Topic: Prostaglandin E2

A growing number of studies indicate the possible involvement of astrocytes in triggering or modulating neurovascular coupling (NVC), i.e. the local dilation of blood vessels in the brain in response to neuronal activity [1]. Their endfeet, surrounding arterioles and capillaries, are ideally positioned to deliver vasodilators to mural cells, either vascular smooth muscle cells or pericytes. Additionnaly, recent EM data suggest contact between endfeet and synapses [2], indicating direct interactions. At the interface between synapses and vessels, endfeet are perfect candidates to mediate NVC. R

Animal models of neurovascular uncoupling (NVU) would be important tools for developing drugs in neurodegenerative disorders. Pharmacologically induced NVU was established in mice [Tarantini et al., 2015] but only preliminary results are available in rats [Varga et al., 2022]. In the current study we attempted to evoke NVU in a translationally relevant rat population.We used 28-month-old male Long-Evans rats with learning history and stable performance in 5-choice serial reaction time task (5-CSRTT). Morris water-maze (MWM), pot jumping, and touchscreen pairwise discrimination. NVU was induced

Neurovascular coupling (NVC), the tight coupling between neural activity and cerebral blood flow (CBF), is essential for brain function and integrity. Decreased CBF and altered NVC are among the earliest biomarkers of Alzheimer’s disease (AD) and may exacerbate its progression. Among the various cellular players of NVC, cyclooxygenase-2 (COX2) pyramidal cells, play a key role via the release of prostaglandin E2 (PGE2), which can bidirectionally control the NVC. We investigated the role of pyramidal cells in neurovascular uncoupling of AD using cortical slices from triple transgenic mice expres