Central neuronal circuit innervating the rat heart defined by transneuronal transport of pseudorabies virus

Standish, A.; Enquist, Lynn W.; Escardo, Julia; Schwaber, James S.

doi:10.1523/jneurosci.15-03-01998.1995

Cited by 177 publications

(108 citation statements)

References 43 publications

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“…It has been well established that the vagal input to the heart originates predominantly from the nAmb (13,43,44). In the present study, unilateral and bilateral microinjections of muscimol into the nAmb attenuated tachycardic responses elicited by microinjections of NMDA into the ARCN, indicating that the nAmb is important in mediating these responses.…”

Section: Discussionsupporting

confidence: 59%

“…The neuronal pools mediating the inhibition of vagal input to the heart in response to ARCN stimulation and the neurotransmitters and receptors involved in these neuronal pools have not been identified. Although cardiac vagal neurons (CVNs) in the rat are located in the dorsal motor nucleus of the vagus as well as the nucleus ambiguus (nAmb), the predominant vagal input to the heart is provided by the CVNs located in the nAmb (13,43,44). The axons of CVNs located in the nAmb pass through the vagus nerves and synapse on cardiac ganglia located in the atrioventricular node and fat tissue surrounding the sinoatrial node (2).…”

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confidence: 99%

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GABA and glycine receptors in the nucleus ambiguus mediate tachycardia elicited by chemical stimulation of the hypothalamic arcuate nucleus

Chitravanshi

Kawabe

Sapru

2015

American Journal of Physiology-Heart and Circulatory Physiology

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elicits tachycardia, which is partially mediated via inhibition of vagal inputs to the heart. The neuronal pools and neurotransmitters in them mediating tachycardia elicited from the ARCN have not been identified. We tested the hypothesis that the tachycardia elicited from the ARCN may be mediated by inhibitory neurotransmitters in the nucleus ambiguus (nAmb). Experiments were done in urethane-anesthetized, artificially ventilated, male Wistar rats. In separate groups of rats, unilateral and bilateral microinjections of muscimol (1 mM), gabazine (0.01 mM), and strychnine (0.5 mM) into the nAmb significantly attenuated tachycardia elicited by unilateral microinjections of NMDA (10 mM) into the ARCN. Histological examination of the brains showed that the microinjections sites were within the targeted nuclei. Retrograde anatomic tracing from the nAmb revealed direct bilateral projections from the ARCN and hypothalamic paraventricular nucleus to the nAmb. The results of the present study suggest that tachycardia elicited by stimulation of the ARCN by microinjections of NMDA is mediated via GABAA and glycine receptors located in the nAmb.

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Section: Discussionsupporting

confidence: 59%

mentioning

confidence: 99%

GABA and glycine receptors in the nucleus ambiguus mediate tachycardia elicited by chemical stimulation of the hypothalamic arcuate nucleus

Chitravanshi

Kawabe

Sapru

2015

American Journal of Physiology-Heart and Circulatory Physiology

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“…Both effects were mediated by AT 1 receptors. The chemoreflex enhancement was reversed by nTS injection of an AT 1 receptor antagonist or an NK 1 receptor antagonist that also blocked the vasodepressor response to SP (81). In contrast, NK 1 receptor blockade had no effect on depression by ANG II of baroreflex-induced bradycardia.…”

Section: Potential Interactions Between Ang II and Sp In The Ntsmentioning

confidence: 91%

Angiotensin potentiates excitatory sensory synaptic transmission to medial solitary tract nucleus neurons

Barnes

DeWeese

Andresen

2003

American Journal of Physiology-Regulatory, Integrative and Comp

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Barnes, Karen L., Dannette M. DeWeese, and Michael C. Andresen. Angiotensin potentiates excitatory sensory synaptic transmission to medial solitary tract nucleus neurons. Am J Physiol Regul Integr Comp Physiol 284: R1340-R1353, 2003. First published January 16, 2003 10.1152/ajpregu.00505.2002-Femtomole doses of angiotensin (ANG) II microinjected into nucleus tractus solitarii (nTS) decrease blood pressure and heart rate, mimicking activation of the baroreflex, whereas higher doses depress this reflex. ANG II might generate cardioinhibitory responses by augmenting cardiovascular afferent synaptic transmission onto nTS neurons. Intracellular recordings were obtained from 99 dorsal medial nTS region neurons in rat medulla horizontal slices to investigate whether ANG II modulated short-latency excitatory postsynaptic potentials . ANG II appeared to selectively augment presynaptic sensory transmission in one class of nTS neurons but had only postsynaptic effects on another group of cells. Thus ANG II is likely to modulate cardiovascular function by more than one nTS neuronal pathway. cardiovascular regulation; L-glutamate; substance P, non-Nmethyl-D-aspartate receptor THE NUCLEUS TRACTUS SOLITARII (nTS) in the dorsal medulla comprises rostrocaudally oriented columns of diverse neurons and fiber tracts that lie lateral to the walls of the fourth cerebral ventricle and join above the central canal caudal to the obex (4, 73). This complex structure, with bidirectional connections to medullary and forebrain nuclei that subserve autonomic functions, plays a major role in the regulation and integration of visceral systems, including normal and impaired cardiovascular mechanisms (60,61,82). Anatomic studies (25,26,43,52,85) and in vivo recordings (91) verify that a substantial proportion of the arterial baroreceptor sensory fibers that originate from receptors in the aortic arch and carotid sinus regions course through the solitary tract (TS) into the nTS and make their first synapse on neurons in the dorsal medial region of the nucleus. Neurons in this region also receive synaptic inputs from other viscera and brain autonomic nuclei via the TS (79). The nTS is a primary central site at which angiotensin (ANG) II influences cardiovascular function. Within the brain, the anatomic distributions of ANG II and its receptors and their mRNAs correlate reasonably well with the probable functions of the peptide (2, 57). However, the cellular mechanisms responsible for the cardiovascular effects of ANG II mediated by the nTS remain unclear.Microinjection of femtomole doses of ANG II into the dorsal medial region of the nTS produces a transient fall in blood pressure and heart rate very similar to the response to activation of the cardiovascular baroreflex in anesthetized rats (41,71,78) and evokes a comparable bradycardia in an in vitro beating heart-brain stem rat preparation (75). Paradoxically, however, higher doses evoke pressor responses, creating dose-response relationships that are biphasic. ANG II injection into the nTS al...

