Topic: hippocampal astrocytes

Astrocytes are active players in brain function. They sense and respond to neuronal activity by elevating intracellular calcium levels. These calcium elevations exhibit complex spatiotemporal patterns across the soma and main processes and focal microdomains. This activity underlies the astrocytic involvement in synaptic transmission, metabolism, and brain homeostasis. Here, we performed a multi-level analysis of the IP3 receptor type 2 knockout (IP3R2 KO) mouse model lacking global calcium elevations in astrocytes to disclose its implications to the molecular, cellular, and behavior levels. T

Medial temporal lobe epilepsy (MTLE) is a common cause of treatment-resistant seizures where excessive and hyper-synchronized neuronal activity is associated with reactive astrogliosis. Emerging evidence has indicated a role for neuron-astrocyte interactions in seizure activity. Previous studies have found increased astrocyte Ca2+ signals in mouse models for MTLE, but it has been difficult to disentangle how these drive or mitigate seizure activity in chronic epilepsy. We used an AAV8-GFAP-hM3Dq-mCherry vector to manipulate reactive astrocytes in the chronic phase of the mouse intrahippocampal

Cholinergic transmission is fundamental in memory mechanisms. Accordingly, the early degeneration of cholinergic fibers characterizing Alzheimer’s disease (AD) contributes to cognitive impairment, and mice lacking functional α7 nicotinic acetylcholine receptors (A7KO) develop an age-dependent AD-like phenotype, featuring increased levels of β-amyloid and phospho-tau, hippocampal plasticity deficits, neuronal loss and astrogliosis. Astrocytes, recognized partners of neurons in brain function, are characterized by a signaling system based on variations in intracellular Ca2+ concentration. Experi