Lipopolysaccharide-induced changes in monoamines in specific areas of the brain: blockade by interleukin-1 receptor antagonist1Preliminary results were presented at the Experimental Biology meeting, Atlanta, GA, USA, 1995.1

MohanKumar, Sheba M.J.; MohanKumar, P.S.; Quadri, S. K.

doi:10.1016/s0006-8993(99)01206-8

Cited by 48 publications

(35 citation statements)

References 33 publications

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Section: Discussionmentioning

confidence: 97%

“…Furthermore intraperitoneal injection of LPS in rats was shown to increase the concentrations of norepinephrine, dopamine, serotonin and their metabolites in the hypothalamic paraventricular nucleus measured by HPLC 5 h after the treatment (16). These changes were completely canceled by a concomitant treatment with an interleukin-1 receptor antagonist (16). More interestingly, intraperitoneal administration of LPS in freely moving rats increased extracellular concentrations of serotonin, noradrenaline, and their metabolites in the dorsal hippocampus as revealed by the in vivo microdialysis analysis (17).…”

Section: Discussionmentioning

confidence: 98%

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Deterioration of Spatial Learning Performances in Lipopolysaccharide-Treated Mice

Arai

Matsuki

Ikegaya

et al. 2001

Japanese Journal of Pharmacology

124

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ABSTRACT-It is well demonstrated that acute or chronic stress leads to reduction of learning ability. Lipopolysaccharide (LPS), a component of the outer membrane of gram-negative bacteria, induces profound physiological and behavioral changes, including fever, decrease in food motivation, and decrease in social behavior. These changes might be interpreted as an acute stress reaction to the LPS. In the present study, therefore, we investigated the effects of LPS (400 -800 mg/ kg, i.p.) on spatial learning performances using C57BL / 6J male mice. In the Morris water-maze task, spatial learning performances were examined in six trials of training for two consecutive days. LPS-treated mice took a longer time to reach the hidden platform than control mice (F(1,60) = 4.80801, P<0.05 at 600 mg / kg). In addition, injection of LPS decreased the percent of correct choices in the Y-maze test (P<0.05 at 800 m g/kg). LPS, however, did not alter the body weight, grip tone, motor activity or swimming speed. Taken together, these results indicate that LPS treatment specifically impaired spatial learning performances.

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Section: Discussionmentioning

confidence: 97%

Section: Discussionmentioning

confidence: 98%

Deterioration of Spatial Learning Performances in Lipopolysaccharide-Treated Mice

Arai

Matsuki

Ikegaya

et al. 2001

Japanese Journal of Pharmacology

124

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“…leptin release (16). Furthermore, it was shown that LPS increased catecholamine levels in the CNS (9,11) and in the periphery (10) and also activated the hypothalamic-pituitaryadrenal axis (5,6). Therefore, we considered the present paradigm as a suitable model to assess the neural control of leptin.…”

Section: Discussionmentioning

confidence: 99%

“…LPS also alters the release of other pituitary hormones in rats, increasing prolactin release and decreasing growth hormone, thyroidstimulating hormone, and luteinizing hormone release (5). There are a variety of other changes in the CNS caused by LPS as well, many of which probably are mediated by LPS-induced cytokine release, such as alterations of central and peripheral catecholamine levels (9,10) and alteration of neurotransmitter release in different areas of the brain (11). These result in induction of fever, loss of appetite, libido, and somnolence, and many metabolic changes.…”

mentioning

confidence: 99%

Lipopolysaccharide-induced leptin release is neurally controlled

Mastronardi

Srivastava

et al. 2001

Proc. Natl. Acad. Sci. U.S.A.