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“…With the development of neurotropic viruses as an alternative to traditional tract tracing tools, our understanding of complex neuronal circuitry, particularly the innervation of thoracic and abdominal viscera, has greatly advanced (Buijs et al, 2003;Cano et al, 2000Cano et al, , 2004Card et al, 1990;Glatzer et al, 2003;Hadziefendic and Haxhiu, 1999;Jansen et al, 1997;Nadelhaft et al, 1992;Schramm et al, 1993;Standish et al, 1995). Notwithstanding this progress, there is a paucity of knowledge concerning how neurotrauma, particularly spinal cord injury (SCI), affects neuronal circuitry and/or plasticity as demarcated with the use of neurotropic viruses (Bareyre et al, 2004;Duale et al, 2009;Kim et al, 2002;Lane et al, 2008;Pan et al, 2005;Yu et al, 2003).…”

Section: Introductionmentioning

confidence: 99%

Noxious Colorectal Distention in Spinalized Rats Reduces Pseudorabies Virus Labeling of Sympathetic Neurons

Duale

Lyttle²,

Smith³

et al. 2010

Journal of Neurotrauma

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The retrograde transsynaptic tracer pseudorabies virus (PRV) has been widely used as a marker for synaptic connectivity in the spinal cord. Notably, the PRV-152 construct expresses enhanced green fluorescent protein (EGFP). We recently reported a significant attenuation of PRV-152 labeling of the intermediolateral cell column (IML) and celiac ganglia after complete T4 spinal cord transection versus sham injury in rats at 96 h after PRV-152 inoculation of the left kidney. Here we found a significant increase in noxious colorectal distention (CRD)-evoked c-Fos expression in spinal cords of injured versus sham rats without PRV infection. In order to assess whether enhancing neuronal activity in spinalized rats might increase PRV-152 labeling, we subjected awake spinalized rats to 1.5 h of intermittent noxious CRD either: (1) just prior to inoculation, or (2) 96 h after inoculation (n ¼ 3/group). Equal numbers of spinalized rats in both groups received PRV-152 inoculations without CRD (non-stimulated; n ¼ 3/group). At 96 h post-inoculation fixed spinal cords and left celiac ganglionic tissues were assessed for the distribution and quantification of EGFP-labeled cells. The injured cohort that received CRD just prior to PRV injection showed a significant reduction in EGFP-labeled cells in both the IML and left celiac ganglion compared to non-stimulated injured rats. In contrast, the injured cohort that received CRD 96 h after PRV-152 inoculation showed no differences in EGFP-labeled cell numbers in the IML or celiac ganglia versus non-stimulated injured rats. Interestingly, microglia near c-Fos-positive cells after acute CRD appeared more reactive compared to non-stimulated spinalized rats, and activated microglial cells markedly reduce viral transduction and progression following PRV inoculation of the CNS. Hence our results imply that increased CRD-induced c-Fos expression in the injured paradigm, prior to but not after PRV injection, further attenuates PRV-152 uptake, perhaps through changes in neuronal activity and/or innate neuro-immune responses.

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Central neuronal circuit innervating the rat heart defined by transneuronal transport of pseudorabies virus

Cited by 177 publications

References 43 publications

GABA and glycine receptors in the nucleus ambiguus mediate tachycardia elicited by chemical stimulation of the hypothalamic arcuate nucleus

GABA and glycine receptors in the nucleus ambiguus mediate tachycardia elicited by chemical stimulation of the hypothalamic arcuate nucleus

Angiotensin potentiates excitatory sensory synaptic transmission to medial solitary tract nucleus neurons

Noxious Colorectal Distention in Spinalized Rats Reduces Pseudorabies Virus Labeling of Sympathetic Neurons

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