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When the stress brake fails
Stress causes the brain to secrete a
hormone that also stimulates the
pituitary gland. This prompts the
adrenal cortex to produce cortisone
and other transmitters. The protein
SPRED2 inhibits this signal pathway;
© Melanie Ullrich
SPRED2: This protein is found in humans and other mammals. Among those who discovered it is a team of scientists from the University of Wurzburg led by Kai Schuh. The professor is researching the function that this protein performs. In this area, he and his doctoral student Melanie Ullrich as well as other colleagues from Wurzburg, Ulm, and Stockholm have now made new findings.
Insights into the function of the protein were gained by the scientists using mice that lack the SPRED2 gene and are therefore unable to create the protein. These animals demonstrate unusual behaviour: they drink twice as much as normal mice and scratch themselves extremely often, such as behind the ears.
Why this abnormal behaviour? To clarify this, the researchers analyzed the organism of these animals very closely. One of the discoveries they made were significantly elevated quantities of the stress hormone cortisone and of the hormone aldosterone. The latter causes an increase in the concentration of salt in the blood, thereby raising blood pressure. Consequently, the mice drink more water so they can expel the excess salt more successfully.
The studies revealed other striking irregularities. The synapses in the brain release a greater number of transmitters. There is also an overabundance of the hormones CRH and ACTH, which are formed in the brain and the pituitary gland: these two transmitters in a signal chain control the production of the hormones cortisone and aldosterone in the adrenal cortex.
The researchers concluded that if the organism is missing the protein SPRED2 the hormonal signal chain from the brain to the pituitary gland to the adrenal cortex is activated far too strongly. It would appear that the protein has the effect of slowing down this system that the organism sets in motion whenever it has to overcome physical or mental stress.
This therefore means that, hormonally speaking, SPRED2-free mice are in a state of permanent stress. The researchers are therefore interpreting the continuous scratching that they observe with these animals as a stress-related compulsion. “The elevated quantity of cortisone simulates stress for them,” says Schuh. No evidence has been found of other conceivable causes for the scratching, such as diabetes.
“We are not currently aware of any illnesses in humans that are connected to SPRED2,” says Schuh. But this could all change, as the example of the closely related SPRED1 gene shows: geneticists only recently proved for the first time that a defect to this gene is the sole cause of neurofibromatosis, tumour-like growths of the nerve tissue.
MEDICA.de; Source: University of Wurzburg