Stress-Induced Bipolar Disorder

I have a strong FH of MH mood disorders but also a lot of prev trauma so I guess it is nature and nurture in my case.

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LW - I understand that you're more focused on treatment at the stage you're at in your life. The stage I'm at is simply fascination & wanting to figure out exactly what is going on in my brain, ya know? I've been dealing with trying to find a proper diagnosis for so long. Now that I finally sat down with a psychiatrist with the intent of getting to the bottom of this finally felt good. I agree with Bipolar more so than I agreed with Borderline PD. My moods are cyclical & classic hypomania. (Along with two episodes of strong mania.)

Also - I'm a major of Psychology of Abnormal Behaviour. I'm naturally intrigued by mental disorders & their origin, their meaning & their prognosis along with treatment. I got interested in it due to my own problems. (How original, right...)

But - alas - I think I need to get through the "gathering knowledge" stage before I can settle for "okay, I'm done talking, lets get some medication" stage.

I came across this and thought you would be interested in it. Since you have an educated background in these things I think you'll understand it.

The following paragraph is taken from http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1525098/

"Studies have also reported decreased radioligand binding to the serotonin transporter (which takes up serotonin from the synaptic cleft) both in platelets and in the midbrain of depressed patients (17,18). Most recently, an intriguing preliminary positron emission tomography (PET) study reported decreases in 5-hydroxytryptamine (5- HT)1A receptor binding potential in raphe and hippocampus- amygdala of brain in depressed patients, in particular in bipolar depressives and in unipolar patients with bipolar relatives (20). One factor which may contribute to the reduction in 5-HT1A receptor binding in depression is increased cortisol secretion (known to occur in many depressed patients, vide infra), since postsynaptic 5-HT1A receptor mRNA expression is under tonic inhibition by corticosteroid receptor stimulation in some brain regions. The magnitude of the reduction in 5-HT1A receptor density and mRNA levels induced by stress-induced glucocorticoid secretion in rodents is similar to that of the differences between depressed and healthy humans. For example, in rats, chronic unpredictable stress reduced 5-HT1A receptor density an average of 22% across hippocampal subfields, similar to the 25% reduction in hippocampal 5-HT1A receptor binding potential found in depression. Similarly, in tree shrews, chronic social subordination stress (for 28 days) decreased the density of 5-HT1A receptors in the posterior cingulate, parietal cortex, prefrontal cortex (PFC), and hippocampus (by 11% to 34%), similar to the magnitude of reduced 5-HT1A receptor binding potential found by Sargent et al (21) and Drevets et al (22) in these regions."

Edit:
Under the heading "Glutamatergic interventions: do they represent a neurotrophic strategy?" you'll read about how glutamate plays a role in the brain activity of bipolars. Interestingly, Lamictal helps to block the uptake of glutamate.

EGD sorry trained to abbreviate, my profession are lazy sods! FH is family history and MH is mental health.

Study sounds interesting.

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