NMDA neurotransmission mediates Borderline Personality Disorder!

[dopamimetic]

NMDA neurotransmission as a critical mediator of borderline personality disorder

Studies of the neurobehavioural components of borderline personality disorder (BPD) have shown that symptoms and behaviours of BPD are partly associated with disruptions in basic neurocognitive processes, in particular, in the executive neurocognition and memory systems. A growing body of data indicates that the glutamatergic system, in particular, the N-methyl-D-aspartate (NMDA) subtype recep- tor, plays a major role in neuronal plasticity, cognition and memory and may underlie the pathophysiology of multiple psychiatric disor- ders. In this paper, we review the literature regarding BPD and its cognitive deficits and the current data on glutamatergic and NMDA neurotransmission. We propose that multiple cognitive dysfunctions and symptoms presented by BPD patients, like dissociation, psy- chosis and impaired nociception, may result from the dysregulation of the NMDA neurotransmission. This impairment may be the result of a combination of biological vulnerability and environmental influences mediated by the NMDA neurotransmission. (Source, PDF)

Seems like I've guessed right with that dissociatives-for-borderliners theory

And there's an interesting table about cognitive functions, brain regions and the associated neurotransmitters:

 

[vortech]

Thanks, good food for thought today to clarify my understanding of the NMDA.
Edit: added to the book.

 

[Cotcha Yankinov]

A book called "Introduction to Neuropsychopharmacology" by Iversen says the following,

"A number of studies have demonstrated the importance of NMDA receptors and of the glutamatergic input to the ventral tegmental area in the regulatory control of mesoprefrontal DA neurons. This input is believed to be at least partially responsible for converting pacemaker-like firing in DA cells into burst firing patterns. NMDA receptors in the VTA appear to modulate differentially the DA projections to the PFC and nucleus accumbens. The NMDA receptor is selectively activated by NMDA and regulated at several pharmacologically distinct sites, including a high affinity strychnine-insensitive glycine binding site. Competitive antagonists of this strychnine insensitive glycine site, which cross the blood-brain barrier, have made possible the in vivo pharmacological modulation of the NMDA receptor via this site. In behavioral paradigms (restraint stress and conditioned fear) that cause metabolic activation of mesoprefrontal and mesaccumbens DA neurons, these agents (e.g. HA-966) selectively abolish the activation of mesoprefrontal DA neurons. These data indicate the under certain perturbed states the NMDA receptor complex and associated glycine modulatory site play an important role in the afferent control of the DA neurons in the prefrontal cortex and provide a potential target for pharmacological regulation of this important DA projection."

Seems like NMDA is far reaching.

BTW Dopa I think you were interested in some books so I will definitely let you know if some of these books I got are good, I got some of these really expensive normally $300+ college books for $20 used but they're in great condition, yay amazon

 

[dopamimetic]

NMDA seems to be involved in next to anything (okay, as glutamate is the primary excitatory transmitter, it makes sense) ... we finally and definitely need brain-region selective glutamate modulators now, if this'd only be easier to do with small molecules! But interesting to read this passage too.