Posted by desolationrower on September 30, 2009, at 0:33:54
In reply to Re: asprin boosts norepinephrine » linkadge, posted by Bob on September 29, 2009, at 11:35:14
Heh, warfarin -> lowered mood. more evidence vitamin k is important.
> > This study (and others) have suggested that asprin (but not other NSAID's) is associated with improved mood.
> >
> > Linkadge
>
> What is the significance of the fact that it boosts 'noradrenaline,' but not adrenaline?i'd think mostly that NA is more important centrally (although there is some adrenaline activity in the rbain). but you can't make conclusions about brain or synapse levels of na from plasma levels.
maybe something not really related, but interesting:
Noradrenaline induces expression of peroxisome proliferator activated receptor gamma (PPAR[gamma]) in murine primary astrocytes and neurons.
Original ArticlesJournal of Neurochemistry. 86(4):907-916, August 2003.
Klotz, Luisa *; Sastre, Magdalena *; Kreutz, Anne *; Gavrilyuk, Vitaliy +; Klockgether, Thomas *; Feinstein, Douglas L. +; Heneka, Michael T. *
Abstract:
Cerebral inflammatory events play an important part in the pathogenesis of Alzheimer's disease (AD). Agonists of the peroxisome proliferator-activated receptor gamma (PPAR[gamma]), a nuclear hormone receptor that mediates anti-inflammatory actions of non-steroidal anti-inflammatory drugs (NSAIDs) and thiazolidinediones, have been therefore proposed as a potential treatment of AD. Experimental evidence suggests that cortical noradrenaline (NA) depletion due to degeneration of the locus ceruleus (LC) - a pathological hallmark of AD - plays a permissive role in the development of inflammation in AD. To study a possible relationship between NA depletion and PPAR[gamma]-mediated suppression of inflammation we investigated the influence of NA on PPAR[gamma] expression in murine primary cortical astrocytes and neurons. Incubation of astrocytes and neurons with 100 [mu]M NA resulted in an increase of PPAR[gamma] mRNA as well as PPAR[gamma] protein levels in both cell types. These effects were blocked by the [beta]-adrenergic antagonist propranolol but not by the [alpha]-adrenergic antagonist phentolamine, suggesting that they might be mediated by [beta]-adrenergic receptors. Our results indicate for the first time that PPAR[gamma] expression can be modulated by the cAMP signalling pathway, and suggest that the anti-inflammatory effects of NA on brain cells may be partly mediated by increasing PPAR[gamma] levels. Conversely, decreased NA due to LC cell death in AD may reduce endogenous PPAR[gamma] expression and therefore potentiate neuroinflammatory processes.cox-2 (inhibited by aspirin, and fishoil and celebrex etc) also decreases GR sensitivity (see thread on corticoids boosting mood)
-d/r
poster:desolationrower
thread:918864
URL: http://www.dr-bob.org/babble/20090921/msgs/919094.html