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Msg  2917 of 3003  at  12/18/2019 4:18:20 PM  by


PTSD Nightmares


The Possible Mechanism of the Appearance of Nightmares in Post-Traumatic Stress Disorder and Approaches to Their Prevention
Abstract—It is hypothesized that the basis of nightmares in post-traumatic stress disorder (PTSD) is modification of synaptic transmission in neural circuits that contain one of the following structures: the visual cortex, prefrontal cortex (PfC), basolateral amygdala (BLA), hippocampus, connected with them nuclei of the thalamus and basal ganglia (BG). The emergence of dreams is promoted by the induction of long-term potentiation of excitatory inputs to the striatonigral cells and the long-term depression of the inputs to the striatopallidal cells that are connected with the visual cortex, and give rise, respectively, to a direct and indirect path way through the BG. This leads to synergistic disinhibition of certain groups of neurons in the thalamus by the output BG nuclei and the formation of activity patterns that reflect dream content in the areas of the visual cortex and hippocampus, which are connected with thalamus. The occurrence of emotionally negative episodes in dreams is a consequence of an increase in BLA activity during PTSD, whose signals are summed with the signals from the hippocampus and PfC on the neurons of the ventral striatum. This mechanism suggests that, in order to prevent nightmares, it is necessary to induce long-term depression of the excitatory inputs to the neurons of the limbic structures and to the striatonigral cells. It is undesirable to act on the receptors on the striatopallidal cells because it may simultaneously induce long-term potentiation of the excitatory inputs to the neurons of PfC, BLA, and hippocampus, which have receptors of the same types. Given the data on the types of receptors on striatal neurons, it follows from the modulation rules we earlier formulated that nightmares may be prevented by antagonists of dopamine D1 receptor and alpha1 adrenoceptor and agonists of glucocorticoid, serotonin 5-HT1B, and cannabinoid CB1 receptors. The use of mineralocorticoid and serotonin 5-HT2A receptor agonists, as well as antagonists of alpha2 adrenoreceptors and dopamine D2 receptors (which are part of some antidepressants and antipsychotics) is undesirable in order to avoid side effects. The treatment should be short-term and used only at bedtime, to avoid impairments of physical activity and sensory perception in the awake state. The consequences of the proposed mechanism are consistent with the known results of clinical studies. 

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