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Zinc supplementation prevents depression and deficits in spatial learning and memory associated with traumatic brain injury in the rat
Author(s) -
Cope Elise C.,
VanLandingham Jacob W.,
Scrimgeour Angus G.,
Condlin Michelle L.,
GowerWinter Shan D.,
Levenson Cathy W.
Publication year - 2011
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.25.1_supplement.228.7
Subject(s) - traumatic brain injury , hippocampal formation , zinc deficiency (plant disorder) , depression (economics) , morris water navigation task , anxiety , hippocampus , medicine , endocrinology , psychology , psychiatry , pathology , micronutrient , economics , macroeconomics
Depression, anxiety, and impairments in learning and memory are all associated with traumatic brain injury (TBI). We have hypothesized that moderate zinc deficiency (ZD, 5 ppm) would exacerbate these symptoms and that zinc supplementation (ZS, 180 ppm) prior to injury would prevent them compared to rats fed a zinc adequate diet (ZA, 30 ppm). Rats were fed ZA, ZD or ZS diets for 4 weeks followed by a moderately‐severe TBI using the well‐established model of controlled cortical impact (CCI). CCI induced depression‐ and anxiety‐like behaviors as well as impairments in spatial learning and memory. While moderate zinc deficiency did not worsen these behavioral deficits, rats fed the ZS diet for 4 weeks showed fewer depression‐like behaviors (p<0.05) and had improved Morris water maze performance, such that they were not different from sham‐operated controls. Proteomic analysis 48h post injury revealed 146 hippocampal proteins regulated by injury, many of which are responsible for neurotransmitter exocytosis or mitochondrial energy metabolism. Interestingly, zinc deficiency prevented the response of many of these proteins to injury. This work was funded by the U.S. Army MRMC.