Effect of glutamate stimulation of bed nucleus of the stria terminalis on arterial pressure and heart rate

Ciriello, John; Janßen, Simone

doi:10.1152/ajpheart.1993.265.5.h1516

Cited by 43 publications

(61 citation statements)

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“…In addition, the cardiovascular responses to stimulation of the PSTN returned to control levels ϳ20 min after the administration of CoCl 2 into mNTS. Furthermore, repetitive injections of Glu at the same PSTN site was found in this study to elicit cardiovascular responses that were both qualitatively and quantitatively similar, an observation that has been observed in previous studies following multiple Glu injections (8,13,16,27). It has also been previously reported that repeated injections of a low concentration of Glu, as used in this study, do not appear to have any significant neurotoxic affects (14,19).…”

Section: Discussionsupporting

confidence: 89%

“…The PSTN region was explored systematically on a grid pattern from 3.7 to 4.3 mm caudal to bregma, 1.3 to 2.2 mm lateral to the midline, and 7.0 to 8.2 mm ventral to the dorsal surface of the brain for sites that elicited changes in AP and/or HR. Solutions of Glu (0.25 M; 10 nl; Sigma, St. Louis, MO) (16) in 0.9% physiological saline were microinjected by the application of pressurized nitrogen pulses controlled by a picospritzer (General Valve, Fairfield, NJ) (8,16). The injected volume (10 nl) was measured by direct observation of the fluid meniscus in the micropipette by using a microscope fitted with an ocular micrometer that was calibrated to allow a 2-nl resolution.…”

Section: Methodsmentioning

confidence: 99%

“…In seven additional animals, to determine which components of the peripheral autonomic nervous system were involved in mediating the cardiovascular responses to PSTN stimulation, cardiovascular responsive sites in the PSTN were retested following the administration of the muscarinic receptor blocker atropine methyl bromide (1-2 mg/kg iv). After 10 -15 min, the nicotinic receptor blocker hexamethonium bromide (20 mg/kg iv) was also administered, and the same site in the PSTN was restimulated with Glu (8).…”

Section: Methodsmentioning

confidence: 99%

“…At the completion of an experiment in which single-barreled micropipettes were used, the micropipette was withdrawn from the last site of injection, filled with Pontamine Sky blue in PBS (pH 7.2) without removing it from the stereotaxic holder, and lowered back to the same site at which a 20-nl microinjection of the dye was made to mark the center of the injection site in the PSTN region (8,10,16). In some experiments, the second-barrel of a double-barreled micropipette was filled with Pontamine Sky blue.…”

Section: Methodsmentioning

confidence: 99%

“…In some experiments, the second-barrel of a double-barreled micropipette was filled with Pontamine Sky blue. This was injected to mark the center of the stimulation site in the PSTN region (20 nl) or of the injection site in the NTS (100 nl) (8,13,16). The injection sites and the resulting micropipette tracks were later identified histologically.…”

Section: Methodsmentioning

confidence: 99%

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Medullary pathways mediating the parasubthalamic nucleus depressor response

Ciriello¹,

Solano-Flores²,

Rosas‐Arellano³

et al. 2008

American Journal of Physiology-Regulatory, Integrative and Comp

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The parasubthalamic nucleus (PSTN) projects extensively to the nucleus of the solitary tract (NTS); however, the function of PSTN in cardiovascular regulation is unknown. Experiments were done in ␣-chloralose anesthetized, paralyzed, and artificially ventilated rats to investigate the effect of glutamate (10 nl, 0.25 M) activation of PSTN neurons on mean arterial pressure (MAP), heart rate (HR), and renal sympathetic nerve activity (RSNA). Glutamate stimulation of PSTN elicited depressor (Ϫ20.4 Ϯ 0.7 mmHg) and bradycardia (Ϫ26.0 Ϯ 1.0 beats/min) responses and decreases in RSNA (67 Ϯ 17%). Administration (intravenous) of atropine methyl bromide attenuated the bradycardia response (46%), but had no effect on the MAP response. Subsequent intravenous administration of hexamethonium bromide blocked both the remaining bradycardia and depressor responses. Bilateral microinjection of the synaptic blocker CoCl 2 into the caudal NTS region attenuated the PSTN depressor and bradycardia responses by 92% and 94%, respectively. Additionally, prior glutamate activation of neurons in the ipsilateral NTS did not alter the magnitude of the MAP response to stimulation of PSTN, but potentiated HR response by 35%. Finally, PSTN stimulation increased the magnitude of the reflex bradycardia to activation of arterial baroreceptors. These data indicate that activation of neurons in the PSTN elicits a decrease in MAP due to sympathoinhibition and a cardiac slowing that involves both vagal excitation and sympathoinhibition. In addition, these data suggest that the PSTN depressor effects on circulation are mediated in part through activation of NTS neurons involved in baroreflex function. lateral hypothalamus; blood pressure; bradycardia; baroreceptor reflex; nucleus of the solitary tract

