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depression

melange

Bluelighter
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Aug 11, 2006
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Richmond, Va - in a mansion with the phantom parke
I am trying to find correlating evidence between physical depression and emotional depression.



A strong emotional response can cause neurons to recede a.k.a. down regulate(grief in my opinion) - the same way drugs can


confirm/deny - is what i am looking for - any facts?
 
Two of many possible mechanisms, plagiarized from Kaplan & Saddock:

1) Dysfunction of the mesolimbic DA pathway and inactivity of D1 receptors.

2) Increased cholinergic activity and hypersensitivity of acetylcholine receptors in the HPA.

The second etiology is especially compelling because,

a) Autopsied MDD patients have been found to have unusually high levels of choline in their brains.
b) Cholinergic agonists produce a suite of psychomotor effects that are identical to those of depression (lethargy, hypoactivity, learned helplessness in physical endeavors).
c) Cholinergic agonists (scary) control manic hyperkinesis pretty robustly.
d) Patients whose depression is in remission, or biological relatives who have themselves never experienced clinical depression, show hypersensitivity to cholinergic agonists.

Many more mechanisms I'm sure. Second messengers and their resultant transduction cascades, for instance. Ever been on a lithium regimen? Fascinating things this little metal does.
 
From my knowledge of depression (3rd year pharmacy student), the physical symptoms can be caused mainly by a lack of specific neurotransmitters in the CNS. When there is a decrease in serotonin, your body manifests that as sedation, lethargy, weight gain. Lack of norepinephrine causes decreased energy, decreased attention and alertness. Lack of dopamine causes decreased pleasure, sadness, and lack of motivation or drive. Acetylcholine also can play a role, but I don't think so much in MDD. Depleted acetylcholine in the CNS can lead to memory impairment in the long-term - this is the foundation of Alzheimer's dementia hypothesis. If given an acetylcholinesterase inhibitor to increase the acetylcholine in the CNS, the dementia patients had significantly better cognitive function.

Norepinephrine and dopamine play a huge role in depression, in my opinion. NE is what gives you that alertness - it and epinephrine are the chemicals that get released in the "fight or flight" response in attacks, emergencies, what have you. Dopamine is that happy, pleasure, rewarding chemical. So being deficient in either of those would leave you unable to concentrate, tired, sluggish, and unhappy with no motivation to do anything, including to get out of bed. Serotonin also plays a part, but I am not a fan of SSRI's - they left me feeling "zombie-like" and since serotonin is involved in obsessions and compulsions, I have yet to understand how Prozac and Luvox are indicated for OCD. I will have to research further.
 
Two of many possible mechanisms, plagiarized from Kaplan & Saddock:

1) Dysfunction of the mesolimbic DA pathway and inactivity of D1 receptors.

2) Increased cholinergic activity and hypersensitivity of acetylcholine receptors in the HPA.

The second etiology is especially compelling because,

a) Autopsied MDD patients have been found to have unusually high levels of choline in their brains.
b) Cholinergic agonists produce a suite of psychomotor effects that are identical to those of depression (lethargy, hypoactivity, learned helplessness in physical endeavors).
c) Cholinergic agonists (scary) control manic hyperkinesis pretty robustly.
d) Patients whose depression is in remission, or biological relatives who have themselves never experienced clinical depression, show hypersensitivity to cholinergic agonists.

Many more mechanisms I'm sure. Second messengers and their resultant transduction cascades, for instance. Ever been on a lithium regimen? Fascinating things this little metal does.

Could you list the reference for this? I've never thought of that before, and it makes pretty good sense. Would be interesting to investigate.
 
what about taking an extreme ndma antagonist(whatever) dose at the immediate moment of grief?

Search clinicaltrials.gov for ketamine: several studies are looking into ketamine as a thermonuclear antidepressant: as in when you're ready to pry your head off your neck because the sadness is indescribably intense.

Taylor, it's from the etiolology section of the mood disorder chapter of Kaplan and Saddock's Synopsis of Psychiatry (2007). The problem with that text is that the references are listed at the end of every chapter and it's unclear which reference refers to what.

The biogenic amine hypotheses would be awesome if the psychiatric meds that modulate them actually worked. They work for some, but they're absolutely worthless for many (like myself).
 
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