Topic: arachidonic acid

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

Traumatic brain injury (TBI) can cause life-changing neurological deficits. There are currently no neuroprotective treatments in TBI. The high content of oxidation-sensitive polyunsaturated fatty acids (PUFAs) in the brain generates an environment vulnerable to TBI-related oxidative damage. We hypothesised that partial replacement of tissue PUFAs with deuterium - enriched PUFAs (D-PUFAs), could act as a brake against oxidation and improve outcome.A moderately severe TBI was induced using a controlled cortical impact (CCI) in adult male and female CD1 mice. Animals received a control or a D-PUF

Alcohol raises concerns due to the episodic and intense alcohol intake observed in adolescents. Recent studies reveal a correlation between escalated EtOH intake and neuroinflammation, emphasizing the endocannabinoid (eCB) system´s engagement. Our previous data in mice revealed that intermittent EtOH-exposure during adolescence leads to elevated levels of the ω-6 arachidonic acid (AA) in adulthood. AA is intricately linked to the neuroinflammatory response as a precursor of proinflammatory prostaglandins, and its brain levels are intertwined with balance between the synthesis and hydrolysis of

Prostaglandins play a key role in modulating the inflammatory response in the central nervous system. They are synthesized from arachidonic acid via the enzyme cyclooxygenases (COX). The Cox-1 isoform is highly enriched in microglia. In response to infection or tissue damage, microglia become reactive which is associated with phagocytosis and pro-inflammatory function. Concurrently, selective Cox-1 inhibition has been shown to ameliorate pathological effects in several neurodegenerative diseases. So far, it is not known which impact Cox-1 expression has on the regulation of microglia activity.