Docosahexaenoic acid signaling modulates cell survival in experimental ischemic stroke penumbra and initiates long-term repair in young and aged rats.

Background: Docosahexaenoic acid, a major omega-3 essential fatty acid family member, improves behavioral deficit and reduces infarct volume and edema after experimental focal cerebral ischemia. We hypothesize that DHA elicits neuroprotection by inducing AKT/p70S6K phosphorylation, which in turn leads to cell survival and protects against ischemic stroke in young and aged rats.

Methods And Results: Rats underwent 2 h of middle cerebral artery occlusion (MCAo).

Novel aspirin-triggered neuroprotectin D1 attenuates cerebral ischemic injury after experimental stroke.

Acute ischemic stroke triggers complex neurovascular, neuroinflammatory and synaptic alterations. Aspirin and docosahexaenoic acid (DHA), an omega-3 essential fatty acid family member, have beneficial effects on cerebrovascular diseases. DHA is the precursor of neuroprotectin D1 (NPD1), which downregulates apoptosis and, in turn, promotes cell survival.

Superior Neuroprotective Efficacy of LAU-0901, a Novel Platelet-Activating Factor Antagonist, in Experimental Stroke.

Platelet-activating factor (PAF) accumulates during cerebral ischemia, and inhibition of this process plays a critical role in neuronal survival. Recently, we demonstrated that LAU-0901, a novel PAF receptor antagonist, is neuroprotective in experimental stroke. We used magnetic resonance imaging in conjunction with behavior and immunohistopathology to expand our understanding of this novel therapeutic approach.

Behavioral sensitization and cross-sensitization between methylphenidate amphetamine, and 3,4-methylenedioxymethamphetamine (MDMA) in female SD rats.

The psychostimulants amphetamine and methylphenidate (MPD/Ritalin) are the drugs most often used to treat attention deficit hyperactivity disorder (ADHD). In addition, students of all ages take these drugs to improve academic performance but also abuse them for pleasurable enhancement. In addition, other psychostimulants such as 3,4-methylenedioxymethamphetamine (MDMA/ecstasy) are used/abused for similar objectives.

Docosahexaenoic Acid therapy of experimental ischemic stroke.

We examined the neuroprotective efficacy of docosahexaenoic acid (DHA), an omega-3 essential fatty acid family member, in acute ischemic stroke; studied the therapeutic window; and investigated whether DHA administration after an ischemic stroke is able to salvage the penumbra. In each series described below, SD rats underwent 2 h of middle cerebral artery occlusion (MCAo). In series 1, DHA or saline was administered i.

MDMA (ecstasy) modulates locomotor and prefrontal cortex sensory evoked activity.

Ingestion of 3, 4-methylenedioxymethamphetamine (MDMA) leads to heightened response to sensory stimulation; thus, MDMA is referred to as "ecstasy" because it produces pleasurable enhancement of such sensation. There have been no electrophysiological studies that report the consequences of MDMA on sensory input. The present study was initiated to study the effects of acute and chronic MDMA on locomotor activity and sensory evoked field potential from freely behaving rats previously implanted with permanent electrodes in the prefrontal cortex (PFC).

Robust docosahexaenoic acid-mediated neuroprotection in a rat model of transient, focal cerebral ischemia.

Background And Purpose: Docosahexaenoic acid (DHA; 22:6n-3), an omega-3 essential fatty acid family member, is the precursor of neuroprotectin D1, which downregulates apoptosis and, in turn, promotes cell survival. This study was conducted to assess whether DHA would show neuroprotective efficacy when systemically administered in different doses after middle cerebral artery occlusion (MCAo) in rats.

Methods: Sprague-Dawley rats were anesthetized with isoflurane and subjected to 2 hour of MCAo.

LAU-0901, a novel platelet-activating factor receptor antagonist, confers enduring neuroprotection in experimental focal cerebral ischemia in the rat.

LAU-0901, a novel platelet-activating factor (PAF) receptor antagonist, is highly neuroprotective in a rodent model of cerebral ischemia. This study was conducted to establish whether the neuroprotection induced by LAU-0901 persists with chronic survival. Male Sprague-Dawley rats were anesthetized with isoflurane and subjected to 2 h of temporary middle cerebral artery occlusion (MCAo) induced by means of a poly-L-lisine-coated intraluminal nylon suture.

LAU-0901, a novel platelet-activating factor antagonist, is highly neuroprotective in cerebral ischemia.

Platelet-activating factor (PAF) is a bioactive phospholipid that accumulates during ischemia-reperfusion and is involved in the activation of platelets, neutrophils, and pro-inflammatory signaling. PAF has been suggested to enhance brain ischemia-reperfusion damage. LAU-0901, a novel PAF receptor antagonist, was examined in models of focal cerebral ischemia in rats and mice.