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Lenart, N.

Publications and source records attributed to Lenart, N..

4 recordsLinked to original sources

Characterization of AZ12464237 as a high affinity, non-nucleotide antagonist radioligand for the P2Y12 receptor

The purinergic receptor P2Y12 (P2Y12R) is a well-recognized target for anti-thrombotic agents. This receptor is also expressed in microglia, where it plays a key role in neuroinflammation and microglia activation. To investigate P2Y12R-mediated actions in the central nervous system (CNS), the development of novel brain-penetrant ligands is essential, along with further in vitro studies. A radiolabeled, easily accessible tool compound would significantly advance such drug discovery efforts. Herein, we describe the 3H-labeling of a non-nucleotide P2Y12R antagonist AZ12464237, and its in vitro binding properties to the receptor in membrane preparations form transfected cells, as well as on mouse brain tissues. The radioligand shows high affinity toward both the human and rat P2Y12R in transfected cells, with Kd values of 3.12 {+/-} 0.70 nM (human) and 16.6 {+/-} 3.4 nM (rat), as determined by saturation binding studies. The binding kinetics of [3H]AZ12464237 are rapid with a short target residence time ([~]1 min). We further confirmed the selectivity of the radioligand by performing competitive displacement studies, in which reported P2Y12R ligands and other P2Y receptors ligands were tested for binding against [3H]AZ12464237. Additionally, the radioligand proved useful for in vitro autoradiography studies on mouse brain tissues, although a small amount of off-target binding was observed in P2Y12R knock-out mice. This could be traced to glycogen synthase kinase 3 . Considering the growing interest in P2Y12R as a biomarker for microglia activation, [3H]AZ12464237 represents a promising tool for in vitro studies, including screening assays aimed at identifying novel P2Y12R ligands for CNS applications.

pharmacology and toxicology↗

Microglia control cerebral blood flow and neurovascular coupling via P2Y12R-mediated actions

Microglia, the main immunocompetent cells of the brain regulate neuronal function in health and disease, but their contribution to cerebral blood flow (CBF) remained elusive. Here we identify microglia as important modulators of CBF both under physiological conditions and during hypoperfusion. We show that microglia establish direct purinergic contacts with cells in the neurovascular unit that shape cerebral perfusion in both mice and humans. Surprisingly, the absence of microglia or blockade of microglial P2Y12 receptor (P2Y12R) substantially impairs neurovascular coupling in the barrel cortex after whisker stimulation. We also reveal that hypercapnia, which is associated with acidification, induces microglial adenosine production, while depletion of microglia reduces brain pH and impairs hypercapnia-induced vasodilation. Furthermore, the absence or dysfunction of microglia markedly impairs adaptation to hypoperfusion via P2Y12R after transient unilateral common carotid artery occlusion, which is also influenced by CX3CR1-mediated actions. Thus, our data reveal a previously unrecognized role for microglia in CBF regulation with broad implications for common neurological diseases.

neuroscience↗

Microglial NKCC1 shapes microglial phenotype, cerebral inflammatory responses and brain injury

The NKCC1 ion transporter contributes to the pathophysiology of common neurological disorders, but its function in microglia, the main inflammatory cells of the brain, has remained unclear to date. Therefore, we generated a novel transgenic mouse line in which microglial NKCC1 was deleted. We show that microglial NKCC1 shapes both baseline and reactive microglia morphology, process recruitment to the site of injury, and adaptation to osmotic stress in a cell-autonomous manner via regulating membrane potential and chloride fluxes. In addition, microglial NKCC1 deficiency results in increased expression of the D subunit of volume regulated anion channel (VRAC), NLRP3 inflammasome priming and production of interleukin-1{beta} (IL-1{beta}), rendering microglia prone to exaggerated inflammatory responses. In line with this, central (intracortical) administration of the NKCC1 blocker, bumetanide, potentiated intracortical lipopolysaccharide (LPS)-induced cytokine levels, whereas systemic bumetanide application decreased inflammation in the brain. Microglial NKCC1 KO animals exposed to experimental stroke showed significantly increased brain injury, inflammation, cerebral edema and worse neurological outcome. Thus, NKCC1 emerges as an important player in controlling microglial ion homeostasis and inflammatory responses through which microglia modulate brain injury. The contribution of microglia to central NKCC1 actions is likely to be relevant for common neurological disorders.

neuroscience↗

Microglia monitor and protect neuronal function via specialized somatic purinergic junctions

Microglia are the main immune cells in the brain with emerging roles in brain homeostasis and neurological diseases, while mechanisms underlying microglia-neuron communication remain elusive. Here, we identify a novel site of interaction between neuronal cell bodies and microglial processes in mouse and human brain. Somatic microglia-neuron junctions possess specialized nanoarchitecture optimized for purinergic signaling. Activity of neuronal mitochondria is linked with microglial junction formation, which is rapidly induced in response to neuronal activation and blocked by inhibition of P2Y12-receptors (P2Y12R). Brain injury-induced changes at somatic junctions trigger P2Y12R-dependent microglial neuroprotection, regulating neuronal calcium load and functional connectivity. Collectively, our results suggest that microglial processes at these junctions are in ideal position to monitor and protect neuronal functions in both the healthy and injured brain.\n\nOne-sentence summaryNeuronal cell bodies possess specialized, pre-formed sites, through which microglia monitor their status and exert neuroprotection.

neuroscience↗