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Increased septal 5‐HIAA efflux in rats that do not develop learned helplessness after inescapable stress
Author(s) -
Ronan Patrick J.,
Steciuk Mark,
Kramer Gerald L.,
Kram Martin,
Petty Frederick
Publication year - 2000
Publication title -
journal of neuroscience research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.72
H-Index - 160
eISSN - 1097-4547
pISSN - 0360-4012
DOI - 10.1002/1097-4547(20000701)61:1<101::aid-jnr12>3.0.co;2-s
Subject(s) - learned helplessness , microdialysis , serotonin , dopamine , neurotransmitter , psychology , endocrinology , serotonergic , medicine , neuroscience , central nervous system , developmental psychology , receptor
Learned helplessness is a behavioral deficit that can be induced by exposure to inescapable stress. Previous studies have implicated the lateral septum in mediating this phenomenon, and in this brain region, serotonin plays an important role in the development, maintenance, prevention, and reversal of learned helplessness behavior. Using the technique of in vivo microdialysis, we measured the efflux of serotonin (5‐HT), dopamine (DA), and their respective metabolites, 5‐hydroxyindoleacetic acid (5‐HIAA) and 3,4‐dihydroxyphenylacetic acid (DOPAC), from the lateral septum of rats that either developed or did not develop learned helplessness. During the microdialysis session all rats were subjected to restraint stress. Control groups included naïve, home cage rats as well as tested control rats that were subjected to the identical handling, restraint, and shuttlebox testing as the rats that received inescapable shock. Overall, levels of 5‐HIAA were significantly higher in non‐helpless rats. There were no significant effects of restraint or differences in levels of 5‐HT, DA, or DOPAC. We propose that this increase in 5‐HIAA is indicative of an overall increase in serotonin metabolism in the lateral septum of rats that do not become helpless after inescapable stress. This increased serotonin metabolism in the lateral septum may protect the animal from adverse behavioral consequences of inescapable stress. J. Neurosci. Res. 61:101–106, 2000. Published 2000 Wiley‐Liss, Inc.