8 months of age all experimental groups were equally proficient. However, at 18 months of age, the EOGHD group had poor spatial learning compared to the AOGHD, GH-replete, and HZ groups. Our data indicate that GHD during adolescence has negative effects on learning and memory that emerge by middle-age unless prevented by GH supplementation.