Astrocytes in Post-Stroke Depression: Roles in Inflammation, Neurotransmission, and Neurotrophin Signaling.

Post-stroke depression (PSD) is a frequent and disabling complication of stroke that affects up to one-third of stroke survivors. The pathophysiology of PSD involves multiple mechanisms, including neurochemical, neuroinflammatory, neurotrophic, and neuroplastic changes. Astrocytes are a type of glial cell that is plentiful and adaptable in the central nervous system. They play key roles in various mechanisms by modulating neurotransmission, inflammation, neurogenesis, and synaptic plasticity. This review summarizes the latest evidence of astrocyte involvement in PSD from human and animal studies, focusing on the alterations of astrocyte markers and functions in relation to monoamine neurotransmitters, inflammatory cytokines, brain-derived neurotrophic factor, and glutamate excitotoxicity. We also discuss the potential therapeutic implications of targeting astrocytes for PSD prevention and treatment. Astrocytes could be new candidates for antidepressant medications and other interventions that aim to restore astrocyte homeostasis and function in PSD. Astrocytes could be new candidates for antidepressant medications and other interventions that aim to restore astrocyte homeostasis and function in PSD.

Role of microtubules in late-associative plasticity of hippocampal Schaffer collateral-CA1 synapses in mice.

The microtubule network represents a key scaffolding structure that forms part of the neuronal cytoskeleton and contributes to biomolecule exchange within neurons. However, researchers have not determined whether an intact microtubule network is required for late associative plasticity. Therefore, the late associative plasticity of field excitatory postsynaptic potentials from two synaptic inputs was analyzed. Synaptic potentiation was induced through alternating tetanization of hippocampal Schaffer-collateral CA1 synaptic populations in acute slices prepared from young-adult C57BL/6 mice. Vincristine was applied to depolymerize microtubules. Vincristine did not alter the phosphorylation levels of plasticity-related pre- or postsynaptic proteins but reduced the level of a protein marker of the ER-Golgi intermediate compartment (ERGIC-53/p58). Vincristine did not alter the magnitude or maintenance of the synaptic potentiation evoked by repeated tetanization (3 × 100 stimuli at 100 Hz) of one synaptic population. However, this synaptic potentiation was sensitive to the coapplication of a protein synthesis inhibitor, such as rapamycin, anisomycin or cycloheximide, indicating that protein synthesis has become essential in depolymerized microtubules during the first hour of the synaptic potentiation. The application of vincristine up to a 70 stimuli, 100 Hz tetanization of a second synaptic input prevented the transformation of short-term potentiation into long-term potentiation (LTP), further indicating that intact microtubules are required for the late associative properties of synaptic plasticity. Therefore, activity-dependent synaptic plasticity does not rely on microtubules within the first two hours after tetanization; however, the associative interaction of independent synaptic inputs relies on their proper function. In addition, either new protein synthesis or microtubule-based processes are sufficient to stabilize LTP within the first 3 h after tetanization, and a deficit in synaptic plasticity is only observable when both processes are blocked.

Environmental toxicology of bisphenol A: Mechanistic insights and clinical implications on the neuroendocrine system.

Bisphenol A (BPA) is a widely used environmental estrogen found in a variety of products, including food packaging, canned goods, baby bottle soothers, reusable cups, medical devices, tableware, dental sealants, and other consumer goods. This substance has been found to have detrimental effects on both the environment and human health, particularly on the reproductive, immune, embryonic development, nervous, endocrine, and respiratory systems. This paper aims to provide a comprehensive review of the effects of BPA on the neuroendocrine system, with a primary focus on its impact on the brain, neurons, oligodendrocytes, neural stem cell proliferation, DNA damage, and behavioral development. Additionally, the review explores the clinical implications of BPA, specifically examining its role in the onset and progression of various diseases associated with the neuroendocrine metabolic system. By delving into the mechanistic analysis and clinical implications, this review aims to serve as a valuable resource for studying the impacts of BPA exposure on organisms.

Enhanced Expression of Secreted α-Klotho in the Hippocampus Alters Nesting Behavior and Memory Formation in Mice.

The klotho gene family consists of α-, ß-, and γ-Klotho, which encode type I single-pass transmembrane proteins with large extracellular domains. α-Klotho exists as a full-length membrane-bound and as a soluble form after cleavage of the extracellular domain. Due to gene splicing, a short extracellular Klotho form can be expressed and secreted. Inactivation of α-Klotho leads to a phenotype that resembles accelerated aging, as the expression level of the α-Klotho protein in the hippocampal formation of mice decreases with age. Here, we show that intrahippocampal viral expression of secreted human α-Klotho alters social behavior and memory formation. Interestingly, overexpression of secreted human α-Klotho in the CA1 changed the nest-building behavior and improved object recognition, object location and passive avoidance memory. Moreover, α-Klotho overexpression increased hippocampal synaptic transmission in response to standardized stimulation strengths, altered paired-pulse facilitation of synaptic transmission, and enhanced activity-dependent synaptic plasticity. These results indicate that memory formation benefits from an augmented level of secreted α-Klotho.