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Hindbrain astrocytes and glucose counter-regulation
Richard C Rogers1, Gerlinda E Hermann1
1Pennington Biomedical Research Center, 6400 Perkins Rd, Baton Rouge, LA 70808, USA.
Physiology & Behavior
|February 25, 2019
Summary
Hindbrain astrocytes detect low glucose and activate neurons to initiate the glucose counter-regulation response (CRR). Thrombin also activates these astrocytes, potentially causing hyperglycemia after traumatic injury.
Area of Science:
- Neuroscience
- Astrocyte Biology
- Metabolic Regulation
Background:
- Hindbrain astrocytes regulate homeostasis and detect physiological parameters.
- Astrocytes in the hindbrain are crucial for the glucose counter-regulation response (CRR).
- Glucoprivation-sensitive astrocytes in the hindbrain are key to CRR.
Purpose of the Study:
- Investigate the role of hindbrain astrocytes in glucose homeostasis.
- Elucidate the mechanisms by which astrocytes regulate the CRR.
- Explore the involvement of astrocytes in pathological hyperglycemia following traumatic injury.
Main Methods:
- Utilized ex vivo and in vivo models to study astrocyte function.
- Examined calcium signaling in response to glucoprivation.
- Investigated purinergic gliotransmission pathways.
- Assessed the effects of thrombin on hindbrain astrocytes.
Main Results:
- Hindbrain astrocytes exhibit robust calcium signaling upon glucopenic stimuli.
- Purinergic gliotransmission by astrocytes activates hindbrain catecholamine neurons, crucial for CRR.
- Thrombin acting on hindbrain astrocytes may induce pathological hyperglycemia post-trauma.
Conclusions:
- Hindbrain astrocytes are critical regulators of glucose homeostasis and the CRR.
- Astrocytes mediate CRR through purinergic signaling to catecholamine neurons.
- Astrocytic activation by thrombin presents a potential mechanism for traumatic injury-induced hyperglycemia.
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