Growth hormone prevents neuronal loss in the aged rat hippocampus

Azcoitia, Íñigo; Pérez‐Martín, Margarita; Salazar, Verónica; Castillo, Carmen; Ariznavarreta, C.; Garcia-Segura, Luis Miguel; Tresguerres, Jesús A.F.

doi:10.1016/j.neurobiolaging.2004.06.007

Cited by 57 publications

(41 citation statements)

References 65 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Increased BrdU-labeling in the SVZ following long-term bGH treatment could, therefore, reflect an influence on the stem cell pool via increased cell survival. Although effects on cell survival have been previously demonstrated for both GH (Gustafson et al 1999, Azcoitia et al 2005 and IGF-I , Brywe et al 2005 following injury, the hypothesis of bGH effects on the SVZ stem cells remains speculative, due to a lack of conclusive markers for adult neural stem cells.…”

Section: Proliferation and Cell Survival -Magnitudesmentioning

confidence: 99%

See 1 more Smart Citation

Peripheral administration of GH induces cell proliferation in the brain of adult hypophysectomized rats

Åberg

Johansson²,

Åberg³

et al. 2009

Journal of Endocrinology

View full text Add to dashboard Cite

IGF-I treatment has been shown to enhance cell genesis in the brains of adult GH-and IGF-I-deficient rodents; however, the influence of GH therapy remains poorly understood. The present study investigated the effects of peripheral recombinant bovine GH (bGH) on cellular proliferation and survival in the neurogenic regions (subventricular zone (SVZ), and dentate gyrus of the hippocampus), as well as the corpus callosum, striatum, parietal cortex, and piriform cortex. Hypopituitarism was induced in female rats by hypophysectomy, and the rats were supplemented with thyroxine and cortisone acetate. Subsequently, the rats received daily s.c. injections of bGH for either 6 or 28 days respectively. Following 5 days of peripheral bGH administration, the number of bromodeoxyuridine (BrdU)-positive cells was increased in the hippocampus, striatum, parietal cortex, and piriform cortex after 6 and 28 days. In the SVZ, however, BrdU-positive cells increased only after 28 days of bGH treatment. No significant change was observed in the corpus callosum. In the hippocampus, after 28 days of bGH treatment, the number of BrdU/NeuN-positive cells was increased proportionally to increase the number of BrdUpositive cells.3 H-thymidine incorporation in vitro revealed that 24 h of bGH exposure was sufficient to increase cell proliferation in adult hippocampal progenitor cells. This study shows for the first time that 1) peripheral bGH treatment increased the number of newborn cells in the adult brain and 2) bGH exerted a direct proliferative effect on neuronal progenitor cells in vitro.

show abstract

Section: Proliferation and Cell Survival -Magnitudesmentioning

confidence: 99%

“…Although one study found that GH therapy attenuated the numbers of neurons being lost in the hippocampus of aged animals (Azcoitia et al 2005), neither cell survival nor cell genesis were assessed. Altogether, the effects of GH therapy on cellular plasticity in rats during adulthood remain poorly understood.…”

Section: Introductionmentioning

confidence: 99%

Peripheral administration of GH induces cell proliferation in the brain of adult hypophysectomized rats

Åberg

Johansson²,

Åberg³

et al. 2009

Journal of Endocrinology

View full text Add to dashboard Cite

show abstract

“…In the present study, we have investigated whether recombinant human GH administration was able to improve some immune parameters altered by age. We used an administration regime similar to that used by the other laboratories involved in this project [21] .…”

Section: Experimental Designmentioning

confidence: 99%

Effect of Growth Hormone Treatment on Lymphocyte Functions in Old Male Rats

Baeza

Alvarado²,

Ariznavarreta³

et al. 2008

Neuroimmunomodulation

Self Cite

View full text Add to dashboard Cite

Introduction: Age-related changes in the communication between the neuroendocrine and the immune system have been scarcely studied. Aging in mammals is associated with an impairment of the immune response, especially regarding lymphocyte functions. Furthermore, the endocrine system is also affected by aging, one of the most significant changes being the decrease in the secretion of several hormones such as growth hormone (GH). Objective: The aim of the present work was to study whether GH replacement therapy in old male rats could improve several lymphocyte functions. Methods: Spleen and axillary node lymphocytes from old (24 months of age) male Wistar rats were used in the present study to investigate the effect of GH (2 mg/kg daily during 10 weeks) on chemotaxis, lymphoproliferative response to the mitogen concanavalin A, interleukin 2 release and natural killer cell activity. Results: We have found that the administration of GH can reduce or even reverse the age-related changes observed in these key immune function parameters. Moreover, we have observed that the recovery of such immune functions is able to reach similar values as those exhibited by young control animals of 6 months of age. Conclusion: Considering that the immune system is a marker of health and a predictor of longevity, hormone replacement therapies with GH, by increasing the immune function and thus delaying or slowing down some aspects of the aging process, could facilitate successful aging.

show abstract

“…GH replacement therapy in GH-deficient patients has been shown to ameliorate the condition for these patients (17)(18)(19). The hormone has further been shown to prevent neuronal loss in the aged rat hippocampus, indicating a neuroprotective effect of GH on old animals (20). Decreased levels of circulating GH and decreasing density of GH-binding sites with age have been shown in several areas of the human brain, including the hippocampus (21,22).…”

mentioning

confidence: 99%

Reversal of opiate-induced apoptosis by human recombinant growth hormone in murine foetus primary hippocampal neuronal cell cultures

Svensson

Bucht

Hallberg

et al. 2008

Proc. Natl. Acad. Sci. U.S.A.

View full text Add to dashboard Cite

Previous studies have shown that chronic opiates may inhibit cell growth and trigger apoptosis leading to impaired cognitive capabilities in both humans and other mammals. In contrast, growth hormone (GH) has been demonstrated to stimulate cell growth and counteract apoptosis. GH has also been shown to improve learning and memory in both human and rodents. In this work, we demonstrate that GH may reverse opiate-induced apoptosis in cells derived from prenatal mouse hippocampus. Primary hippocampal cell cultures derived from 16-day-old fetal mouse neurons were treated with morphine for 7 days during growth in the absence or presence of recombinant human GH (rhGH). The release of lactate dehydrogenase (LDH) into the culture media and the level of cleaved caspase-3 were measured. Results indicate that morphine (15 M) decreased the cell content in a concentration-dependent manner and increased LDH release and caspase-3 activity. Thus, fetal mouse neurons treated with morphine showed less viability compared with controls. Interestingly, the addition of rhGH (1 M) counteracted the morphine-induced effect on the cell density. Furthermore, the hormone attenuated the effects on LHD release and caspase-3 activity elicited by morphine. These results suggest that the hormone is capable of preventing or even repairing morphine-induced damage to hippocampal cells.apoptosis ͉ morphine ͉ caspase-3 ͉ lactate dehydrogenase

show abstract

Growth hormone prevents neuronal loss in the aged rat hippocampus

Cited by 57 publications

References 65 publications

Peripheral administration of GH induces cell proliferation in the brain of adult hypophysectomized rats

Peripheral administration of GH induces cell proliferation in the brain of adult hypophysectomized rats

Effect of Growth Hormone Treatment on Lymphocyte Functions in Old Male Rats

Reversal of opiate-induced apoptosis by human recombinant growth hormone in murine foetus primary hippocampal neuronal cell cultures

Contact Info

Product

Resources

About