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Click on the blue letters to pay attention to the olfactory system of our mice participating in various behaviors such as eating, mating, and fighting.
As a component of feeding behavior, smell provides clues to predict feeding.
In humans and rodent species, hunger promotes sensitivity to food odors, and quickly perceives food, and sensitivity to food odors and exploration after fullness will decrease.
In a hungry state, mice have the ability to distinguish whether it is the smell of food or the pheromone emitted by their companions.
In this process, the same or different neuron groups in the olfactory epithelium, olfactory bulb, and olfactory cortex may be activated, and the same or different odors may be felt to regulate behavior flexibly.
On March 3, 2021, the Stephen D.
Liberle research team of the Department of Cell Biology at Harvard Medical School published an article in the journal Nature and found that the thalamic neuropeptide Y signaling pathway can be used to selectively promote the preference for food odors in the hungry state.
Hunger-dependent odor response behavior experiment flow chart The researchers designed a simple and effective hunger-dependent odor response behavior experiment: mice are placed in a device that emits odor at both ends, and one end stores the food they have eaten.
, One end stores the urine of the opposite sex, and the mouse cannot directly touch the two ends, and can only perceive the smell of food and urine through the sense of smell.
After 24 hours of fasting, mice were given food (Fed mice) and continued fasting mice (Fasted mice).
Then, Fed mice and Fasted mice were subjected to odor detection experiments.
The results showed that Fasted mice obviously liked The Fed mice did not show this preference when they went to the food storage section and tried to seek food.
The response of starved mice and full-bodied mice to food odors.
Previous studies have shown that light-activated agouti-related protein (AgRP) neurons in the arcuate nucleus of the hypothalamus promote eating behavior, and inhibit eating behavior after inhibiting this type of neurons.
There was starvation death.After the researchers light-activated AgRP neurons in Fed mice, they showed a preference for food smell similar to that of Fasted mice.
That is to say, the full-fed mice still have a strong sensitivity to food odors after activating AgRP neurons.
Previous studies have shown that AgRP neurons extensively project to the paraventricular nucleus (PVT) of the thalamus, the stria terminalis (BNST), the paraventricular nucleus of the hypothalamus (PVH), the central nucleus of the amygdala (CeA), and the lateral hypothalamic nucleus (LH).
), the medial amygdala (MeA), the gray matter around the midbrain aqueduct (PAG), and the parabrachial nucleus.
Researchers in the downstream brain regions of light-activated AgRP neuron projections do nothing, and by injecting the optogenetic virus cre enzyme-dependent AAV-DIO-ChR2 into these brain regions of AgRP-cre mice, all the above brain regions are activated separately After the food odor test, the results showed that only activating the AgRP neurons in the PVT and arcuate nucleus can promote the food odor preference of the mice after being fed.
After the photoinhibition of PVT and AgRP neurons in the arcuate nucleus, Fasted mice were not as interested in the smell of food as before.
These results indicate that the thalamic AgRP neurons regulate food odor preference behavior.
AgRP neurons mainly release three neurotransmitters: GABA, agouti-associated protein, and neuropeptide Y (NPY).
Researchers found that fasted mice still showed preference for food odor after knocking out GABA or agouti-related protein, but fasted mice could not show this preference after knocking out NPY, resulting in odor behavior defects and performance.
Similar to the role of AgRP neurons that inhibit PVT.
Because NPY is not only expressed on AgRP neurons, but also expressed on other types of neurons.
The researchers further confirm that the behavioral defects caused by knock-out NPY are caused by the loss of NPY in AgRP neurons.
They crossed AgRP-cre mice with NPY knockout mice, and then injected the Cre enzyme-dependent virus AAV-DIO-Npy into the arcuate nucleus region, so that NPY would be re-expressed in this brain region, which is a "saving" experiment.
It can indeed reverse odor behavior defects.This further confirms that NPY released by AgRP neurons mediates food odor preference behavior.
Neuropeptide Y receptors belong to the rhodopsin family of GPCRs and include four subtypes in the human body: NPY1R, NPY2R, NPY4R and NPY5R.
After the researchers knocked out NPY1R, fasted mice still showed preference for food smell, but fasted mice showed odor behavior defects after knocking out NPY5R.
Fasted mice showed food odor behavior defects after knocking out NPY, but in PVT This defect no longer exists after injection of NPY or NPY5R agonist into the brain area.
In addition, there is no preference for food smell after injection of NPY5R antagonist in wild-type fasted mice.
These results indicate that NPY5R plays a key role in the behavior of food odor preference caused by hunger.
In summary, the findings in this article reveal the neural signaling pathways that can sense food odors during starvation: the NPY signal released by thalamic AgRP neurons and its receptor NPY5R.
[References] 1.
https://doi.
org/10.
