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Pain has always been a hot topic in the medical field.
At present, it is believed that so-called pain is a complex physiological and psychological activity, including the pain sensation caused by noxious stimuli acting on the body, and the body's pain response to noxious stimuli.
Pain stimulation is produced by a series of complex and diverse etiological, genetic and environmental factors in different combinations, and these factors participate in specific neurobiological processes.
Typical physical pain is caused by physical factors, including inflammatory activities and trauma, and can also be caused by chronic mental illness (such as depression).
Various evidences indicate that chronic pain and depression symptoms are frequently encountered in clinical practice, and most patients with depression do not respond well to traditional analgesics.
This difference in treatment methods means that pain caused by tissue damage has a different mechanism than pain caused by emotional factors, although these mechanisms are still unclear.
On March 8, 2021, the research team of Zhang Zhi, Li Juan and Jin Yan of the University of Science and Technology of China jointly published a new result in the journal Nature Neuroscience: Distinct thalamocortical circuits underlie allodynia induced by tissue injury and by depression-like states.
They found that different thalamic cortical circuits are the basis for allodynia caused by tissue damage and depression-like states.
DOI: 10.
1038/s41593-021-00811-x The thalamus is considered to be the main source of "nociceptive neurons" at the highest level of the nervous system of anesthetized animals.
Therefore, the researchers studied the neural activity of different subnuclei of the thalamus.
First, the researchers observed the expression of c-Fos on the established mouse model of tissue injury-related allodynia.
c-Fos is an early gene marker of neural activity in the posterior thalamic nucleus (PO), not the parafascicular nucleus (PF).
), the label of the ventromedial nucleus of the thalamus (VPM) or the ventromedorial nucleus of the thalamus (VPL).
Subsequent immunofluorescence staining showed that about 90% of the c-Fos signal was co-localized with the glutamate (Glu) specific antibody.
The whole-cell recording of visualized glutamatergic neurons showed that in the mouse model, the PO-derived The number of peaks increases, while the rheology from PF decreases.
These in vitro data indicate that POGlu neurons, but not PFGlu neurons, are activated by neuroinflammation or injury.
PO is involved in tissue injury-related allodynia.
Subsequently, the researchers established a depression-related allodynia model in mice through chronic restraint stress.
The mice showed significant allodynia and a variety of depression-like behaviors.
In order to study whether the appearance of allodynia requires a depression-like state, the researchers conducted pharmacological experiments by delivering the antidepressant paroxetine, and found that antidepressants can alleviate allodynia and depression-like behaviors in mice.
Further experiments showed that: No expression of c-Fos was observed in PO or PF of mice with depressive drugs.
Whole-cell recordings showed that the peak number of PFGlu neurons decreased, while the rheology of POGlu neurons increased.
This is different from the results of pain experiments caused by tissue damage.
Different subnuclei of the thalamus are involved in allodynia from tissue damage and depression-like states.
PF is involved in allodynia caused by depression-like states.
Next, the research team studied the mechanism of two different thalamic cortical circuits, dissected the functional connections of different thalamic cortical circuits, and clarified the abnormalities related to tissue damage and depression.
The circuit basis of sexual pain.
Multiple experiments have shown that the projection from the posterior thalamic nucleus (POGlu) to the glutamatergic neurons (S1Glu) of the primary somatosensory cortex mediates allodynia caused by tissue damage, and from the parafascicular thalamic nucleus (PFGlu) to The pathway from GABA neurons in the anterior cingulate cortex to glutamatergic neurons (ACCGABA→Glu) mediates allodynia associated with depression-like states.
In vivo calcium imaging and multi-tetrode electrophysiological recordings show that the POGlu and PFGlu populations undergo different adaptations under these two conditions.
Human intervention in each circuit will affect allodynia caused by tissue damage or depression-like states, but not both.
Analysis of the PoGlu→S1HL pathway.
In short, this study shows that the different thalamic cortical circuits POGlu→S1Glu and PFGlu→ACCGABA→Glu can reduce allodynia related to tissue damage and depression-like states, respectively, so as to understand the pathology caused by different causes.
The circuit basis of pain provides insights.
