Stress genetic vulnerability

Henn FA, Volhnayr B (2005) Stress models of depression Forming genetically vulnerable strains. Neurosci Biobehav Rev 29 799-804. 

Nevertheless, there is strong evidence that some mental illnesses are partly inherited. One prevailing theory is the two hit hypothesis. The first of these two hits is a genetic trait that leaves one vulnerable to the illness. The second hit is some stressful life event or environmental insult (e.g., infection or toxic exposure) that triggers the onset of the illness in the vulnerable individual. 

Merikangas KR (2002) Genetic and other vulnerability factors for anxiety and stress disorders. In Davis KL, Charney D, Coyle JT, Nemeroff C (eds) Neuropsychopharmacology— the fifth generation of progress. Lippincott Williams and Wilkins, Philadelphia, pp 867-882... 

We propose that a redox/antioxidant dysregulation due to GSH deficit could represent a vulnerability factor at the early phase of brain development in at least a subgroup of schizophrenia patients. Combined with other genetic factors and environmental factors, such as stress, obstetrical complications or viral infections, it could favor the development of the disease. The role of the GSH deficit proposed allows integration in a causal way many phenomenological aspects of schizophrenia. It is compatible with both the DA and the glutamate/NMDA hypotheses and with the neuropathological observations. In contrast to... 

Another effect of genetic uniformity is to make the entire population of plants also vulnerable to the same environmental stresses. 

Kreek MJ, Nielsen DA, Butelman ER, LaForge KS (2005) Genetic influences on impulsivity, risk taking, stress responsivity and vulnerability to drug abuse and addiction. Nat Neurosci 8 1450-1457... 

Analysis of mouse models with genetic disruption of individual chemokines or chemokine receptors has usually revealed specific phenotypes, but generally, only under stressed conditions (infection, allograft, etc.), which suggests that the full potential of chemokine-receptor redundancy may not always be realized in vivo. Instead, under normal physiological conditions and during immune responses, chemokines and chemokine receptors appear to function as a coordinated, but vulnerable, network. 

Prolonged seizures of around 30 min produce necrotic and apoptotic cell death in the same cell population with different time courses or in different cell populations. The current concept of the fate of a neuron is determined by many factors following an initial seizure including early gene expression with alteration of mRNA and proteins (enzymes, receptors, and ion channel subunits) modulated by calcium mediated effects. These changes alter the vulnerability of that neuron to subsequent excitotoxic stresses. Therefore, genetics influences seizure susceptibility (manifested in animal models and febrile seizures in humans) and consequences of seizures (hippocampal sclerosis). 

Genetic contribution and importance of triggers (stress vulnerability model)... 

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