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Old 05-23-2006, 09:18 AM   #1
R.B.
Senior Member
 
Join Date: Mar 2006
Posts: 1,843
COX inhibition - substantial sustained deficits in spatial learning in the watermaze

Herceptin is reported as impacting on the production of long chain fatty acids.

So is Tamoxifen.

Cox 2s and inflamation are reported as factors in BC.

Unfortunately the trial does not look at the impact of omega 3s.

The exercise comment is interesting but I have no idea what its implications are.

It is a pay for view so I have not seen full trial.

I post it just for the general wider implications that there is evidence that intervention in the brains fat pathways does produce "learning deficits".

RB



http://www.ncbi.nlm.nih.gov/entrez/q...=pubmed_docsum

1: Eur J Neurosci. 2003 Jun;17(11):2438-46. Related Articles, Links
Click here to read
Deficits in spatial learning and synaptic plasticity induced by the rapid and competitive broad-spectrum cyclooxygenase inhibitor ibuprofen are reversed by increasing endogenous brain-derived neurotrophic factor.

Shaw KN, Commins S, O'Mara SM.

Department of Psychology and Trinity College Institute of Neuroscience, Trinity College, Dublin 2, Ireland.

Cyclooxygenase (COX), which is present in two isoforms (COX1 and 2), synthesizes prostaglandins from arachidonic acid; it plays a crucial role in inflammation in both central and peripheral tissues. Here, we describe its role in synaptic plasticity and spatial learning in vivo via an effect on brain-derived neurotrophic factor (BDNF) and prostaglandin E2 (PGE2; both measured by Elisa). We found that broad-spectrum COX inhibition (BSCI) inhibits the induction of long-term potentiation (LTP; the major contemporary model of synaptic plasticity), and causes substantial and sustained deficits in spatial learning in the watermaze. Increases in BDNF and PGE2 following spatial learning and LTP were also blocked. Importantly, 4 days of prior exercise in a running wheel increased endogenous BDNF levels sufficiently to reverse the BSCI of LTP and spatial learning, and restored a parallel increase in LTP and learning-related BDNF and PGE2. In control experiments, we found that BSCI had no effect on baseline synaptic transmission or on the nonhippocampal visible-platform task; there was no evidence of gastric ulceration from BSCI. COX2 is inhibited by glucorticoids; there was no difference in blood corticosterone levels as measured by radioimmunoassay in any condition. Thus, COX plays a previously undescribed, permissive role in synaptic plasticity and spatial learning via a BDNF-associated mechanism.

PMID: 12814375 [PubMed - indexed for MEDLINE]
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