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Our hypothesis is that leptin release is controlled neurohormonally. Conscious, male rats bearing indwelling, external, jugular catheters were injected with the test drug or 0.9% NaCl (saline), and blood samples were drawn thereafter to measure plasma leptin. Anesthesia decreased plasma leptin concentrations within 10 min to a minimum at 120 min, followed by a rebound at 360 min. Administration (i.v.) of lipopolysaccharide (LPS) increased plasma leptin to almost twice baseline by 120 min, and it remained on a plateau for 360 min, accompanied by increased adipocyte leptin mRNA. Anesthesia largely blunted the LPS-induced leptin release at 120 min. Isoproterenol (␤-adrenergic agonist) failed to alter plasma leptin but reduced LPS-induced leptin release significantly. Propranolol (␤-receptor antagonist) produced a significant increase in plasma leptin but had no effect on the response to LPS. Phentolamine (␣-adrenergic receptor blocker) not only increased plasma leptin (P < 0.001), but also augmented the LPS-induced increase (P < 0.001). ␣-Bromoergocryptine (dopaminergic-2 receptor agonist) decreased plasma leptin (P < 0.01) and blunted the LPSinduced rise in plasma leptin release (P < 0.001). We conclude that leptin is at least in part controlled neurally because anesthesia decreased plasma leptin and blocked its response to LPS. The findings that phentolamine and propranolol increased plasma leptin concentrations suggest that leptin release is inhibited by the sympathetic nervous system mediated principally by ␣-adrenergic receptors because phentolamine, but not propranolol, augmented the response to LPS. Because ␣-bromoergocryptine decreased basal and LPS-induced leptin release, dopaminergic neurons may inhibit basal and LPS-induced leptin release by suppression of release of prolactin from the adenohypophysis.T he close interrelationships among the immune, endocrine, and nervous systems allow the organism to respond as a whole to different types of stress and changes in the environment. Rather than acting independently, these systems are closely interrelated through their messenger molecules: cytokines, hormones, neurotransmitters, neuropeptides, and nitric oxide. Thus, a complex network allows the organism to respond to noxious stimuli and changes in the environment to preserve homeostasis (1).In inflammatory stress induced by peripheral or central administration of lipopolysaccharide (LPS) in rodents, there are a number of changes in the immune system such as: stimulation of release of acute phase proteins, induction of nitric oxide synthase activity and synthesis, and increased release of cytokines (2-7). Proinflammatory cytokines, such as tumor necrosis factor ␣ and IL-1, released from immune cells reach the central nervous system (CNS) and increase release of corticotrophin-releasing hormone that activates the pituitary-adrenal axis (8). LPS also alters the release of other pituitary hormones in rats, increasing prolactin release and decreasing growth hormone, thyroidstimulating hormone, and luteinizing hor...

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“…However, other reports showed that antagonists of IL-1 or its receptors prevented neurochemical or HPA responses to LPS [8][9][10].…”

Section: Introductionmentioning

confidence: 93%

Lipopolysaccharide- and Tumor Necrosis Factor-α-Induced Changes in Prolactin Secretion and Dopaminergic Activity in the Hypothalamic-Pituitary Axis

Laurentiis

Pisera

Caruso

et al. 2002

Neuroimmunomodulation

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Bacterial lipopolysaccharide (LPS) affects pituitary hormone secretion, including prolactin release, by inducing synthesis and release of cytokines such as tumor necrosis factor-α (TNF-α). Since prolactin is mainly under tonic inhibitory control of dopamine, we investigated the effect of LPS and TNF-α on the hypothalamic-pituitary dopaminergic system. LPS (100–250 µg/rat, i.p.) decreased serum prolactin levels after 1 or 3 h. Sulpiride, a dopaminergic antagonist, increased serum prolactin and blocked the inhibitory effect of LPS. LPS increased hypothalamic dopamine and DOPAC concentrations and the DOPAC/dopamine ratio both in mediobasal hypothalamus and the posterior pituitary. LPS also enhanced dopamine and DOPAC concentration in the anterior pituitary. LPS elevated plasma levels of epinephrine, norepinephrine and dopamine but it did not modify the concentration of epinephrine or norepinephrine in the tissues studied. The administration of TNF-α (i.c.v., 1 h, 100 ng/rat) decreased serum prolactin but did not affect plasma catecholamine levels. TNF-α did not modify the DOPAC/dopamine ratio in hypothalamus or posterior pituitary but increased dopamine and DOPAC concentrations in the anterior pituitary. Incubations of hypothalamic explants showed that TNF-α did not modify in vitro basal dopamine release and reduced K⁺-evoked dopamine release. On the contrary, incubations of posterior pituitaries showed that TNF-α significantly increased basal and K⁺-evoked dopamine release. These results indicate that LPS and TNF-α increase dopamine turnover in the hypothalamic-pituitary axis. This increase in dopaminergic activity could mediate the inhibitory effect of LPS and TNF-α on prolactin release. Furthermore, the increase in dopaminergic activity elicited by LPS could be mediated by an increase in hypothalamic TNF-α during endotoxemia.

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Lipopolysaccharide-induced changes in monoamines in specific areas of the brain: blockade by interleukin-1 receptor antagonist1Preliminary results were presented at the Experimental Biology meeting, Atlanta, GA, USA, 1995.1

Cited by 48 publications

References 33 publications

Deterioration of Spatial Learning Performances in Lipopolysaccharide-Treated Mice

Deterioration of Spatial Learning Performances in Lipopolysaccharide-Treated Mice

Lipopolysaccharide-induced leptin release is neurally controlled

Lipopolysaccharide- and Tumor Necrosis Factor-α-Induced Changes in Prolactin Secretion and Dopaminergic Activity in the Hypothalamic-Pituitary Axis

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