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Discusses supercontinuum (SC) generation extending to 300 nanometer in the ultraviolet from a pure-silica holey fiber. Broad spectrum obtained by launching ultra-short pulses from an amplified Ti:sapphire laser; Extension of holey-fiber-based SC generation into the ultraviolet; Visible SC from several subsidiary cores.

Intracerebroventricular (i.c.v.) administration of histamine (HA, 0.025-0.1 μM/rat) to arthritic rats induces a dose-related inhibition of the neuronal thalamic firing evoked by peripheral noxious stimuli. To characterize the type(s) of HA receptors involved in this depressing activity of the amine we used electrophysiological techniques to examine the effects of i.c.v. administration of H and H agonists and antagonists on the spontaneous and evoked nociceptive firing of the thalamic neurons in rats rendered arthritic by Freund's adjuvant. The H agonist 2-pyridylethylamine (0.4-1.0 μM/rat, i.c.v) displayed a dose-dependent antinociceptive effect very similar to that of HA, while the H agonist dimaprit (0.05-0.2 μM/rat, i.c.v.) did not modify thalamic firing. Neither mepyramine (H antagonist, 0.1 μM/rat, i.c.v.) nor zolantidine (H antagonist, 0.01 μM/rat, i.c.v.) modified the evoked firing of rat thalamic neurons. When administered before HA (0.1 μM/rat, i.c.v.) mepyramine but not zolantidine was able to inhibit the antinociceptive effect of HA. On the basis of the present electrophysiological results, we suggest that a specific interaction of histamine with H receptors may be important for its antinociceptive effect on afferent peripheral inputs to the thalamus. [ABSTRACT FROM AUTHOR]

The effects of intracarotid (i.a.) administration of the histamine (HA) H-receptor agonist (R)-α-methyl-histamine (αMeHA) and of the H-antagonist thioperamide, (THIO) on basal or morphine (M)-induced prolactin (PRL) and growth hormone (GH) secretion were studied in male rats. M was administered 3 h after the H-drugs. Neither THIO (2.5 mg/kg) nor αMeHA (10 mg/kg) changed basal PRL levels and only THIO enhanced the PRL-releasing effect of M (6 mg/kg). Basal GH secretion was not modified by THIO. αMeHA slightly increased GH secretion. THIO significantly decreased M-stimulated GH secretion (1 mg/kg, i.a.) and αMeHA slightly increased it. These results, in agreement with previous evidence obtained after central HA administration, indicate that endogenous brain HA facilitates PRL and inhibits GH secretion. [ABSTRACT FROM AUTHOR]

We studied the effects of histamine (HA) antagonists on the facilitatory action of morphine (M) and β-endorphin ( βE) on prolactin (PRL) release and the effect of α-fluoromethylhistidine (α-FMH, inhibitor of HA synthesis) on βE-induced PRL secretion. Male rats were injected intracerebroventricularly (i.c.v.) with mepyramine (MEP, H-antagonist, 0.8 μmol/rat) or ranitidine (RAN, H-antagonist, 0.4 μmol/rat) 10 min before M (6 mg/kg, intracarotid, i.a.) or βE (0.25 μg/rat, i.c.v.). α-FMH (200 μg/rat, i.c.v.) was administered 3 h before βE. Plasma PRL levels were measured at various times before and after drug treatment. RAN but not MEP significantly reduced PRL release induced by M whereas neither HA-antagonists nor α-FMH modified βE-induced PRL release. The results obtained show that brain HA contributes through activation of H-receptors to the PRL facilitatory action of M but not of βE. [ABSTRACT FROM AUTHOR]

We examined the effects of an irreversible inhibitor of brain histamine (HA) synthesis, α-fluoromethyl-histidine (α-FMH), on prolactin (PRL) release induced by an opiate agonist (morphine, M) or by a serotonergic agonist (MK212). α-FMH was administered intracerebroventricularly (i.c.v., 200 μg/rat) into freely moving rats with indwelling catheters in the carotid. M (6 mg/kg, intracarotid, i.a.) was administered simultaneously with or 3 h after α-FMH. MK212 (2.5 mg/kg, i.a.) was administered 3 h after α-FMH. Blood samples for assay for PRL were drawn at 0, 10, 20, 40 min after M or MK212 administration. α-FMH (3 h before) significantly reduced the PRL-releasing effect of M and MK212 but did not modify PRL release by M when administered simultaneously. The present results showing that the facilitatory actions of the opiate and serotonergic systems on PRL are impaired when brain HA synthesis is reduced, suggest that there is an HA-dependent step in opiate and serotonergic control of PRL. [ABSTRACT FROM AUTHOR]