1038/s41586-021-03299-4 The pictures in the article are all from the references
As a component of feeding behavior, smell provides clues to predict feeding.
In humans and rodent species, hunger promotes sensitivity to food odors, and quickly perceives food, and sensitivity to food odors and exploration after fullness will decrease.
In a hungry state, mice have the ability to distinguish whether it is the smell of food or the pheromone emitted by their companions.
In this process, the same or different neuron groups in the olfactory epithelium, olfactory bulb, and olfactory cortex may be activated, and the same or different odors may be felt to regulate behavior flexibly.
On March 3, 2021, the Stephen D.
Liberle research team of the Department of Cell Biology at Harvard Medical School published an article in the journal Nature and found that the thalamic neuropeptide Y signaling pathway can be used to selectively promote the preference for food odors in the hungry state.
Hunger-dependent odor response behavior experiment flow chart The researchers designed a simple and effective hunger-dependent odor response behavior experiment: mice are placed in a device that emits odor at both ends, and one end stores the food they have eaten.
, One end stores the urine of the opposite sex, and the mouse cannot directly touch the two ends, and can only perceive the smell of food and urine through the sense of smell.
After 24 hours of fasting, mice were given food (Fed mice) and continued fasting mice (Fasted mice).
Then, Fed mice and Fasted mice were subjected to odor detection experiments.
The results showed that Fasted mice obviously liked The Fed mice did not show this preference when they went to the food storage section and tried to seek food.
The response of starved mice and full-bodied mice to food odors.
Previous studies have shown that light-activated agouti-related protein (AgRP) neurons in the arcuate nucleus of the hypothalamus promote eating behavior, and inhibit eating behavior after inhibiting this type of neurons.
There was starvation death.After the researchers light-activated AgRP neurons in Fed mice, they showed a preference for food smell similar to that of Fasted mice.
That is to say, the full-fed mice still have a strong sensitivity to food odors after activating AgRP neurons.
Previous studies have shown that AgRP neurons extensively project to the paraventricular nucleus (PVT) of the thalamus, the stria terminalis (BNST), the paraventricular nucleus of the hypothalamus (PVH), the central nucleus of the amygdala (CeA), and the lateral hypothalamic nucleus (LH).
), the medial amygdala (MeA), the gray matter around the midbrain aqueduct (PAG), and the parabrachial nucleus.
Researchers in the downstream brain regions of light-activated AgRP neuron projections do nothing, and by injecting the optogenetic virus cre enzyme-dependent AAV-DIO-ChR2 into these brain regions of AgRP-cre mice, all the above brain regions are activated separately After the food odor test, the results showed that only activating the AgRP neurons in the PVT and arcuate nucleus can promote the food odor preference of the mice after being fed.
After the photoinhibition of PVT and AgRP neurons in the arcuate nucleus, Fasted mice were not as interested in the smell of food as before.
These results indicate that the thalamic AgRP neurons regulate food odor preference behavior.
AgRP neurons mainly release three neurotransmitters: GABA, agouti-associated protein, and neuropeptide Y (NPY).
Researchers found that fasted mice still showed preference for food odor after knocking out GABA or agouti-related protein, but fasted mice could not show this preference after knocking out NPY, resulting in odor behavior defects and performance.
Similar to the role of AgRP neurons that inhibit PVT.
Because NPY is not only expressed on AgRP neurons, but also expressed on other types of neurons.
The researchers further confirm that the behavioral defects caused by knock-out NPY are caused by the loss of NPY in AgRP neurons.
They crossed AgRP-cre mice with NPY knockout mice, and then injected the Cre enzyme-dependent virus AAV-DIO-Npy into the arcuate nucleus region, so that NPY would be re-expressed in this brain region, which is a "saving" experiment.
It can indeed reverse odor behavior defects.This further confirms that NPY released by AgRP neurons mediates food odor preference behavior.
Neuropeptide Y receptors belong to the rhodopsin family of GPCRs and include four subtypes in the human body: NPY1R, NPY2R, NPY4R and NPY5R.
After the researchers knocked out NPY1R, fasted mice still showed preference for food smell, but fasted mice showed odor behavior defects after knocking out NPY5R.
Fasted mice showed food odor behavior defects after knocking out NPY, but in PVT This defect no longer exists after injection of NPY or NPY5R agonist into the brain area.
In addition, there is no preference for food smell after injection of NPY5R antagonist in wild-type fasted mice.
These results indicate that NPY5R plays a key role in the behavior of food odor preference caused by hunger.
In summary, the findings in this article reveal the neural signaling pathways that can sense food odors during starvation: the NPY signal released by thalamic AgRP neurons and its receptor NPY5R.
[References] 1.
https://doi.
org/10.
1038/s41586-021-03299-4 The pictures in the article are all from the references