End reference materials: [1]https://
At present, it is believed that so-called pain is a complex physiological and psychological activity, including the pain sensation caused by noxious stimuli acting on the body, and the body's pain response to noxious stimuli.
Pain stimulation is produced by a series of complex and diverse etiological, genetic and environmental factors in different combinations, and these factors participate in specific neurobiological processes.
Typical physical pain is caused by physical factors, including inflammatory activities and trauma, and can also be caused by chronic mental illness (such as depression).
Various evidences indicate that chronic pain and depression symptoms are frequently encountered in clinical practice, and most patients with depression do not respond well to traditional analgesics.
This difference in treatment methods means that pain caused by tissue damage has a different mechanism than pain caused by emotional factors, although these mechanisms are still unclear.
On March 8, 2021, the research team of Zhang Zhi, Li Juan and Jin Yan of the University of Science and Technology of China jointly published a new result in the journal Nature Neuroscience: Distinct thalamocortical circuits underlie allodynia induced by tissue injury and by depression-like states.
They found that different thalamic cortical circuits are the basis for allodynia caused by tissue damage and depression-like states.
DOI: 10.
1038/s41593-021-00811-x The thalamus is considered to be the main source of "nociceptive neurons" at the highest level of the nervous system of anesthetized animals.
Therefore, the researchers studied the neural activity of different subnuclei of the thalamus.
First, the researchers observed the expression of c-Fos on the established mouse model of tissue injury-related allodynia.
c-Fos is an early gene marker of neural activity in the posterior thalamic nucleus (PO), not the parafascicular nucleus (PF).
), the label of the ventromedial nucleus of the thalamus (VPM) or the ventromedorial nucleus of the thalamus (VPL).
Subsequent immunofluorescence staining showed that about 90% of the c-Fos signal was co-localized with the glutamate (Glu) specific antibody.
The whole-cell recording of visualized glutamatergic neurons showed that in the mouse model, the PO-derived The number of peaks increases, while the rheology from PF decreases.
These in vitro data indicate that POGlu neurons, but not PFGlu neurons, are activated by neuroinflammation or injury.
PO is involved in tissue injury-related allodynia.
Subsequently, the researchers established a depression-related allodynia model in mice through chronic restraint stress.
The mice showed significant allodynia and a variety of depression-like behaviors.
In order to study whether the appearance of allodynia requires a depression-like state, the researchers conducted pharmacological experiments by delivering the antidepressant paroxetine, and found that antidepressants can alleviate allodynia and depression-like behaviors in mice.
Further experiments showed that: No expression of c-Fos was observed in PO or PF of mice with depressive drugs.
Whole-cell recordings showed that the peak number of PFGlu neurons decreased, while the rheology of POGlu neurons increased.
This is different from the results of pain experiments caused by tissue damage.
Different subnuclei of the thalamus are involved in allodynia from tissue damage and depression-like states.
PF is involved in allodynia caused by depression-like states.
Next, the research team studied the mechanism of two different thalamic cortical circuits, dissected the functional connections of different thalamic cortical circuits, and clarified the abnormalities related to tissue damage and depression.
The circuit basis of sexual pain.
Multiple experiments have shown that the projection from the posterior thalamic nucleus (POGlu) to the glutamatergic neurons (S1Glu) of the primary somatosensory cortex mediates allodynia caused by tissue damage, and from the parafascicular thalamic nucleus (PFGlu) to The pathway from GABA neurons in the anterior cingulate cortex to glutamatergic neurons (ACCGABA→Glu) mediates allodynia associated with depression-like states.
In vivo calcium imaging and multi-tetrode electrophysiological recordings show that the POGlu and PFGlu populations undergo different adaptations under these two conditions.
Human intervention in each circuit will affect allodynia caused by tissue damage or depression-like states, but not both.
Analysis of the PoGlu→S1HL pathway.
In short, this study shows that the different thalamic cortical circuits POGlu→S1Glu and PFGlu→ACCGABA→Glu can reduce allodynia related to tissue damage and depression-like states, respectively, so as to understand the pathology caused by different causes.
The circuit basis of pain provides insights.
End reference materials: [1]https://
