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How the parasite affects mice fear of cats


Doctors online, November 6, 2018

Fear of Ada

Parasites Tokoplasmosis gondii produce incredible behavioral changes.
So, mice lose the fear of Katzen.n. And for people, he could be a neurological risk factor.

How the parasite affects mice fear of cats

After parasite infestation, mice lost their natural fear of cats.

© Sergii Figurnii /

Magdeburg. Magdeburg scientists examined in a study that Tokoplasma gondii, a trigger of toxoplasmosis, affects metabolism in the brain of their hosts. The staff of the Institute of Inflammation and Neurodegeneration at Otto von Guericke Magdeburg University (OVGU) and the Leibniz Institute of Neurobiologists (LIN) have shown that it modifies the molecular composition of the synapse there (J neuroinflammation 2018: 15: 216).

About 30 to 50 percent of people are already infected with toxoplasm during their lifetime. During the fifties, even 50 percent. Toxoplasmosis usually goes unnoticed and the infected do not suspect that they are affected. In healthy people, the infection causes short-term symptoms such as fever, fever and pain in the body. By contrast, such an infection can be dangerous to pregnant women or to persons with a weakened immune system.

There is no therapy to get rid of parasites when they attack the brain. Once infected, this remains a lifespan. The parasite nests in the muscle tissue of infected animals, but not only: "The gonorrhea toxins are absorbed by humans through digestion, entering the bloodstream and also migrating to the brain to arrive there for the lifetime of the nervous cells," Dr. Karl-Heinz Small from the Special Laboratory of Molecular Biological Techniques at LIN was quoted in the Institute's press release.

Lost fear

Magdeburg scientists have found mice in previous experiments that there are incredible changes in animals infected with Tokoplasma gondii: "Mice, who are really preyed with cat's animals, have lost their natural fear of cats after infection." If the rodents had the smell of the cat's urine, They seemed to have had the advantage of cats, "researchers said.

In order to explain these behavioral changes, they specifically investigated the molecular composition of the synapse, because these are the basic structures for signal processing in the brain.

In collaboration with the Helmholtz Center for the Investigation of Infection in Braunschweig, they succeeded in proving that in a total of 300 synaptic proteins, levels in the brain after infection with toxoplasmosis have changed. In particular, the proteins are particularly reduced in the excitatory release of the release glutamate. On the other hand, increased levels of proteins involved in the immune response have been found.

Sulphadiazine is often used for the treatment of toxoplasmosis, which in part prevents the proliferation of toxoplasmens. Psychiatrist and neuroscientist Bjorn Schott explains: "Now we wanted to find out how the treatment of sulphadiazine affects the molecular changes in the brain caused by the infection."

The protein composition changes after treatment

Result: The protein content of the mouse in the mouse after therapy was comparable to those uninfected. "All tested proteins, which are responsible for transmitting glutamater signals, are again in the normal range, and inflammatory activity has declined measurably."

It seems that the infection leads to an improved immune response that reduces the proteins involved in the synaptic excitability of glutamate, while sulfadiazine reduces toxoplasma and thereby normalizes the immune response, causing the synaptic protein recovery.

Even for people, these findings can be medically relevant. "They support the suggestion that Tokoplasma gondii is a risk factor for neuropsychiatric disorders. Malfunction of glutamatergic synapses is involved in the causes of depression, schizophrenia and autism." The components of the immune response also show connections to these diseases, summarizes the Dunai neuroimunologist.

The researchers suspect that an immune response can cause changes in the synapses that can lead to neuropsychiatric disorders. (Eb)

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