poa/fever

Lipopolysaccharide (LPS) administration induces hypothalamic nitric oxide (NO); NO is antipyretic in the preoptic area (POA), but its mechanism of action is uncertain. LPS also stimulates the release of preoptic norepinephrine (NE), which mediates fever onset. Because NE upregulates NO synthases and

Although studies have shown that chemokines are pyrogenic when injected into the brain, there are no data indicating which cell types and receptors in the CNS are employed by chemokines such as CCL3 (synonym: MIP-1α) to induce fever in rats. We aimed to study, whether CCL3 induces fever when

The preoptic area (POA) plays an important role in fever in mammals, but the role of this region in fever in ectothermic vertebrates has never been assessed. Toads, like all ectotherms, regulate their body temperature (T(b)) primarily by behavior and develop behavioral fever when injected with

The central mechanism of fever induction is triggered by an action of prostaglandin E(2) (PGE(2)) on neurons in the preoptic area (POA) through the EP3 subtype of prostaglandin E receptor. EP3 receptor (EP3R)-expressing POA neurons project directly to the dorsomedial hypothalamus (DMH) and to the

The effect of macrophage inflammatory protein-1 beta (MIP-1 beta) on body temperature, following its injection into the anterior hypothalamic pre-optic area (AH/POA), was examined by a radiotelemetry system in the freely moving rat. The purpose of this study was to examine the action of an inhibitor

Prostaglandin E2 (PGE2) is postulated to be a central mediator of fever. It is generally believed that it is produced in the preoptic area of the anterior hypothalamus (POA) because, among other evidence, its level increases both in the third ventricle and in the POA in response to pyrogens.

A role of central histamine in the preoptic area/anterior hypothalamus (POA/AH) for the regulation of hyperthermia-induced polypnea was examined in anesthetized, paralyzed, vagotomized and artificially ventilated rabbits. Phrenic nerve activities were recorded to monitor respiratory neuronal output.

Considerable evidence supports the role of prostaglandins in fever production, but the neuroanatomic sites of prostaglandin synthesis that produce fever remain unknown. With the use of a novel microinjection technique, we injected the cyclooxygenase inhibitor ketorolac into the preoptic area (POA)

Brain temperature of conscious freely moving rats was recorded during perfusion of the preoptic area (POA) with neuroactive compounds using the microdialysis technique. Unilateral perfusion of the POA with the sodium channel blocking agent, tetrodotoxin (1 microM), induced a pronounced hyperthermia.

Recently, we have reported that the heme oxygenase (HO)-carbon monoxide (CO) pathway plays an important role in the genesis of LPS fever, acting through a cGMP signaling pathway in the brain, but the site of action remains unclear. Thus, the present study was designed to test the hypothesis that the

To distinguish pattern differences in experimentally induced fevers, we investigated febrile responses induced by intravenous (IV), intracerebroventricular (ICV), and intra-preoptic/anterior hypothalamic (POA) administration of bacterial endotoxin (lipopolysaccharide, LPS), endogenous pyrogen (EP),

Experiments were carried out on male rabbits, anesthetized with urethane, bilaterally vagotomized, paralysed and artificially ventilated. The preoptic area (POA) was stimulated at three different levels of CO2: in hypo- normo- and hypercapnia under normothermia, moderate hyperthermia and

This investigation examined the extent to which the activity of a prostaglandin (PG) in the anterior hypothalamic, preoptic area (AH/POA) of the rat plays a role in the intense fever induced by macrophage inflammatory protein-1 (MIP-1) applied directly to this anatomical region. For the

CC Chemokine ligand 22 (Ccl22) is a selective, high affinity ligand at the CC chemokine receptor 4 (Ccr4). We have identified cDNAs encoding both ligand and receptor of the Ccl22-Ccr4 pair in cDNA libraries of the anterior hypothalamus/pre-optic area (AH/POA) by PCR. The AH/POA is the key brain

Recently, it was shown that cerebrospinal fluid (CSF) contaminated with the fungus Trichosporon beigelii produces an intense fever when the organism is microinjected directly into the thermosensitive region of the anterior hypothalamic preoptic area (AH/POA). The purpose of this study was to