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Running exercise- and antidepressant-induced increases in growth and survival-associated signaling molecules are IGF-dependent.
Growth Factors. 2007 Apr; 25(2):118-31.GF

Abstract

It is known that physical exercise increases hippocampal brain-derived neurotrophic factor (BDNF) mRNA and protein, as well as the expression of several pro-survival signaling proteins and that many of these effects depend on the uptake of peripheral insulin-like growth factor-1 (IGF-1) into the CNS. Because treatment with antidepressants has similar effects upon neurotrophin expression, we investigated whether antidepressant-induced BDNF changes also depend on IGF-1 uptake, as well as whether IGF-1 plays a role in the exercise/antidepressant-induced expression of molecules associated with plasticity/growth (GAP-43, SCG-10) and the intracellular activation of molecules associated with neuronal survival (Akt, ERK1/2). We evaluated the effects of a well known monoamine oxidase inhibitor, tranylcypromine, on BDNF mRNA and protein levels and phospho-Akt and phospho-ERK1/2 immunoreactivity, both with and without systemic blockade of IGF-1 uptake through the use of an antiserum raised against IGF-1. Anti-IGF-1 reversed the increase in BDNF mRNA and protein elicited by exercise as well as tranylcypromine. Exercise also significantly enhanced transcription of axon growth protein, GAP-43, an effect that was also evidenced to be IGF-1-dependent. The combination of exercise-plus-tranylcypromine also increased several cell survival signaling measures, but the BDNF changes associated with the combination treatment appeared to be independent of IGF-1 uptake. Together, these results indicate that the uptake of peripheral IGF-1 in the CNS is essential for antidepressant- as well as exercise-induced enhancement in hippocampal BDNF expression and thus, enhanced hippocampal neuronal survival and plasticity.

Authors+Show Affiliations

Department of Biological Sciences, California State University, 5151 State University Drive, Los Angeles, CA 90032, USA. mchen@calstatela.eduNo affiliation info available

Pub Type(s)

Journal Article
Research Support, N.I.H., Extramural

Language

eng

PubMed ID

17852404

Citation

Chen, Michael J., and Amelia A. Russo-Neustadt. "Running Exercise- and Antidepressant-induced Increases in Growth and Survival-associated Signaling Molecules Are IGF-dependent." Growth Factors (Chur, Switzerland), vol. 25, no. 2, 2007, pp. 118-31.
Chen MJ, Russo-Neustadt AA. Running exercise- and antidepressant-induced increases in growth and survival-associated signaling molecules are IGF-dependent. Growth Factors. 2007;25(2):118-31.
Chen, M. J., & Russo-Neustadt, A. A. (2007). Running exercise- and antidepressant-induced increases in growth and survival-associated signaling molecules are IGF-dependent. Growth Factors (Chur, Switzerland), 25(2), 118-31.
Chen MJ, Russo-Neustadt AA. Running Exercise- and Antidepressant-induced Increases in Growth and Survival-associated Signaling Molecules Are IGF-dependent. Growth Factors. 2007;25(2):118-31. PubMed PMID: 17852404.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Running exercise- and antidepressant-induced increases in growth and survival-associated signaling molecules are IGF-dependent. AU - Chen,Michael J, AU - Russo-Neustadt,Amelia A, PY - 2007/9/14/pubmed PY - 2007/12/14/medline PY - 2007/9/14/entrez SP - 118 EP - 31 JF - Growth factors (Chur, Switzerland) JO - Growth Factors VL - 25 IS - 2 N2 - It is known that physical exercise increases hippocampal brain-derived neurotrophic factor (BDNF) mRNA and protein, as well as the expression of several pro-survival signaling proteins and that many of these effects depend on the uptake of peripheral insulin-like growth factor-1 (IGF-1) into the CNS. Because treatment with antidepressants has similar effects upon neurotrophin expression, we investigated whether antidepressant-induced BDNF changes also depend on IGF-1 uptake, as well as whether IGF-1 plays a role in the exercise/antidepressant-induced expression of molecules associated with plasticity/growth (GAP-43, SCG-10) and the intracellular activation of molecules associated with neuronal survival (Akt, ERK1/2). We evaluated the effects of a well known monoamine oxidase inhibitor, tranylcypromine, on BDNF mRNA and protein levels and phospho-Akt and phospho-ERK1/2 immunoreactivity, both with and without systemic blockade of IGF-1 uptake through the use of an antiserum raised against IGF-1. Anti-IGF-1 reversed the increase in BDNF mRNA and protein elicited by exercise as well as tranylcypromine. Exercise also significantly enhanced transcription of axon growth protein, GAP-43, an effect that was also evidenced to be IGF-1-dependent. The combination of exercise-plus-tranylcypromine also increased several cell survival signaling measures, but the BDNF changes associated with the combination treatment appeared to be independent of IGF-1 uptake. Together, these results indicate that the uptake of peripheral IGF-1 in the CNS is essential for antidepressant- as well as exercise-induced enhancement in hippocampal BDNF expression and thus, enhanced hippocampal neuronal survival and plasticity. SN - 0897-7194 UR - https://www.unboundmedicine.com/medline/citation/17852404/Running_exercise__and_antidepressant_induced_increases_in_growth_and_survival_associated_signaling_molecules_are_IGF_dependent_ L2 - http://www.tandfonline.com/doi/full/10.1080/08977190701602329 DB - PRIME DP - Unbound Medicine ER -