[Central effects of anisodamine, atropine, anisodine and scopolamine after intraventricular injection].
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Putrescine produced in anesthetized dogs significant cardiovascular changes at higher doses than other transmitters. The hypotensive response observed after intravenous injection is due to histamine release. Tachycardic effects seem to be due both to release of histamine and to a reflex stimulation of carotid-sinus baroreceptors. The hypotensive and bradycardic effects observed after microinjection of putrescine into the III cerebral ventricle or into the vertebral artery are due to an increase in parasympathetic output.
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The effects of the meningococcal lipopolysaccharide (LPS), given into the II cerebral ventricle of adult fowls, were studied on behaviour and body temperature. Immediately after the administration a marked and dose- dependent behavioural sedation or sleep lasting over 2 hours or more according to the dose was observed. The body temperature effects of LPS were biphasic, i.e. and immediate initial phase of hypothermia lasting about 100 min, followed by a longer-lasting fever response. A pretreatment with phentolamine, an antagonist at alpha-adrenoceptors prevented the hypothermic phase following the endotoxin administration. In conclusion, present experiments show that in comparison to 0-somatic antigen of Shigella dysenteriae, meningococcal endotoxin possesses more marked behavioural effects and a different profile in body temperature effects.
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The effects of cefazolin, given into the III cerebral ventricle at different doses were studied on GABA content, GAD and GABA-T in the brain-stem of young chickens (Gallus domesticus). A dose-dependent fall in GABA content was observed; GABA decrease was evident 15 min after the administration, reached its nadir at 60 min and disappeared at 120 minutes. Glutamate decarboxylase and GABA-transaminase activity were not significantly changed. Present experiments suggest the excitatory and convulsant effects of cefazolin in chicks are related to GABA depletion in the brain-stem.
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Actions of the central angiotensin system on brain cAMP concentrations were studied after intraventricular injection of renin. Biosynthesis of endogenous brain angiotensin II was stimulated by 0.1 U renin and the blood pressure was elevated 40 min after the application. Stimulation of the brain angiotensin system affected cAMP metabolism in several brain areas, mostly expressed as decreased cAMP levels. Significant decreases in cAMP concentrations were found in the cerebral cortex, hippocampus, basal ganglia, various hypothalamic nuclei, substantia nigra, central grey matter and in the locus coeruleus. The unchanged cAMP levels in the nucleus of the solitary tract might indicate that intraventricular injection of renin induced an acute blood pressure elevation which is not associated with changes in the cAMP system in the primary baroreceptor area.
Recent data have shown that 5 days after intraventricular injection of 6-hydroxydopamine (6-OHDA), the tyrosine hydroxylase activity (TH) was increased within the locus coeruleus (LC). We sought to determine if such an alteration occurs within the A1 and A2 noradrenergic (NA) and C1 and C2 adrenergic (A) neurons of the rat medulla oblongata. The TH activity within the cell bodies was significantly increased 2 days after 6-OHDA injection with a maximum at 5 days (LC, + 109%, P less than 0.001; A1-C1, + 40%, P less than 0.01; A2-C2; + 24%, P less than 0.01) while a significant decrease was present 21 days after 6-OHDA. Conversely, dopamine-beta-hydroxylase (DBH) activity exhibited a decrease which was maximal at 21 days (LC,-41%; A1-C1,-33%; A2-C2,-35%, P less than 0.001). Both the TH (-47% at 5 days) and the DBH (-82% at 12 days) activities were decreased within the terminals of the tractus intermediolateralis (TIML). The phenylethanolamine-N-methyltransferase (PNMT) activity was never altered in the cell bodies nor in the terminals analyzed. These data demonstrate that the NA neurons of the rat medulla oblongata and of the LC exhibit a similar pattern of response to the neurotoxin 6-OHDA. Conversely, the lack of change in the PNMT activity confirms the hypothesis of a resistance of the A neurons to 6-OHDA or questions the validity of the PNMT as an A marker.
Electron microscope evaluation of choroid plexus and ependyma following single cerebral intraventricular injections of Conray 60 and Pantopaque was carried out on 35 rats and 4 dogs. The animals were sacrificed at periods ranging from 1 hour to 4 months. Conray was not detected with the light or electron microscope; however, Pantopaque was presumptively localized as electron-dense masses associated with lipid-like bodies at the ventricular interface of both choroidal and ependymal epithelium. Conray 60 injections consistently induced convulsions in rats. Histological studies demonstrated moderate cellular damage and multilayered proliferation of ependymal epithelium. Morphological damage following Pantopaque was more severe and widespread in both choroid plexus and ependyma suggesting that, of the two agents, Conray may have the greater clinical potential provided that the associated convulsions are controlled by appropriate measures.
Intraventricular injection of beta-endorphin (3, 7, 10 and 30 nmol/kg) into the third ventricular of pentobarbital-anaesthetized male Sprague-Dawley rats resulted in a dose-dependent increase in mean arterial pressure (MAP) while injection of the same volume of 0.9% NaCl solution did not cause significant changes in MAP. Naloxone, which did not produce any significant change in MAP, antagonized the vasopressor effect of beta-endorphin, indicating that the response is mediated via the naloxone sensitive opiate receptors. Rats acclimated to cold (5 degrees) for 3 weeks showed a potentiated and prolonged increase in MAP following beta-endorphin injection, indicating an increased responsiveness to the peptide. This increased responsiveness in the cardiovascular system is probably of adaptive value in cold acclimation. Naloxone itself did not alter MAP either, but abolished the cardiovascular response to beta-endorphin completely in cold acclimated rats, indicating an increased effectiveness in its antagonistic effect following cold acclimation as well.
The purpose of these experiments was to elucidate further the possibility that intraventricular injections of bombesin (BBS) lower the set point around which an animal regulates its core body temperature. In an attempt to prevent a confounding of general activity and thermoregulatory behavior which occurred in earlier work, a horizontal temperature gradient was used. Intraventricular injections of bombesin resulted in the selection of temperatures that were approximately 9-13 degrees C colder than those selected by animals following control injections. Additionally, the increase in core body temperature observed following control injections was reversed by the highest dose of bombesin. No significant alterations in general locomotor activity were observed. These findings suggest that bombesin may act centrally to reduce the set point around which behavioral responses are regulated.