Posted by JohnX2 on November 18, 2001, at 22:42:38
dxm = dextromethorphan.Just out of curiosity I tried wellbutrin
again. 1st time before taking dxm and it immediately
gave me a whopper of a tension headache. 2nd and 3rd time
with dxm, and no headache. plus, I got the
anti-depressant response a few hours ago after feeling
utter dispair earlier today. So now mr. dysthymia
is on vacation for a while, we'll see when he
returns because he always does.I'm wondering how the various metabolites of WB
are reacting. It can cause kindling from what I
understand and seizures for some, but the main
active metabolites hydroxy-bupropion and something
else have etremely long 1/2 lives (like 20+ hrs).The dxm can only be in my body at most a few hrs
and I'm wondering if this is enough for it to
counteract the parent bupropion kindling itself.
We'll see if the headache returns. I'll keep taking
a dxm dose with wellbutrin while this lasts just for kicks.
If it continues to work, then it is a good indicator
that memantine will help me.I did find a reference to nmda antagonists antagonizing
crf release and kindling in the amygdala.
I wonder how their research NMDA antagonist
2-amino-5-phosphonovaleric acid, compares to dxm or
memantine or mk-801.N-methyl-D-aspartate (NMDA)-mediated corticotropin-releasing factor (CRF) release in cultured rat amygdala neurons.
Peptides 1999;20(1):93-100 (ISSN: 0196-9781)Cratty MS; Birkle DL [Find other articles with these Authors]
Department of Pharmacology and Toxicology, West Virginia University, Robert C. Byrd Health Sciences Center, Morgantown 26506, USA.Corticotropin-releasing factor (CRF) plays an important role in the activation of centrally mediated responses to stress. The amygdala, a limbic structure involved in the stress response, has a
significant number of CRF cell bodies and CRF receptors. Activation of glutamatergic projections to the amygdala has been implicated in the stress response. Few studies have evaluated
neurotransmitter-stimulated CRF release in the amygdala. We measured the effects of glutamate (0.1-1000 microM) and N-methyl-D-aspartate (NMDA, 0.1-1000 microM) on CRF release
from the amygdala using primary neuronal cultures from embryonic rat brains (E18-19). Experiments were performed after the cultures grew for 17-20 days. CRF was measured using
radioimmunoassay. The excitatory amino acid neurotransmitters, glutamate and NMDA, stimulated CRF release in a concentration-dependent manner. The apparent EC50 values for
glutamate and NMDA were 17.5 microM and 12 microM, respectively. Consistent with a NMDA receptor-driven event, glutamate-stimulated CRF release was blocked by the NMDA
antagonist, 2-amino-5-phosphonovaleric acid (AP-5, 1-100 microM) and antagonized by the addition of 1.2 mM MgCl2 to the incubation medium. These results implicate an inhibition of
CRF release in the amygdala as a possible mechanism for the reported anxiolytic effects of NMDA antagonists.
poster:JohnX2
thread:84623
URL: http://www.dr-bob.org/babble/20011113/msgs/84623.html