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Results for “Stimulation, Chemical”

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At least 55 records · Page 3Linked to original sources
PubMed1976

Effects of chemical stimulation of the mesolimbic dopamine system upon locomotor activity.

The effects of local injections of drugs into terminal areas of the mesolimbic dopamine system were investigated. Bilateral administration of dopamine, but not of noradrenaline and serotonin, into the nucleus accumbens of non-pretreated rats resulted in stimulation of locomotor activity. No clear or only minor effects were seen after injections of the dopamine metabolites 3-methoxytyramine, DOPAC and HVA and after injections of media with different pH and osmolality. d-Amphetamine proved more effective than dopamine in producing locomotor stimulation, whereas both stimulant and depressant effects were observed following injection of apomorphine into the nucleus accumbens. ET 495 and the noradrenaline agonists clonidine, phenylephrine and isoprenaline did not enhance locomotor activity, but theophylline was effective. Pretreatment with haloperidol, but not with clozapine, significantly reduced the effects of dopamine and theophylline. Locomotor stimulation was also found following bilateral administration of dopamine, d-amphetamine and apomorphine into the tuberculum olfactorium, whereas noradrenaline, serotonin and ET 495 produced no, or rather depressant effects. These results provide further evidence for an important role of the mesolimbic dopamine system with respect to locomotor activity.

Animals↗
PubMed1990

Cardiovascular responses elicited by chemical stimulation of the rostral ventrolateral medulla in conscious, unrestrained rats.

The cardiovascular effects of microinjection of L-glutamic acid into the rostral ventrolateral medulla have been investigated in anaesthetized and in conscious, unrestrained rats. In conscious rats L-glutamic acid (0.36, 1.2 and 2.4 nmol) produced significant increases in blood pressure, generally accompanied by a bradycardia. A lower dose of L-glutamic acid (0.12 nmol) had no effect on blood pressure or heart rate. The cardiovascular responses elicited by L-glutamic acid (2.4 nmol) were completely abolished by intravenous infusion of the ganglion blocker, pentolinium. However, in urethane-anaesthetized rats, the pressor response (+27 +/- 2/+21 +/- 2 mmHg) to microinjection of L-glutamic acid (2.4 nmol) was markedly less than that seen in conscious rats (+64 +/- 6/+47 +/- 3 mmHg) and there was a tachycardia (+21 +/- 2 beats/min) rather than a bradycardia. These results corroborate previous studies, carried out in anaesthetized animals, indicating that stimulation of the rostral ventrolateral medulla provides direct and/or indirect excitatory drive to the preganglionic sympathetic neurons of the spinal cord to increase blood pressure, but demonstrate a marked difference in sensitivity in conscious vs urethane-anaesthetized animals.

Animals↗
PubMedDate not supplied

Cerebral chemosensory evoked potentials elicited by chemical stimulation of the human olfactory and respiratory nasal mucosa.

A stimulation method was employed by which chemosensory evoked potentials were recorded without tactile somatosensory contamination. The purpose of the study was to determine whether potential components evoked by stimulation of the chemoreceptors of the trigeminal nerve can be distinguished from those of the olfactory nerve. The stimulants (vanillin, phenylethyl alcohol, limonene, menthol, anethol, benzaldehyde, carbon dioxide and a mixture of vanillin and carbon dioxide) were presented in a randomized order to 13 volunteers. Chemosensory evoked potentials to substances which anosmics are unable to perceive (vanillin, phenylethyl alcohol) were termed olfactory evoked potentials; potentials to CO2, which effected no olfactory sensations were termed chemo-somatosensory potentials. Analysis of variance revealed that the different substances resulted in statistically significant changes in the amplitudes and latencies of the evoked potentials, and also in the subjective estimates of intensity. An increased excitation of the somatosensory system resulted in reduced latencies and enhanced amplitudes of the evoked potentials. Responses to the mixture of carbon dioxide and vanillin appeared significantly earlier (50-150 msec) than responses to either substance alone.

Adult↗
PubMed1991

Effects of chemical stimulation of the subfornical organ on metabolic activity of the hypothalamo-neurohypophysial system in rats.

Topical stimulation of the subfornical organ (SFO) with angiotensin II (ANG II) or acetylcholine (ACh) increased blood pressure, water intake, and the activity of the hypothalamo-neurohypophysial system (HNS). The pressor and drinking responses were higher and the metabolic activity of the HNS, measured with the [14C]deoxyglucose (DG) method, was lower with ANG-II than with ACh. Glucose utilization in the neural lobe increased by 165% with ACh as opposed to 65% with ANG II. These results demonstrate the ANG II and ACh mobilize differentially the mechanisms increasing blood pressure, drinking responses, and the activity of the HNS.

Acetylcholine↗
PubMed1993

Chemical stimulation of the nucleus locus coeruleus: cardiovascular responses and baroreflex modification.

