streetsurfer
Ex-Bluelighter
Man, The other day I started prozac, my god, all of a sudden (after 3 days) I wasn't shy, I was charming the pants off everyone I came across. I felt so positive about the direction my life was heading and felt centred in myself.
One glorious Day
Then, I return back to the old me. Timid, angry, repetative intrusive thoughts sad sad sad. All these things are still good that have happened, but they don't make me feel good.
I am so borderline, my moods cycle from suicidality to elation several times a day. I am on lamictal 250mg but it doesn't seem to be working. I am just so sick of it.
Amygdala Dysfuntion yes? How do I deactivate it, could you, through psychosurgury do so? what about D- cyclozine, Anyone know much about that? Does the Amygdala serve any fucking purpose asides cause misery? Lastly, to get back on topic, do you think this study would be applicable to other drugs like ssri's so they work longer than a god damn week.
Many Thanks
One glorious Day
Then, I return back to the old me. Timid, angry, repetative intrusive thoughts sad sad sad. All these things are still good that have happened, but they don't make me feel good.
I am so borderline, my moods cycle from suicidality to elation several times a day. I am on lamictal 250mg but it doesn't seem to be working. I am just so sick of it.
Amygdala Dysfuntion yes? How do I deactivate it, could you, through psychosurgury do so? what about D- cyclozine, Anyone know much about that? Does the Amygdala serve any fucking purpose asides cause misery? Lastly, to get back on topic, do you think this study would be applicable to other drugs like ssri's so they work longer than a god damn week.
Many Thanks
Chronic elevation of brain-derived neurotrophic factor by ampakines.
J Pharmacol Exp Ther. 2003 Oct;307(1):297-305. Epub 2003 Jul 31.
"The ampakine CX614 positively modulates alpha-amino-3-hydroxy-5methyl-4-isoxazolepropionic acid (AMPA) receptor-gated currents and increases brain-derived neurotrophic factor (BDNF) expression. In rat hippocampal slice cultures, CX614 rapidly increases BDNF gene expression but with time, mRNA levels fall despite the continued presence of active drug. The present study examined this apparent refractory period and the possibility that spaced ampakine treatments could sustain elevated BDNF protein levels. In cultured hippocampal slices, CX614, a second ampakine CX546, and the cholinergic agonist carbachol each increased BDNF mRNA levels with acute (3-h) treatment. After 4-day pretreatment with CX614, fresh ampakine (CX614 or CX546) did not induce BDNF mRNA, whereas carbachol did. Western blots confirmed that after an extended period of ampakine treatment, AMPA receptor protein levels are indeed reduced, suggesting that with longer treatments receptor down-regulation mediates ampakine insensitivity. Finally, using a "24-h on/24-h off" CX614 treatment protocol, the ampakine refractory state was circumvented, BDNF mRNA was induced with each ampakine application, and elevated BDNF protein levels were maintained through 5 days in vitro. These results suggest that spaced ampakine treatments can be used to sustain elevated neurotrophin levels and to test the utility of this manipulation for neuroprotection by endogenous neurotrophins." [Abstract]