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Click on the blue text to follow our contact protein-associated protein-like 2 gene (CNTNAP2 gene) as a susceptibility gene for autism
.
Cntnap2 knockout mice show core symptoms of autism such as social disorders, and at the same time, oxytocin is closely related to this social disorder
.
MRI technology found that the functional connectivity of the brain in autistic patients and animal models is impaired
.
Cntnap2 is enriched and expressed in oxytocinergic neurons.
Cntnap2 knockout mice have lower brain oxytocin levels, and the number of oxytocinergic neurons in the hypothalamic paraventricular nucleus (PVN) also decreases
.
Exogenously increasing oxytocin levels or chemical genetics endogenously increasing oxytocin levels can alleviate social disorders in mice with autism
.
On December 20, 2021, the Daniel H.
Geschwind research team of the University of California, Los Angeles, David Geffen School of Medicine revealed that oxytocin restores functional connectivity by activating oxytocin receptor signals in the nucleus accumbens brain area to normalize social functions in autistic model mice
.
Figure 1: Functional connectivity changes in Cntnap2 knockout mice after oxytocin treatment.
Researchers divided the mouse brain into olfactory (OLF), cortex (CTX), hippocampus (HPC), forebrain nucleus (FN), and the Allen Mouse Brain Atlas.
In 7 main brain regions, including thalamus (TH), hypothalamus (HYPO) and midbrain (MID), resting state functional MRI analysis revealed that Cntnap2 knockout mice have FN-centered FN-HPC, FN-TH , The functional connection of FN-MID is disordered, and the functional connections of the medial prefrontal cortex (mPFC), nucleus accumbens (NAc), stria terminalis (BNST), and hypothalamus related to social functions are weakened.
Oxytocin treatment can alleviate most of the above functional connectivity disorders (Figure 1)
.
Pharmacological MRI can explain the changes of brain activity level under the action of drugs with the change of endogenous blood oxygen level dependent signal
.
Through pharmacological nuclear magnetic resonance technology, it was found that after oxytocin treatment, Cntnap2 knockout mice PVN, BNST, NAc, and hippocampal blood oxygen levels depend on signal enhancement, especially in the PVN brain area
.
Figure 2: Whole brain c-fos labeling map The above MRI results reveal the effect of oxytocin on brain function from a macroscopic perspective.
The researchers further used transparent brain technology to label the whole brain with c-fos (Figure 2) and found that it induces labor.
Cntnap2 can enhance the activity of neurons in the brain regions of Cntnap2 knockout mice NAc, BNST, anterior insula, somatosensory cortex, visual cortex, etc.
, and reduce neuronal activity in hippocampal CA1 and CA3 regions
.
After treatment with oxytocin, different imaging techniques revealed some differences in the brain changes of Cntnap2 knockout mice: MRI revealed that NAc, BNST, medial septum, and hippocampus were the brain regions with the most obvious functional changes, while pharmacology Magnetic resonance imaging found that the blood oxygen level-dependent signal enhancement of PVN was the most obvious, and the whole brain c-fos labeling revealed that the somatosensory cortex and visual cortex had the largest number of activated neurons
.
Interestingly, the chronic activation of Cntnap2 by chemical genetics can activate the neuronal activity in the NAc brain area after knocking out the oxytocin-expressing neurons in the PVN brain area of mice
.
The injection of oxytocin receptor agonist into the NAc brain area of normal mice can promote social behavior.
Light-activated PVN brain area oxytocinergic neurons project to the neural circuit of NAc, which can alleviate the social disorder of Cntnap2 knockout mice
.
In general, this article uses nuclear magnetic resonance technology to find from the macro level that the functional connection of autism model mice is disordered, and the functional connection disorder can be alleviated by activating the oxytocin signal in the nucleus accumbens after administration of oxytocin
.
[References] 1.
https://doi.
org/10.
1016/j.
neuron.
2021.
11.
031 The pictures in the text are from the references
.
Cntnap2 knockout mice show core symptoms of autism such as social disorders, and at the same time, oxytocin is closely related to this social disorder
.
MRI technology found that the functional connectivity of the brain in autistic patients and animal models is impaired
.
Cntnap2 is enriched and expressed in oxytocinergic neurons.
Cntnap2 knockout mice have lower brain oxytocin levels, and the number of oxytocinergic neurons in the hypothalamic paraventricular nucleus (PVN) also decreases
.
Exogenously increasing oxytocin levels or chemical genetics endogenously increasing oxytocin levels can alleviate social disorders in mice with autism
.
On December 20, 2021, the Daniel H.
Geschwind research team of the University of California, Los Angeles, David Geffen School of Medicine revealed that oxytocin restores functional connectivity by activating oxytocin receptor signals in the nucleus accumbens brain area to normalize social functions in autistic model mice
.
Figure 1: Functional connectivity changes in Cntnap2 knockout mice after oxytocin treatment.
Researchers divided the mouse brain into olfactory (OLF), cortex (CTX), hippocampus (HPC), forebrain nucleus (FN), and the Allen Mouse Brain Atlas.
In 7 main brain regions, including thalamus (TH), hypothalamus (HYPO) and midbrain (MID), resting state functional MRI analysis revealed that Cntnap2 knockout mice have FN-centered FN-HPC, FN-TH , The functional connection of FN-MID is disordered, and the functional connections of the medial prefrontal cortex (mPFC), nucleus accumbens (NAc), stria terminalis (BNST), and hypothalamus related to social functions are weakened.
Oxytocin treatment can alleviate most of the above functional connectivity disorders (Figure 1)
.
Pharmacological MRI can explain the changes of brain activity level under the action of drugs with the change of endogenous blood oxygen level dependent signal
.
Through pharmacological nuclear magnetic resonance technology, it was found that after oxytocin treatment, Cntnap2 knockout mice PVN, BNST, NAc, and hippocampal blood oxygen levels depend on signal enhancement, especially in the PVN brain area
.
Figure 2: Whole brain c-fos labeling map The above MRI results reveal the effect of oxytocin on brain function from a macroscopic perspective.
The researchers further used transparent brain technology to label the whole brain with c-fos (Figure 2) and found that it induces labor.
Cntnap2 can enhance the activity of neurons in the brain regions of Cntnap2 knockout mice NAc, BNST, anterior insula, somatosensory cortex, visual cortex, etc.
, and reduce neuronal activity in hippocampal CA1 and CA3 regions
.
After treatment with oxytocin, different imaging techniques revealed some differences in the brain changes of Cntnap2 knockout mice: MRI revealed that NAc, BNST, medial septum, and hippocampus were the brain regions with the most obvious functional changes, while pharmacology Magnetic resonance imaging found that the blood oxygen level-dependent signal enhancement of PVN was the most obvious, and the whole brain c-fos labeling revealed that the somatosensory cortex and visual cortex had the largest number of activated neurons
.
Interestingly, the chronic activation of Cntnap2 by chemical genetics can activate the neuronal activity in the NAc brain area after knocking out the oxytocin-expressing neurons in the PVN brain area of mice
.
The injection of oxytocin receptor agonist into the NAc brain area of normal mice can promote social behavior.
Light-activated PVN brain area oxytocinergic neurons project to the neural circuit of NAc, which can alleviate the social disorder of Cntnap2 knockout mice
.
In general, this article uses nuclear magnetic resonance technology to find from the macro level that the functional connection of autism model mice is disordered, and the functional connection disorder can be alleviated by activating the oxytocin signal in the nucleus accumbens after administration of oxytocin
.
[References] 1.
https://doi.
org/10.
1016/j.
neuron.
2021.
11.
031 The pictures in the text are from the references
