Karim Nader of the psychology department at McGill University explained his research on the mechanisms of memory re-consolidation and treatment options for managing undesirable memories in chronic Post-Traumatic Stress Disorder (PTSD) patients, in a seminar at Dartmouth on November 7.

Nader’s discussion focused predominantly on his research of how the lateral amygdala processes intensely emotional memories, particularly those related to fear. Initial studies focused on the elucidation of the basic functions of memory processing. According to Nader, when a typical memory is in the labile or short-term memory (STM) state, there is no directly associated RNA transcription or protein translation. By contrast, both memory consolidation and re-consolidation involve protein synthesis.

Support for this finding came from Nader’s research on mice. Initial experimental protocol involved administration of a controlled stimulus (electric shock) to the specimen. Anisomycin, an antibiotic that inhibits protein synthesis, was then injected into the lateral amygdala of the specimen. Results indicated that STM was not significantly affected by anisomycin. However, the specimens’ stable state or long-term memory (LTM) was inhibited. The possibility of being able to degrade a particular memory was an important step toward the development of a new means of treating PTSD.

Nader then examined the role of strength of training in both the memory consolidation and re-consolidation processes. PTSD memories, which are generally highly emotional and fear-related, are essentially analogous to the strongly trained memories studied by Nader via mouse model. Experimental results have indicated that, in new learning, strongly trained memories bypass the labile (STM) state, passing directly from an initial basal state to a consolidated or LTM state. However, it appears that triggering a specimen (or patient) to recall a strongly trained memory results in conversion to the labile state. It appears that NR2B-containing NMDA receptors in the brain are essential for re-consolidation of such a memory.

Nader’s results suggest that it might be possible to use an appropriate NMDA inhibitor as a means of attenuating undesirable memories in PTSD patients. Related clinical trials have used propranolol, a beta-blocker and NMDA receptor antagonist, in this very manner. Long-term PTSD patients were asked to verbalize the details of their traumatic memory, theoretically converting the memory to a labile state. The patient then received acute treatment with propranolol. Patient screening a week later demonstrated a noticeable reduction in undesirable physiological response symptoms when asked to recall the same undesirable memory. These results suggest that propranolol may be an effective means of treating the debilitating symptoms of PTSD.