Post-Traumatic Stress Disorder (PTSD) is a common psychiatric disorder that is often associated with intrusive memories and deficits in declarative memory function. The neurobiology of this effect is complex. The report focus is to provide an overview of systems activated during stress and consequences of the activation as well as modulation of those effects. Two systems predominate in stress and related memory processing and encoding. They are the autonomic nervous system (ANS) and hypothalamic-pituitary-adrenal axis (HPA) axis. ANS has significant effect on enhancing encoding of emotional memories, sensitization, and fear conditioning with the main neurotransmitter being norepinephrine (NE). HPA system is involved in memory regulation where cortisol (CORT), by itself and with NE, regulates memories of emotional events. Therapeutic interference with stress-related memory dysfunction has been a focus of research for some time. New focus of this research may be the HPA axis and ANS. Recent evidence demonstrates significant efficacy in prevention of PTSD by administration of CORT, as well as treatment of PTSD by utilization of Stellate Ganglion Block (SGB), which reduces NE. Both therapeutic approaches may act by a common pathway involving Nerve Growth Factor (NGF). This factor may be the "missing link" between memory consolidation and PTSD. Suppression of NGF can reduce memory effect directly or by effect on NE, leading to prevention or effective treatment of PTSD.
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