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Octopamine metabolically reprograms astrocytes to confer neuroprotection against α-synuclein

ABSTRACT: Octopamine metabolically reprograms astrocytes to confer neuroprotection against α-synuclein

PROVIDER: PRJNA882845 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR21660016.fastq.gz	Fastqsanger.gz
	SRR21660017.fastq.gz	Fastqsanger.gz
	SRR21660018.fastq.gz	Fastqsanger.gz
	SRR21660019.fastq.gz	Fastqsanger.gz
	SRR21660020.fastq.gz	Fastqsanger.gz

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Octopamine metabolically reprograms astrocytes to confer neuroprotection against α-synuclein

Project description:Octopamine is a well-established invertebrate neurotransmitter involved in fight-or-flight responses. In mammals, its function was replaced by norepinephrine. Nevertheless, it is present at trace amounts and can modulate the release of monoamine neurotransmitters by a yet unidentified mechanism. Here, through a multidisciplinary approach utilizing in vitro and in vivo models of a-synucleinopathy, we uncovered an unprecedented role for octopamine in driving the conversion from toxic to neuroprotective astrocytes in the cerebral cortex by fostering aerobic glycolysis. Neuron-derived octopamine acts on astrocytes via a TAAR1-Orai1-Ca2+-calcineurinmediated signaling pathway to stimulate lactate secretion. Lactate uptake in neurons via the MCT2-calcineurin-dependent pathway increases ATP and prevents neurodegeneration. Pathological increases of octopamine caused by a-synuclein halts lactate production in astrocytes and short-circuits the metabolic communication to neurons. Our work provides a novel function of octopamine as a modulator of astrocyte metabolism and hence neuroprotection with implications to a-synucleinopathies.

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Octopamine metabolically reprograms astrocytes to confer neuroprotection against α-synuclein.

Project description:Octopamine is a well-established invertebrate neurotransmitter involved in fight or flight responses. In mammals, its function was replaced by epinephrine. Nevertheless, it is present at trace amounts and can modulate the release of monoamine neurotransmitters by a yet unidentified mechanism. Here, through a multidisciplinary approach utilizing in vitro and in vivo models of α-synucleinopathy, we uncovered an unprecedented role for octopamine in driving the conversion from toxic to neuroprotective astrocytes in the cerebral cortex by fostering aerobic glycolysis. Physiological levels of neuron-derived octopamine act on astrocytes via a trace amine-associated receptor 1-Orai1-Ca2+-calcineurin-mediated signaling pathway to stimulate lactate secretion. Lactate uptake in neurons via the monocarboxylase transporter 2-calcineurin-dependent pathway increases ATP and prevents neurodegeneration. Pathological increases of octopamine caused by α-synuclein halt lactate production in astrocytes and short-circuits the metabolic communication to neurons. Our work provides a unique function of octopamine as a modulator of astrocyte metabolism and subsequent neuroprotection with implications to α-synucleinopathies.

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