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

Chitravanshi, Vineet C.; Kawabe, Kazumi; Sapru, Hreday N.

doi:10.1152/ajpheart.00801.2014

Cited by 8 publications

(4 citation statements)

References 49 publications

(65 reference statements)

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“…The NTS receives primary information from cardiorespiratory sensory neurons, and the excitatory pathway from the NTS to CVNs likely plays an essential role in the chemoreceptor and baroreceptor reflex control of heart rate (1). Retrograde tracing studies have demonstrated direct projections from the PVN to the NA (6,22). This long-range neurotransmission from the PVN is excitatory with the endogenous release of oxytocin facilitating glutamatergic neurotransmission and excitation of CVNs (30).…”

Section: Discussionmentioning

confidence: 99%

Neurotransmission to parasympathetic cardiac vagal neurons in the brain stem is altered with left ventricular hypertrophy-induced heart failure

Cauley

Wang

Dyavanapalli

et al. 2015

American Journal of Physiology-Heart and Circulatory Physiology

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Neurotransmission to parasympathetic cardiac vagal neurons in the brain stem is altered with left ventricular hypertrophy-induced heart failure. Am J Physiol Heart Circ Physiol 309: H1281-H1287, 2015. First published September 14, 2015; doi:10.1152/ajpheart.00445.2015.-Hypertension, cardiac hypertrophy, and heart failure (HF) are widespread and debilitating cardiovascular diseases that affect nearly 23 million people worldwide. A distinctive hallmark of these cardiovascular diseases is autonomic imbalance, with increased sympathetic activity and decreased parasympathetic vagal tone. Recent device-based approaches, such as implantable vagal stimulators that stimulate a multitude of visceral sensory and motor fibers in the vagus nerve, are being evaluated as new therapeutic approaches for these and other diseases. However, little is known about how parasympathetic activity to the heart is altered with these diseases, and this lack of knowledge is an obstacle in the goal of devising selective interventions that can target and selectively restore parasympathetic activity to the heart. To identify the changes that occur within the brain stem to diminish the parasympathetic cardiac activity, left ventricular hypertrophy was elicited in rats by aortic pressure overload using a transaortic constriction approach. Cardiac vagal neurons (CVNs) in the brain stem that generate parasympathetic activity to the heart were identified with a retrograde tracer and studied using patch-clamp electrophysiological recordings in vitro. Animals with left cardiac hypertrophy had diminished excitation of CVNs, which was mediated both by an augmented frequency of spontaneous inhibitory GABAergic neurotransmission (with no alteration of inhibitory glycinergic activity) as well as a diminished amplitude and frequency of excitatory neurotransmission to CVNs. Opportunities to alter these network pathways and neurotransmitter receptors provide future targets of intervention in the goal to restore parasympathetic activity and autonomic balance to the heart in cardiac hypertrophy and other cardiovascular diseases. heart failure; cardiac hypertrophy; parasympathetic; autonomic; vagal NEW & NOTEWORTHYA common hallmark of cardiovascular diseases is autonomic imbalance. Left ventricular hypertrophy altered both excitatory and inhibitory neurotransmission to cardiac vagal neurons that generate parasympathetic activity to the heart. These preferentially altered network pathways and neurotransmitter receptors provide future targets to restore parasympathetic activity in these diseases.HYPERTENSION, cardiac hypertrophy, and heart failure (HF) are widespread and debilitating cardiovascular diseases that affects nearly 23 million people worldwide with ϳ2 million new patients diagnosed annually (15). Cardiac rhythm disturbances lead to sudden cardiac death in 40 -50% of advanced HF patients with a 1-yr mortality rate of Ͼ50% (10). A distinctive hallmark of cardiac hypertrophy, HF, and the accompanying cardiac conduction abnormalities is autonomic imbalance,...

