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Peripheral Injection (peripheral + injection)

Distribution by Scientific Domains

Medical Sciences	60%

Selected Abstracts

Alpha-melanocyte-stimulating hormone attenuates behavioral effects of corticotropin-releasing factor in isolated guinea pig pups

DEVELOPMENTAL PSYCHOBIOLOGY, Issue 5 2009
Patricia A. Schiml-Webb
Abstract During a 3-hr period of social isolation in a novel environment, guinea pig pups exhibit an initial active phase of behavioral responsiveness, characterized primarily by vocalizing, which is then followed by a stage of passive responsiveness in which pups display a distinctive crouch, eye-closing, and extensive piloerection. Prior treatment of pups with alpha-melanocyte-stimulating hormone (,-MSH) reduces each of the passive behaviors. The onset of passive responding during separation can be accelerated with peripheral injection of corticotropin-releasing factor (CRF). To examine whether CRF produces its effects through a mechanism similar to that of prolonged separation, we examined the effect of administering ,-MSH to pups injected with CRF. As expected, CRF markedly enhanced passive responding during a 60-min period of separation. ,-MSH delivered by either intracerebroventricular infusion or intraperitoneal injection significantly reduced each of the passive behavioral responses without significantly affecting active behavior. These findings, together with previous results indicating that it is the anti-inflammatory property of ,-MSH that is responsible for its behavioral effects during prolonged separation, suggest that peripheral CRF speeds the induction of passive responding through a mechanism involving enhanced proinflammatory activity. © 2009 Wiley Periodicals, Inc. Dev Psychobiol 51: 399,407, 2009. [source]

Empirical tests of the functional significance of amygdala-based modulation of hippocampal representations: evidence for multiple memory consolidation pathways

EUROPEAN JOURNAL OF NEUROSCIENCE, Issue 5 2007
Robert J. McDonald
Abstract This series of experiments evaluated the effects of amygdala damage on the acquisition and long-term retention of variants of the water task, and tested the hypothesis that the amygdala is an essential neural system for consolidation of hippocampal memories. In Experiment 1, rats with large, neurotoxic lesions of the amygdala (AMYG) showed normal acquisition on the standard spatial version of the water task, as well as normal retention and decay rate profiles on the 24-h and 30-day retention probes. In Experiment 2, AMYG rats showed normal one-trial place learning abilities and could retain this one-trial information over a 24 h delay. Experiment 3 showed that the amygdala lesions used in this study were functionally significant because AMYG rats, from Experiment 2, showed impairments in a discriminative fear conditioning to context paradigm. Experiment 4 was a critical test of the idea that the amygdala is a decisive locus for consolidation of hippocampal memories. AMYG rats were trained to sub-asymptotic levels of performance on the standard version of the water task. Following each training session, the subjects were given a post-training peripheral injection of d -amphetamine. A probe test revealed that normal subjects and AMYG rats showed similar post-training memory improvement effects. Taken together, the results show that hippocampal memory consolidation processes do not require amygdala modulation. Arguments for an alternative view are presented suggesting that there are multiple memory consolidation pathways, one of which may depend on amygdala neural circuitry. [source]

The Anti-Inflammatory Effect of Bee Venom Stimulation in a Mouse Air Pouch Model Is Mediated by Adrenal Medullary Activity

JOURNAL OF NEUROENDOCRINOLOGY, Issue 1 2003
Y.-B. Kwon
Abstract Cutaneous electrical or chemical stimulation can produce an anti-inflammatory effect, which is dependent on adrenal medullary-sympathetic activation. We have previously shown that peripheral injection of bee venom (BV) also produces a significant anti-inflammatory effect that is neurally mediated. In the present study, we examined whether this anti-inflammatory effect is also dependent on the adrenal gland using the mouse inflammatory air pouch model. Subcutaneous (s.c.) BV injection produced a marked suppression of leucocyte migration and tumour necrosis factor (TNF)- , concentration induced by zymosan injection into the air pouch. The role of the adrenal gland in this suppression was evaluated in adrenalectomized mice. Adrenalectomy significantly reversed the suppression of leucocyte migration and TNF- , elevation caused by BV. Serum concentrations of corticosteroid were increased in mice with zymosan-induced air-pouch inflammation and this increase was reduced by BV administration, suggesting that adrenal corticosteroid release is not involved in mediating the anti-inflammatory effects of BV. To test this hypothesis, the corticosteroid receptor antagonist (RU486) was administered and found not to affect the BV-induced inhibition of leucocyte migration. By contrast, pretreatment with the , -adrenergic antagonist propranolol reversed the BV-induced inhibitory effect on leucocyte migration. These results suggest that the anti-inflammatory effect of s.c. BV administration is mediated in part by the release of catecholamines from the adrenal medulla. [source]