Microinjection of glutamate (Glu, 2.5 nmol) or homocysteic acid (HA, 0.1-0.5 nmol) into the nucleus locus coeruleus (LC) decreased both blood pressure and heart rate. These microinjections also produced a facilitatory or occlusive effect on depressor and bradycardiac responses evoked by electrical stimulation of the aortic depressor nerve (ADN). Destruction of the nucleus tractus solitarius (NTS), which totally eliminated ADN-evoked responses, had no effect on the cardiovascular responses evoked by LC stimulation. These results suggest that the neuronal populations that contribute to the LC-induced cardiovascular responses overlap at least partly with the baroreflex substrate other than the NTS.

Animals↗
PubMed1995

Map of spinal neurons activated by chemical stimulation in the nucleus raphe magnus of the unanesthetized rat.

The expression of the proto-oncogene c-fos was used as a cellular marker of spinal cord neurons activated by microinjection of kainic acid into the medullary nucleus raphe magnus of awake and drug-free Sprague-Dawley rats. The c-FOS protein was detected by immunocytochemistry. We found increased immunoreactivity bilaterally in laminae I-VI of the dorsal horn. The strongest c-FOS expression was observed within the inner layer of lamina II near its border with lamina III. In the ventral horn no c-FOS immunoreactivity was observed. Thus, the present results provide evidence for a descending excitation of neurons predominantly in inner lamina II, possibly mediating nucleus raphe magnus-induced inhibition of neurons in other laminae.

Animals↗
PubMed1996

Differential distribution of Fos-like immunoreactivity in the spinal trigeminal nucleus after noxious and innocuous thermal and chemical stimulation of rat cornea.

Corneal afferent nerves project to two spatially distinct sites within the spinal trigeminal nucleus: the subnucleus interpolaris/caudalis transition and the subnucleus caudalis/upper cervical spinal cord transition. The role of these two regions in processing corneal input is uncertain. To determine if neurons in these regions encode different features of an applied corneal stimulus, immunoreactivity for the immediate early gene protein product, Fos, was quantified in barbiturate-anesthetized rats. Intensity was varied across thermal (thermal probe 5, 35, 42, 52 degrees C; radiant heat of approximately 45 degrees C) stimuli and compared with that seen after mustard oil (5 microliters, 20%) or mineral oil application. All stimuli increased the number of Fos-positive neurons located at the ventrolateral pole of the subnucleus interpolaris/caudalis transition compared with unstimulated controls. By contrast, only 52 degrees C thermal probe and mustard oil produced an additional peak of Fos-positive neurons within the superficial laminae at the subnucleus caudalis/cervical cord transition. Further, the magnitudes of the bimodal peaks of Fos produced by 52 degrees C thermal probe and mustard oil stimuli were different quantitatively. Mustard oil caused a greater Fos response at the subnucleus interpolaris/caudalis transition than 52 degrees C thermal probe stimulation, whereas the opposite was true at the subnucleus caudalis/cervical cord transition. Double-labeling revealed that Fos immunoreactive neurons within the spinal trigeminal nucleus were restricted to regions densely labeled for calcitonin gene-related peptide. These results indicate that select features of corneal stimuli such as modality are encoded differently by neurons in the trigeminal subnucleus interpolaris/caudalis transition compared with those located in the subnucleus caudalis/cervical cord transition. It is likely that neurons in these two brainstem regions subserve different aspects of corneal sensation.

Animals↗
PubMed2005

Hippocampal dopamine receptors modulate cFos expression in the rat nucleus accumbens evoked by chemical stimulation of the ventral hippocampus.

Recently, we have shown that D1 and D2 receptors in the ventral hippocampus (VH) modulate both the locomotor activation and the increase in dopamine (DA) levels in the rat nucleus accumbens (NAc) induced by NMDA stimulation of the VH. In the present study we analyze the possible role of VH D1 and D2 receptors in the modulation of the cFos expression in NAc (core and shell subregions) and in dorsal striatum. This was assessed by immunohistochemical analysis of cFos expression in the rat brains after retro-dialysis application of NMDA (50mM, 10 min) into VH, in absence and in presence of either the D1/D5 receptor antagonist SCH 23390 (100 and 250 microM, 60 min) or the D2 receptor antagonist raclopride (100 and 250 microM, 60 min). NMDA induced a robust increase in the cFos expression in the NAc shell, both in the ipsilateral and contralateral side. No statistically significant increases were observed in the NAc core and in the dorsal striatum. Simultaneous application of SCH 23390 and NMDA into the VH attenuated the NMDA-evoked cFos expression in NAc shell. In contrast, raclopride had no significant effect. Our present results show that the NMDA receptor mediated effects in the VH require D1 receptors and suggest that DA in VH strongly modulates the excitatory outputs from this brain area.

Animals↗