The effects of intracerebroventricular injection of histamine H-receptor agonists (4-methylhistamine, 4-MeH; dimaprit, DIM), H-antagonists (cimetidine, CIM; ranitidine, RAN; famotidine, FAM) and of the DIM chemical analogue SK&F 91487 on hot-plate latency in rats were examined. Both DIM (0.4-0.8 μmol/rat) and 4-MeH (0.4-0.8 μmol/rat) significantly enhanced the pain threshold, whereas SF&F 91487 (0.8 μmol/rat) had no effect, indicating that DIM antinociception is specifically due to its activity on histamine (HA) receptors. The H-antagonists CIM (0.8 μmol/rat) and RAN (0.6 μmol/rat) also enhanced the pain threshold, while FAM (0.03 μmol/rat) did not modify pain latency. When injected before 4-MeH, FAM reduced the antinociceptive effect of 4-MeH. These findings suggest that the antinociceptive activity of CIM and RAN is not related to specific blockade of H-receptors and that the activation of HA-H-receptors is inhibitory to nociception. [ABSTRACT FROM AUTHOR]

We investigated whether inhibition of brain histamine (HA) synthesis by α-fluoromethylhistidine (α-FMH) can influence basal or stimulated prolactin (PRL) release in male rats. α-FMH was administered either into the carotid (i.a., 20 and 100 mg/kg) or intracerebroventriculary (i.c.v., 200 μg/rat) into freely moving rats with indwelling catheters. Plasma PRL levels were measured 90, 120, 180 min later. Both i.a. and i.c.v. administration of α-FMH significantly inhibited basal PRL secretion at 120 and 180 min. When PRL secretion was stimulated by exposing rats to restraint stress, α-FMH administered 3 h before the stress (20 and 100 mg/kg, i.a.; 200 μg/rat, i.c.v.) was able to prevent the PRL surges at 10 and 20 min after stress. These results suggest that endogenous brain HA has a facilitatory role in the control of PRL secretion in rats. [ABSTRACT FROM AUTHOR]

The effects of intracerebroventricular (icv) injection of histamine (HA, 0.4 μmol/rat) or of the inhibitor of HA synthesis α-fluoromethylhistidine (αFMH, 100 mg/kg, intracarotid (ia)) on growth hormone (GH) secretion induced by GH-releasing hormone (hGHRH, 2 μg/kg, ia) in freely moving rats were examined. HA significantly inhibited GH release induced by GHRH whereas pretreatment (3 h before) with αFMH enhanced the GH response to GHRH. The inhibitory effect of HA on GHRH-induced GH release is still evident in somatostatin-depleted rats with cysteamine (300 mg/kg, sc, 4 h before) but is completely overcome by the inhibitor of catecholamine synthesis (α-methyl-p-tyrosine, 200 mg/kg, ip, 2 h before) suggesting that HA influences GH secretion by modulation of catecholaminergic neurons. This suggestion is supported by the biochemical data showing an increase in noradrenaline and dopamine contents in the hypothalamus and striatum of rats pretreated with αFMH. [ABSTRACT FROM AUTHOR]

The effects of intracerebroventricular (i.c.v.) injection of histamine (HA), an H-agonist (2-pyridylethylamine, 2PEA) and an H-antagonist (pyrilamine, PYR) on hot-plate latency in rats were examined. HA (40 or 80 μg/rat) significantly enhanced the pain threshold whereas 2PEA (80 or 160 μg/rat) and PYR (20 μg/rat) had no effect. Moreover, PYR did not modify HA antinociception. These results indicate that HA-H receptors are not involved in the inhibition by HA of the hot-plate response. To characterize the neural pathways involved in the antinociceptive action of HA, the effect of HA (40 μg/rat, i.c.v.) on the firing of thalamic neurons in arthritic rats evoked by peripheral noxious stimuli was recorded by electrophysiological techniques. HA markedly depressed the neuronal firing evoked by ankle mobilization, suggesting that the thalamus is one important area involved in modulation of pain by HA. [ABSTRACT FROM AUTHOR]