Topic: astrocyte-neuron lactate shuttle

Depression is associated with alterations in brain glucose metabolism and impairments in processes associated with the astrocyte-neuron lactate shuttle (ANLS). Within this framework, lactate emerges as a promising therapeutic avenue, demonstrating antidepressant efficacy in diverse mouse models of depression, including the forced swim test and chronic corticosterone treatment. Our study explores the impact of stress and elevated corticosterone on astrocyte-neuron metabolic coupling, examining restoration potential of lactate treatment in controlled in vitro and complex in vivo settings. Prolon

The brain is the most energy-demanding organ of our body in proportion to its size. Within it, neurons are the prime energy consumers, but they are not alone in the brain. While the classical view of brain energetics pointed at blood-borne glucose as the main source for neuronal energy metabolism, it is now admitted that lactate is also playing a key role. The Astrocyte-Neuron Lactate Shuttle (ANLS) in which astrocytes take up glucose from the blood, store it as glycogen, and/or convert and release it under the form of lactate, is a parallel energy source. Whether neurons preferentially use gl

The Astrocyte-Neuron Lactate Shuttle model posits that lactate is transferred from astrocytes to neurons to fulfill energetic needs and act as a signal that regulates gene expression related to neuroprotection, neuronal excitability, synaptic plasticity, and memory. N6-methyladenosine (m6A), the most abundant internal modification of RNA, influences mRNA stability, translation, transport, localization, and alternative splicing. This dynamic epitranscriptomic mark is prevalent in the nervous system, impacting various processes, including those affected by lactate, such as neurogenesis, synaptic

Lactate is an important metabolite produced by astrocytes and delivered to neurons to support their energy needs in a process known as the astrocyte-neuron lactate shuttle. Emerging research during the past decade has unveiled a role of lactate as a signal capable of orchestrating critical functions ranging from neuroprotection to memory. In previous work, we found that lactate enhanced the amplitude and decay time of NMDA receptor currents (INMDAR) evoked by brief applications of glutamate and glycine. These effects were not observed when neurons were exposed to lactate receptor (HCA1) agonis