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Biomedical subjects

D Bieger

Publications and source records attributed to D Bieger.

At least 73 records · Page 4Linked to original sources

Central serotonin receptor sensitivity in rats with experimental allergic encephalomyelitis.

Serotonin mediated bulbospinal motor activities were examined in rats with experimental allergic encephalomyelitis (EAE)-induced-paraplegia. Treatment with monoamine oxidase inhibitors and L-tryptophan failed to elicit the components of the serotonin syndrome which involved levels of the neuraxis manifesting flaccid paralysis. Straub tail, hindlimb abduction and hindlimb rigidity did not occur. The motor responses represented at spinal segments just above the level of paraplegia, lateral head weaving and forepaw treading, were present but altered in the diseased rats. No impairment was evident in the production of head tremor or hyper-reactivity to accoustic and tactile stimuli. Similarly, in urethane-anesthetized EAE rats, serotonergically-evoked automatic swallowing activity was unchanged as judged by the effects of serotonin receptor agonists, and a serotonin precursor, a reuptake blocker and an antagonist. Our data support the conclusion that EAE-induced impairment of serotonergic neurotransmission is correlated with motor deficits manfested during the acute paralytic stage of the disease.

5-Hydroxytryptophan↗

Basal forebrain facilitation of reflex swallowing in the cat.

In adult cats anaesthetized with urethane, electrical and chemical stimulation of the basal forebrain facilitated reflex swallowing elicited by electrical stimulation of the superior laryngeal nerve. A systematic stereotaxic mapping study using electrical stimulation revealed that the facilitatory sites were distributed along the course of the ansa peduncularis, specifically its rostral forebrain and hypothalamic components associated with the anterior amygdalar area, substantia innominata, lateral preoptic area, anterior hypothalamus and nucleus accumbens. By means of acute discrete radiofrequency lesions, the descending pathways mediating facilitatory influences from the nucleus accumbens and the amygdala to the brain stem were found to traverse the lateral hypothalamus. Ventral tegmental facilitatory sites in the midbrain are likely to be associated with these descending pathways; however, there is evidence for independent participation of this region of the brain in the control of swallowing. Chemical stimulation by means of microinjections of dopamine and apomorphine into the amygdala and nucleus accumbens also enhanced reflex swallowing. It is concluded that the results of this investigation implicate the basal forebrain as a site of integration of viscero-olfacto-gustatory information needed for the enactment of ingestive behaviour.

Animals↗

The emetic action of L-dopa and its effect on the swallowing reflex in the cat.

In adults cats anesthetized with urethane it was shown that facilitation of reflexly-induced swallowing by dopaminomimetics is caused by a central action independent of the emetic of such drugs. It is suggested that this modulatory influence is mediated by dopamine receptors associated with the amygdala and ventral basal striatum.

Animals↗

Pharmacological evidence for a selective antidopaminergic action of gamma-hydroxybutyric acid.

D-Amphetamine (Amph) and p-chloroamphetamine (PCA) induced dose-dependent increases in oropharyngeal myocloniform twitch activity (MTA) in rats anesthetized with urethane. In doses of 80-120 mg/kg, gamma-hydroxybutyric acid (GHB) blocked Amph-induced MTA. The blockade was readily surmountable. Pretreatment with reserpine markedly enhanced the myoclonigenic effect of Amph and rendered it insensitive blockade by GHB, 160 mg/kg. PCA and tryptamine also effectively stimulated MTA, but unlike Amph were antagonized by low doses of the serotonin (5-HT) antagonist methysergide. In doses which blocked Amph, GHB failed to antagonize the myoclonigenic effect of PCA. It is concluded that: (a) the actions of Amph and PCA on MTA is less sensitive to GHB blockade than DA-mediated MTA; and (c) the GHB-Amph antagonism may be of a functional nature, i.e. result from a depression of the firing activity of DA neurons produced by GHB. Since reserpinization abolished the GHB effect on Amph-induced MTA, the functional integrity of granular DA binding and releasing mechanisms appears to be a pre-requisite for the antagonism between GHB and Amph.

Animals↗