Recent advances in the neurobiology of posttraumatic stress disorder: A review of possible mechanisms underlying an effective pharmacotherapy. (April 2019)

• Record Type: Journal Article
• Authors: Malikowska-Racia, Natalia; Salat, Kinga
• Is Part Of: Pharmacological research. Volume 142(2019)
• Page Start: 30
• Page End: 49
• Publication Date: 2019-04
• Subjects: AEA anandamide -- ACTH adrenocorticotropic factor -- AH anterior hippocampus -- AlloP allopregnanolone -- AMPA α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid -- AVP arginine vasopressin/vasopressin -- BEP Brief Eclectic Psychotherapy -- BDNF brain-derived neurotrophic factor -- BK channels large-conductance potassium channels -- BLA basolateral amygdala -- BST bed nucleus of the stria terminalis -- CB1R cannabinoid receptor type 1 -- CeMA medial subdivision of central amygdala -- CPT cognitive processing therapy -- CRH corticotropin-releasing factor -- CRH1R corticotropin-releasing hormone receptor 1 -- CRH2R corticotropin-releasing hormone receptor 2 -- CRHRs corticotropin-releasing hormone receptors -- CS conditioned stimulus -- CSF cerebrospinal fluid -- D1–5R dopaminergic receptors types 1–5 -- DHEA dehydroepiandrosterone -- EMDR Eye Movement Desensitization and Reprocessing -- ErbB4 receptor receptor tyrosine-protein kinase erbB-4 -- FAAH fatty acid amide hydrolase -- GABAAR GABA receptor type A -- GABABR GABA receptor type B -- GAD glutamate decarboxylase -- GR glucocorticoid receptor -- HPA hypothalamic–pituitary–adrenal axis -- HPT hypothalamic–pituitary–thyroid axis -- LC locus coeruleus -- LTD long-term depression -- LTP long-term potentiation -- mGluR1 metabotropic glutamate receptor type 1 -- mGluR2/3 metabotropic glutamate receptors types 2 and 3 -- mGluR5 metabotropic glutamate receptor type 5 -- mPFC medial prefrontal cortex -- mPR membrane progesterone receptor -- MR mineralocorticoid receptors -- NE norepinephrine -- NET narrative exposure therapy -- NET norepinephrine transporter -- NMDAR N-methyl-d-aspartate receptor -- NOS nitrogen monoxide synthase -- NRG-1 neuregulin 1 -- NY neuropeptide Y -- OT oxytocin -- OX1R orexin receptor type 1 -- PAG periaqueductal gray -- PE prolonged exposure -- PFC prefrontal cortex -- PRL prolactin -- PTSD posttraumatic stress disorder -- PVN paraventricular nucleus -- SBSSs selective brain steroidogenic stimulants -- SK channels small-conductance potassium channels -- SN substantia nigra -- SNP single nucleotide polymorphism -- SPS single prolonged stress protocol -- SRC-1 steroid receptor co-activator -- SSRIs selective serotonin reuptake inhibitors -- T3 triiodothyronine -- T4 thyroxine -- TSH thyroid-stimulating hormone -- US unconditioned stimulus -- VA U.S. Department of Veteran Affairs -- VH ventral hippocampus -- vmPFC ventromedial prefrontal cortex -- VOD U.S. Department of Defense -- VTA ventral tegmental area -- Y2R neuropeptide Y2 receptor; PTSD -- Neuropathology -- Neurotransmission -- Anxiety -- Brain -- Stress; Pharmacology -- Periodicals; Pharmacology -- Periodicals; Research -- Periodicals; Médicaments -- Recherche -- Périodiques; Pharmacologie -- Périodiques; 615.105
• DOI: 10.1016/j.phrs.2019.02.001
• Languages: English
• ISSNs: 1043-6618

Abstract

Graphical abstract: Abstract: Recent progress in the field of neurobiology supported by clinical evidence gradually reveals the mystery of human brain functioning. So far, many psychiatric disorders have been described in great detail, although there are still plenty of cases that are misunderstood. These include posttraumatic stress disorder (PTSD), which is a unique disease that combines a wide range of neurobiological changes, which involve disturbances of the hypothalamic–pituitary–adrenal gland axis, hyperactivation of the amygdala complex, and attenuation of some hippocampal and cortical functions. Such multiplicity results in differential symptomatology, including elevated anxiety, nightmares, fear retrieval episodes that may trigger delusions and hallucinations, sleep disturbances, and many others that strongly interfere with the quality of the patient's life. Because of widespread neurological changes and the disease manifestation, the pharmacotherapy of PTSD remains unclear and requires a multidimensional approach and involvement of polypharmacotherapy. Hopefully, more and more neuroscientists and clinicians will study PTSD, which will provide us with new information that would possibly accelerate establishment of well-tolerated and effective pharmacotherapy. In this review, we have focused on neurobiological changes regarding PTSD, addressing the most disturbed brain structures and neurotransmissions, as well as discussing in detail the recently taken and novel therapeutic paths.