Posted by Chairman_MAO on June 12, 2005, at 10:16:56
In reply to Are there any meds for a neurotic depression?, posted by DoYouKnowHim? on June 11, 2005, at 14:32:18
The following is just my intuition, really:
MAOIs (especially phenelzine), opioids (buprenorphine or tramadol are the only ones likely to be prescribed for most people), Cymbalta/Effexor + benzodiazepine. The most potent combination would probably be MAOI + opioid.
A popular remedy used between the 50s and the 70s was a psychostimulant + barbiturate (Dexamyl, Desbutal et al). I'll bet Dexedrine + benzodiazepine would also work well, but in general I feel the effect of MAOIs is more robust, and benzos can worsen depression. I really like opioids because they inhibit NE-induced firing of neurons in the locus coeruleus, thereby attenuating feelings of stress.
I am choc full of neuroses, dysthymic, and socially phobic (at times worsening into moderate agoraphobia) by default, and phenelzine + buprenorphine changes me into a competent-feeling , generally happy-go-lucky, sociable, generally optimistic person. I can still cry and feel stressed when appropriate, which I Could not do on SSRIs (which didn't even work).
---Evidence for functional release of endogenous opioids in the locus ceruleus during stress termination
by
Curtis AL, Bello NT, Valentino RJ.
The Children's Hospital of Philadelphia,
706 Abramson Pediatric Research Center,
Philadelphia, Pennsylvania 19104, USA.
J Neurosci 2001 Jul 1;21(13):RC152ABSTRACT
Endogenous opioids target noradrenergic locus ceruleus (LC) neurons and potently inhibit LC activity. Nonetheless, it has been difficult to demonstrate functional regulation of the LC-noradrenergic system by endogenous opioids because of the lack of effect of opiate antagonists. The present findings provide evidence that endogenous opioids regulate LC neuronal activity during the termination of a stressor. LC neuronal discharge was recorded from halothane-anesthetized rats before, during, and after hypotensive stress elicited by intravenous nitroprusside infusion. In naive rats, mean arterial blood pressure was temporally correlated with LC activity such that hypotension was associated with increased LC discharge and a return to the normotensive state was associated with a decrease in LC discharge below pre-stress values. After microinfusion of an antagonist of the stress neuropeptide corticotropin-releasing factor (CRF) into the LC, the increase in LC discharge associated with hypotension was prevented, whereas LC inhibition associated with termination of the challenge occurred at an earlier time and was of a greater magnitude. In contrast, microinfusion of naloxone into the LC completely abolished LC inhibition associated with termination of the stressor. Naloxone microinfusion did not prevent LC inhibition associated with hypertension produced by intravenous vasopressin administration, suggesting that endogenous opioids may be selectively engaged during the termination of hypotensive stress. These results provide evidence for a functional release of endogenous opioids within the LC. This action of endogenous opioids may serve to counterbalance excitatory effects of CRF on the LC-norepinephrine system, thereby limiting its activation by stress.
poster:Chairman_MAO
thread:511067
URL: http://www.dr-bob.org/babble/20050611/msgs/511411.html