New research at Karolinska Institutet
in Sweden have identified a protein in the brain that is important both for the function of the mood-regulating substance serotonin and for the release of
stress hormones, at least in mice. Their observation shows, which are published
in the journal Molecular Psychiatry,
may have implications for the development of new drugs for depression and
anxiety.
Researchers at the Karolinska Institute in Sweden
identified a protein in the brain important for the function of serotonin
regulating mood and for the secretion of stress hormones, at least in mice. The
findings, published in the journal Molecular Psychiatry, may have implications
for the development of new drugs for depression and anxiety.
After being exposed to shock or severe stress, some
people experience an abnormal response to stress or chronic stress. This
increases the risk of other diseases such as depression and anxiety, but it
remains unknown what mechanisms are underlying or how the response to stress is
regulated.
A research group at the Karolinska Institute
previously showed that a protein called p11 plays an important role in the function of serotonin, a neurotransmitter in the brain that regulates mood.
Patients with depression and suicide victims have low levels of p11 protein in
their brains and laboratory mice with low levels of p11 show depression-like
behavior and anxiety. The
p11 protein is connected with the signal transport of synapses. Found in the brain
of people and different vertebrates, it has been controlled in the guideline of
temperament. Furthermore, because it collaborated with serotonin-flagging
proteins and its relationship with the side effects of mind-set problems, p11 is
another possible objective for drug treatment. its levels in mice can also be raised by some
antidepressants.
The new study shows that p11 affects the initial
release of the stress hormone cortisol in mice by modifying the activity of
specific neurons in the hypothalamus region of the brain. Through a completely
different signaling pathway arises in the brain stem, p11 also affects the
release of two other stress hormones, adrenaline, and noradrenalin. Besides,
tests showed that mice with p11 deficiency reacted more strongly with stress,
with higher heart rate and more signs of anxiety, compared to mice with normal
p11 levels.
Now the researchers know that an abnormal response to
stress can lead to or exacerbate depression and cause anxiety disorder and
cardiovascular disease, says first author Vasco Souza, a researcher in the
Department of Clinical Neurology, Karolinska Institute. Therefore, it is important
to know whether the link between p11 deficiency and the response to stress that
we see in mice can also be seen in patients.
Researchers believe the results may have implications
for the development of new, more effective drugs. New treatments are urgently
needed because current antidepressants are not effective enough in many
patients.
Per Svenningsson, a professor in the Department of
Clinical Neurology, Karolinska Institutet, who led the study, says: One the promising method involves giving factors that promote topical expression of
p11 and many trials are already conducted on animal models of depression. Another interesting approach that needs further investigation includes the development
of drugs that prevent the onset of a stress hormone response in the brain.