Augurin stimulates the hypothalamo-pituitary-adrenal axis via the release of corticotrophin-releasing factor in rats

BRITISH JOURNAL OF PHARMACOLOGY, Issue 8 2010
JA Tadross
Background and purpose:, The functional characterization of secreted peptides can provide the basis for the development of novel therapeutic agents. Augurin is a recently identified secreted peptide of unknown function expressed in multiple endocrine tissues, and in regions of the brain including the hypothalamus. We therefore investigated the effect of hypothalamic injection of augurin on the hypothalamo-pituitary-adrenal (HPA) axis in male Wistar rats. Experimental approach:, Augurin was given as a single injection into the third cerebral ventricle (i.c.v.) or into the paraventricular nucleus (iPVN) of the hypothalamus. Circulating hormone levels were then measured by radioimmunoassay. The effect of augurin on the release of hypothalamic neuropeptides was investigated ex vivo using hypothalamic explants. The acute effects of iPVN augurin on behaviour were also assessed. Key results:, i.c.v. injection of augurin significantly increased plasma ACTH and corticosterone, compared with vehicle-injected controls, but had no effect on other hypothalamo-pituitary axes hormones. Microinjection of lower doses of augurin into the PVN caused a similar increase in plasma ACTH and corticosterone, without significant alteration in behavioural patterns. Incubation of hypothalamic explants with increasing doses of augurin significantly elevated corticotrophin-releasing factor (CRF) and arginine vasopressin release. In vivo, peripheral injection of a CRF1/2 receptor antagonist prevented the rise in ACTH and corticosterone caused by i.c.v. augurin injection. Conclusions and implications:, These data suggest that augurin stimulates the release of ACTH via the release of hypothalamic CRF. Pharmacological manipulation of the augurin system may therefore be a novel target for regulation of the HPA axis. [source]

A comparative study on the acute and long-term effects of MDMA and 3,4-dihydroxymethamphetamine (HHMA) on brain monoamine levels after i.p. or striatal administration in mice

BRITISH JOURNAL OF PHARMACOLOGY, Issue 2 2005
Isabel Escobedo
1This study investigated whether the immediate and long-term effects of 3,4-methylenedioxymethamphetamine (MDMA) on monoamines in mouse brain are due to the parent compound and the possible contribution of a major reactive metabolite, 3,4-dihydroxymethamphetamine (HHMA), to these changes. The acute effect of each compound on rectal temperature was also determined. 2MDMA given i.p. (30 mg kg,1, three times at 3-h intervals), but not into the striatum (1, 10 and 100 ,g, three times at 3-h intervals), produced a reduction in striatal dopamine content and modest 5-HT reduction 1 h after the last dose. MDMA does not therefore appear to be responsible for the acute monoamine release that follows its peripheral injection. 3HHMA does not contribute to the acute MDMA-induced dopamine depletion as the acute central effects of MDMA and HHMA differed following i.p. injection. Both compounds induced hyperthermia, confirming that the acute dopamine depletion is not responsible for the temperature changes. 4Peripheral administration of MDMA produced dopamine depletion 7 days later. Intrastriatal MDMA administration only produced a long-term loss of dopamine at much higher concentrations than those reached after the i.p. dose and therefore bears little relevance to the neurotoxicity. This indicates that the long-term effect is not attributable to the parent compound. HHMA also appeared not to be responsible as i.p. administration failed to alter the striatal dopamine concentration 7 days later. 5HHMA was detected in plasma, but not in brain, following MDMA (i.p.), but it can cross the blood,brain barrier as it was detected in the brain following its peripheral injection. 6The fact that the acute changes induced by i.p. or intrastriatal HHMA administration differed indicates that HHMA is metabolised to other compounds which are responsible for changes observed after i.p. administration. British Journal of Pharmacology (2005) 144, 231,241. doi:10.1038/sj.bjp.0706071 [source]