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Click on the blue letters to focus on the astrocytes and microglia in our hypothalamus that affect eating, energy and glucose metabolism by regulating synaptic input.
The synaptic plasticity of the hypothalamic neural circuits regulated by peripheral energy metabolism signals is a prerequisite for autonomous adaptation to the constantly changing surrounding environment.
In the past ten years, scientists have focused on the cellular and molecular mechanisms of synaptic plasticity in the hypothalamus.
In fact, the key part that controls the output of neurons is the perinuclear cell body except axons and dendrites-the perinuclear body, which is an important gateway for regulating nerve excitability.
This part integrates all the signal inputs of the dendritic branches and affects them along the way.
Action potentials transmitted by axons.
On May 17, 2021, Tamas L.
Horvath of Yale University School of Medicine published an article revealing the mechanism by which starvation-promoting agouti-related peptide (AgRP) neurons induce astrocyte-mediated feedforward self-activation loops.
Researchers have found that restricting food intake can increase the level of glial fibrillary acidic protein (GFAP) in the arcuate nucleus (ARC) brain area, and increase the fission of astrocyte mitochondria.
In addition, after restricting the diet, astrocytes are more wrapped around AgRP neurons (AgRP), and the number of inhibitory synapses in the perinucleus is also significantly reduced.
Studies have shown that the hunger hormone Ghrelin increases after fasting.
The research team simulated an effect similar to restricted diet by injecting Ghrelin into the abdominal cavity of normal mice one and a half hours after GFAP levels in the ARC brain area increased.
In addition, Ghrelin also causes the depolarization of astrocyte membrane potentials (MPs) in the ARC brain area.
Subsequently, the researchers chronically inhibited the activity of AgRP neurons during intraperitoneal injection of Ghrelin and did not affect the electrical activity of astrocytes.
However, after activating this type of neurons, astrocytes are more wrapped around AgRP neurons, and the number of inhibitory synapses in the perinuclear body is also reduced.
More surprisingly, activation of AgRP neurons caused a depolarization of the membrane potential of astrocytes.
Gone are the days of [labeling astrocytes with unsatisfactory results]! The change of AgRP neuron activity can release AgRP, neuropeptide Y and inhibitory transmitter GABA.
In order to further find the mechanism by which AgRP neurons regulate Ghrelin-induced depolarization of astrocytes in the ARC brain area, in vitro electrophysiological experiments have found that the incubation of AgRP and neuropeptide Y does not affect the hypothalamic astrocytes.
Discharge activity.
But after incubating the inhibitory transmitter GABA, it can cause astrocytes to depolarize strongly and rapidly.
Ghrelin did not promote the depolarization of astrocyte membrane potential after administration of GABA receptor antagonist.
Of course the forces are interacting.
Neurons regulate the firing of astrocytes by releasing GABA, so astrocytes will not be beaten in vain, and they will also release certain factors to regulate neuronal activity.
This factor is prostaglandin E2 (PGE2).
Exogenous administration of PGE2 from the central nervous system can activate AgRP neurons and cause mitochondrial division.
Inhibition of PGE2 does not activate AgRP neurons, and Ghrelin does not exert its previous effects.
In general, this paper found that the astrocytes wrapped around the perinucleus of AgRP neurons replaced the inhibitory synaptic connections in the starvation state.
GABA released by AgRP neurons activates astrocytes, and PGE2 released by astrocytes can activate AgRP neurons through its receptors.
In this way, a diet-related feed-forward self-activation cycle mechanism is formed.[References] 1.
https://doi.
org/10.
1172/JCI144239, the pictures in the text are all from the reference Baidu Netdisk Original download: https://pan.
baidu.
com/s/1lBX3jHXz8AcYfdnTXjoVtQ Extraction code: s8at
The synaptic plasticity of the hypothalamic neural circuits regulated by peripheral energy metabolism signals is a prerequisite for autonomous adaptation to the constantly changing surrounding environment.
In the past ten years, scientists have focused on the cellular and molecular mechanisms of synaptic plasticity in the hypothalamus.
In fact, the key part that controls the output of neurons is the perinuclear cell body except axons and dendrites-the perinuclear body, which is an important gateway for regulating nerve excitability.
This part integrates all the signal inputs of the dendritic branches and affects them along the way.
Action potentials transmitted by axons.
On May 17, 2021, Tamas L.
Horvath of Yale University School of Medicine published an article revealing the mechanism by which starvation-promoting agouti-related peptide (AgRP) neurons induce astrocyte-mediated feedforward self-activation loops.
Researchers have found that restricting food intake can increase the level of glial fibrillary acidic protein (GFAP) in the arcuate nucleus (ARC) brain area, and increase the fission of astrocyte mitochondria.
In addition, after restricting the diet, astrocytes are more wrapped around AgRP neurons (AgRP), and the number of inhibitory synapses in the perinucleus is also significantly reduced.
Studies have shown that the hunger hormone Ghrelin increases after fasting.
The research team simulated an effect similar to restricted diet by injecting Ghrelin into the abdominal cavity of normal mice one and a half hours after GFAP levels in the ARC brain area increased.
In addition, Ghrelin also causes the depolarization of astrocyte membrane potentials (MPs) in the ARC brain area.
Subsequently, the researchers chronically inhibited the activity of AgRP neurons during intraperitoneal injection of Ghrelin and did not affect the electrical activity of astrocytes.
However, after activating this type of neurons, astrocytes are more wrapped around AgRP neurons, and the number of inhibitory synapses in the perinuclear body is also reduced.
More surprisingly, activation of AgRP neurons caused a depolarization of the membrane potential of astrocytes.
Gone are the days of [labeling astrocytes with unsatisfactory results]! The change of AgRP neuron activity can release AgRP, neuropeptide Y and inhibitory transmitter GABA.
In order to further find the mechanism by which AgRP neurons regulate Ghrelin-induced depolarization of astrocytes in the ARC brain area, in vitro electrophysiological experiments have found that the incubation of AgRP and neuropeptide Y does not affect the hypothalamic astrocytes.
Discharge activity.
But after incubating the inhibitory transmitter GABA, it can cause astrocytes to depolarize strongly and rapidly.
Ghrelin did not promote the depolarization of astrocyte membrane potential after administration of GABA receptor antagonist.
Of course the forces are interacting.
Neurons regulate the firing of astrocytes by releasing GABA, so astrocytes will not be beaten in vain, and they will also release certain factors to regulate neuronal activity.
This factor is prostaglandin E2 (PGE2).
Exogenous administration of PGE2 from the central nervous system can activate AgRP neurons and cause mitochondrial division.
Inhibition of PGE2 does not activate AgRP neurons, and Ghrelin does not exert its previous effects.
In general, this paper found that the astrocytes wrapped around the perinucleus of AgRP neurons replaced the inhibitory synaptic connections in the starvation state.
GABA released by AgRP neurons activates astrocytes, and PGE2 released by astrocytes can activate AgRP neurons through its receptors.
In this way, a diet-related feed-forward self-activation cycle mechanism is formed.[References] 1.
https://doi.
org/10.
1172/JCI144239, the pictures in the text are all from the reference Baidu Netdisk Original download: https://pan.
baidu.
com/s/1lBX3jHXz8AcYfdnTXjoVtQ Extraction code: s8at
