Exogenous L-lactate promotes astrocyte plasticity but is not sufficient for enhancing striatal synaptogenesis or motor behavior in mice

Lundquist, Adam J.; Gallagher, T; Petzinger, Giselle M.; Jakowec, Michael W.

doi:10.1101/2020.04.13.039446

Cited by 2 publications

(2 citation statements)

References 51 publications

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“…Lactate is known to be a signalling molecule for neuronal plasticity in cultured mouse primary neurons and in vivo in the mouse sensory-motor cortex [ 82 ]. Recently, Lundquist et al [ 83 ] observed an increase in the expression of BDNF in primary astrocytes treated with l-lactate in-vitro. They also demonstrated that l-lactate administration to healthy mice led to increased astrocyte morphological complexity, as well as astrocyte-specific neurotrophic expression within the striatum, a critical component of the motor and reward systems [ 83 ].…”

Section: Hormones and Metabolites Of The Muscle–brain Axismentioning

confidence: 99%

“…Recently, Lundquist et al [ 83 ] observed an increase in the expression of BDNF in primary astrocytes treated with l-lactate in-vitro. They also demonstrated that l-lactate administration to healthy mice led to increased astrocyte morphological complexity, as well as astrocyte-specific neurotrophic expression within the striatum, a critical component of the motor and reward systems [ 83 ]. Interestingly, increases in peripheral blood lactate levels at rest in humans have been associated with an increase in circulating BDNF [ 84 ].…”

Section: Hormones and Metabolites Of The Muscle–brain Axismentioning

confidence: 99%

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Molecular Mechanisms Underlying the Beneficial Effects of Exercise on Brain Function and Neurological Disorders

Nay

Smiles

Kaiser

et al. 2021

IJMS

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As life expectancy has increased, particularly in developed countries, due to medical advances and increased prosperity, age-related neurological diseases and mental health disorders have become more prevalent health issues, reducing the well-being and quality of life of sufferers and their families. In recent decades, due to reduced work-related levels of physical activity, and key research insights, prescribing adequate exercise has become an innovative strategy to prevent or delay the onset of these pathologies and has been demonstrated to have therapeutic benefits when used as a sole or combination treatment. Recent evidence suggests that the beneficial effects of exercise on the brain are related to several underlying mechanisms related to muscle–brain, liver–brain and gut–brain crosstalk. Therefore, this review aims to summarize the most relevant current knowledge of the impact of exercise on mood disorders and neurodegenerative diseases, and to highlight the established and potential underlying mechanisms involved in exercise–brain communication and their benefits for physiology and brain function.

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Section: Hormones and Metabolites Of The Muscle–brain Axismentioning

confidence: 99%

Section: Hormones and Metabolites Of The Muscle–brain Axismentioning

confidence: 99%

Molecular Mechanisms Underlying the Beneficial Effects of Exercise on Brain Function and Neurological Disorders

Nay

Smiles

Kaiser

et al. 2021

IJMS

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Knockdown of astrocytic monocarboxylate transporter 4 (MCT4) in the motor cortex leads to loss of dendritic spines and a deficit in motor learning

Lundquist

Llewellyn

Kishi

et al. 2021

Preprint

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Monocarboxylate transporters (MCTs) shuttle molecules, including L-lactate, involved in metabolism and cell signaling of the central nervous system. Astrocyte-specific MCT4 is a key component of the astrocyte-neuron lactate shuttle (ANLS) and is important for neuroplasticity and learning of the hippocampus. However, the importance of astrocyte-specific MCT4 in neuroplasticity of the M1 primary motor cortex remains unknown. In this study, we investigated astrocyte-specific MCT4 in motor learning and neuroplasticity of the M1 primary motor cortex using a cell-type specific shRNA knockdown of MCT4. Knockdown of astrocyte-specific MCT4 resulted in impaired motor performance and learning on the accelerating rotarod. In addition, MCT4 knockdown was associated with a reduction of neuronal dendritic spine density and spine width and decreased protein expression of PSD95 and Arc. Using near-infrared-conjugated 2-deoxyglucose uptake as a surrogate marker for neuronal activity, MCT4 knockdown was also associated with decreased neuronal activity in the M1 primary motor cortex and associated motor regions including the dorsal striatum and ventral thalamus. Our study supports a potential role for astrocyte-specific MCT4 and the ANLS in the neuroplasticity of the M1 primary motor cortex. Targeting MCT4 may serve to enhance neuroplasticity and motor repair in several neurological disorders, including Parkinson's disease and stroke.

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Exogenous L-lactate promotes astrocyte plasticity but is not sufficient for enhancing striatal synaptogenesis or motor behavior in mice

Cited by 2 publications

References 51 publications

Molecular Mechanisms Underlying the Beneficial Effects of Exercise on Brain Function and Neurological Disorders

Molecular Mechanisms Underlying the Beneficial Effects of Exercise on Brain Function and Neurological Disorders

Knockdown of astrocytic monocarboxylate transporter 4 (MCT4) in the motor cortex leads to loss of dendritic spines and a deficit in motor learning

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