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Section: Discussionsupporting

confidence: 89%

Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

See 3 more Smart Citations

Medullary pathways mediating the parasubthalamic nucleus depressor response

Ciriello¹,

Solano-Flores²,

Rosas‐Arellano³

et al. 2008

American Journal of Physiology-Regulatory, Integrative and Comp

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Mediation of dehydration-induced peptidergic gene expression in the rat lateral hypothalamic area by forebrain afferent projections

Kelly

Watts

1996

J. Comp. Neurol.

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We have previously shown in dehydrated rats that cellular levels of the mRNAs encoding the precursor peptides for corticotropin-releasing hormone and neurotensin/neuromedin N significantly increase in a restricted region of the lateral hypothalamic area (Watts, 1992, Brain Res. 581:208-216). The experiments reported here address the role that forebrain osmosensitive cells groups or regions associated with autonomic regulation play in developing this mRNA response. The first experiment showed that unilateral knife cuts placed between the rostral forebrain and the lateral hypothalamic area (LHA) will unilaterally attenuate the mRNA response in the LHA to dehydration. In a second experiment, small injections of the retrograde tracer Fluorogold into the region of the LHA containing these mRNAs revealed a direct input from the osmosensitive median preoptic nucleus and subfornical organ and from the fusiform nucleus of the bed nuclei of the stria terminalis, which is part of a complex of cell groups associated with autonomic regulation. We found that at least 30% of the neurons in the median preoptic nucleus and subfornical organ and 14% of the neurons in the fusiform nucleus of the bed nuclei of the stria terminalis that project to the LHA responded to a rapid increase in plasma osmolality with increased c-fos mRNA levels. In the final experiment, injections of Fluorogold into the LHA were made simultaneously with ipsilateral rostral knife cuts. Here the numbers of neurons accumulating Fluorogold in the median preoptic nucleus, subfornical organ, and the fusiform nucleus were all significantly decreased concomitantly with attenuated mRNA responses in the LHA to dehydration. We conclude that the LHA receives direct and functional projections from the median preoptic nucleus, subfornical organ, and the fusiform nucleus. These projections appear capable of mediating a substantial part of the response of peptidergic mRNAs in the LHA to dehydration.

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Regulation of norepinephrine release from the rat bed nucleus of the stria terminalis: In vivo microdialysis studies

1997

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The microdialysis technique was used to study the in vivo extracellular levels of norepinephrine in the bed nucleus of the stria terminalis. A basal level of 2.34 +/-0.25 fmol/microl of norepinephrine was observed. Desipramine (2 and 10 microM), a norepinephrine uptake blocker, significantly increased extracellular levels of norepinephrine. Reversed perfusion with high potassium in the presence of 2 microM desipramine induced the release of norepinephrine. Instead, in the presence of 10 microM desipramine, a significant decrease in the induced release of norepinephrine was observed. Clonidine, an alpha2-adrenergic agonist, significantly decreased basal extracellular levels of norepinephrine and the K+-induced release of norepinephrine. In contrast, yohimbine and RX821002, two alpha2-adrenergic antagonists, significantly increased basal extracellular levels of norepinephrine but not the release of norepinephrine induced by 70 mM K+. Perfusion of tetrodotoxin through the probe located in the bed nucleus of the stria terminalis significantly decreased both the basal extracellular level and the K+-induced release of norepinephrine. Furthermore, perfusion of tetrodotoxin through a microdialysis probe implanted in the medial forebrain bundle also decreased basal extracellular levels of norepinephrine in the bed nucleus of the stria terminalis. The results show that in vivo there is a significant noradrenergic tonic activity in the bed nucleus of the stria terminalis. This tonic activity depends on the impulse flow through medial forebrain bundle nerve fibers. Under these conditions, extracellular levels of norepinephrine in the bed nucleus of the stria terminalis are regulated by the magnitude of norepinephrine uptake and by presynaptic alpha2-adrenergic receptors.

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Effect of glutamate stimulation of bed nucleus of the stria terminalis on arterial pressure and heart rate

Cited by 43 publications

References 0 publications

Medullary pathways mediating the parasubthalamic nucleus depressor response

Medullary pathways mediating the parasubthalamic nucleus depressor response

Mediation of dehydration-induced peptidergic gene expression in the rat lateral hypothalamic area by forebrain afferent projections

Regulation of norepinephrine release from the rat bed nucleus of the stria terminalis: In vivo microdialysis studies

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