Amir Dehghanghadikolaei,1* Jamal Ansary,2 Reza Ghoreishi3
Proceedings of the Nature Research Society, Volume 2, Article Number 02008, 2018
Published Online: 13 June 2018 (Review)
Selakovic Dragica, Joksimovic Jovana, Rosic Gvozden*
Proceedings of the Nature Research Society, Volume 2, Article Number 02007, 2018
Published Online: 8 June 2018 (Review)
Literature data offers evidence that AASs abuse is accompanied with psychiatric manifestations, as well as with different behavioral alterations from mild type, which are social acceptable, to uncontrolled and impulsive behavior with expression of aggression, anxiety, hypomania, and also manic episodes. Numerous investigations were performed on animal experimental models in order to make an insight to mechanisms underlying mechanisms for AASs impact on behavioral alterations. The absolute majority of literature sources declared the anxiogenic effect of AASs when applied in supraphysiological doses. The increased anxiety levels following AASs treatment seems to be a consequence of changes in various neuroregulatory systems (gabaergic, dopaminergic, etc.), as well as alterations in sex hormones receptors in specific brain regions, including hippocampus. Supraphysiological doses of AASs also affect mood by means of increased depressiveness. The prodepressant action of AASs is usually accompanied with significant reduction of growth factors (NGF, BDNF) release with consequent effects on neuromodulatory systems (gabaergic, dopaminergic) in rat prefrontal cortex and hippocampus. When applied in supraphysiological dose AAS significantly affected the quality of cognitive abilities, manifested as significant decline in spatial learning and memory. The negative impact of AASs on cognitive functions was attributed to significant alterations in acetylcholine, dopamine, norepinephrine, glutamate and serotonin levels in specific brain regions, responsible for regulation of learning and memory.
Yanxia Lu,1,2* Tze Pin Ng,3 Anis Larbi2,4
Proceedings of the Nature Research Society, Volume 2, Article Number 02005, 2018
Published Online: 28 May 2018 (Review)
The prevalence of asthma morbidity and mortality has increased significantly in recent decades, concurrently with increasing mental health problems worldwide. Asthma has long been considered as an archetypal psychosomatic disease. However, evidence supporting the link between psychosocial stress and asthma is just emerging. The stress-asthma link is supported by evidence that chronic stress suppresses hypothalamo-pituitary-adrenocortical (HPA) axis activity and its anti-inflammatory effect, resulting in blunted HPA axis responsiveness seen in asthma patients. However, marked inter-individual variability in responses to stress exists. Some are more vulnerable than others to the effects of stress in terms of asthma risks and morbidity. Recent studies suggest the main contribution of neuropeptide Y (NPY) in modulating HPA-axis responsiveness and explaining inter-individual variation in resilience to stress and asthma in animal models and clinical samples. The temporal and spatial expression pattern of NPY and its receptors (Y1 and Y5) is determined in the airways of asthmatic mice. Peripheral NPY concentration and the genetic variation in the NPY gene has been investigated in asthma in multiple studies. Studies have attempted to explain the underlying mechanisms of the "neuroimmune" crosstalk as a contributor to the development of the airway inflammation and asthma. Such a psychoneuro-immunological perspective in asthma research represents a new psychosomatic approach in pharmacological therapy of asthma, and may open the door for future potential use of NPY agonists in treating asthma. Future brain imaging research using specific NPY-receptor ligands is required to better understand the relationship between central release of NPY and asthma.