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Section: Discussionmentioning

confidence: 99%

Neurotransmission to parasympathetic cardiac vagal neurons in the brain stem is altered with left ventricular hypertrophy-induced heart failure

Cauley

Wang

Dyavanapalli

et al. 2015

American Journal of Physiology-Heart and Circulatory Physiology

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“…This interaction has been demonstrated only in animal models and should be explored in humans with the aid of UHF fMRI. The NTS/NAmb link is also influenced by tonic inhibitory influence from arcuate and paraventricular (PVN) hypothalamic nuclei onto NAmb (Ciriello et al 2003; Chitravanshi et al 2015), forming the core central control circuitry for cardiovagal modulation. Furthermore, NTS and NAmb, as well as surrounding portions of the medullary reticular formation, have been physiologically defined as the dorsal medullary respiratory center (Kalia 1977), in addition to the Kölliker-Fuse nucleus in the pons and portions of the PAG in the midbrain (see section 3.5).…”

Section: Assessing Specific Brainstem Neural Circuitries With Uhf mentioning

confidence: 99%

Challenges and opportunities for brainstem neuroimaging with ultrahigh field MRI

et al. 2018

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The human brainstem plays a central role in connecting the cerebrum, the cerebellum and the spinal cord to one another, hosting relay nuclei for afferent and efferent signaling, and providing source nuclei for several neuromodulatory systems that impact central nervous system function. While the investigation of the brainstem with functional or structural magnetic resonance imaging has been hampered for years due to this brain structure's physiological and anatomical characteristics, the field has seen significant advances in recent years thanks to the broader adoption of ultrahigh-field (UHF) MRI scanning. In the present review, we focus on the advantages offered by UHF in the context of brainstem imaging, as well as the challenges posed by the investigation of this complex brain structure in terms of data acquisition and analysis. We also illustrate how UHF MRI can shed new light on the neuroanatomy and neurophysiology underlying different brainstem-based circuitries, such as the central autonomic network and neurotransmitter/neuromodulator systems, discuss existing and foreseeable clinical applications to better understand diseases such as chronic pain and Parkinson's disease, and explore promising future directions for further improvements in brainstem imaging using UHF MRI techniques.

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“…The details of all the procedures used in the present study are reported in our earlier publications (3,13,22,23,39). Initially, the rats were anesthetized with inhalation of isoflurane (2-3% in 100% oxygen), using a vaporizer (Fluotec-3, Cyprane, UK).…”

Section: General Proceduresmentioning

confidence: 99%

Stimulation of the hypothalamic arcuate nucleus increases brown adipose tissue nerve activity via hypothalamic paraventricular and dorsomedial nuclei

Chitravanshi

Kawabe

Sapru

2016

American Journal of Physiology-Heart and Circulatory Physiology

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Hypothalamic arcuate nucleus (ARCN) stimulation elicited increases in sympathetic nerve activity (IBATSNA) and temperature (TBAT) of interscapular brown adipose tissue (IBAT). The role of hypothalamic dorsomedial (DMN) and paraventricular (PVN) nuclei in mediating these responses was studied in urethane-anesthetized, artificially ventilated, male Wistar rats. In different groups of rats, inhibition of neurons in the DMN and PVN by microinjections of muscimol attenuated the increases in IBATSNA and TBAT elicited by microinjections of N-methyl-d-aspartic acid into the ipsilateral ARCN. In other groups of rats, blockade of ionotropic glutamate receptors by combined microinjections of D(-)-2-amino-7-phosphono-heptanoic acid (D-AP7) and NBQX into the DMN and PVN attenuated increases in IBATSNA and TBAT elicited by ARCN stimulation. Blockade of melanocortin 3/4 receptors in the DMN and PVN in other groups of rats resulted in attenuation of increases in IBATSNA and TBAT elicited by ipsilateral ARCN stimulation. Microinjections of Fluoro-Gold into the DMN resulted in retrograde labeling of cells in the ipsilateral ARCN, and some of these cells contained proopiomelanocortin (POMC), α-melanocyte-stimulating hormone (α-MSH), or vesicular glutamate transporter-3. Since similar projections from ARCN to the PVN have been reported by us and others, these results indicate that neurons containing POMC, α-MSH, and glutamate project from the ARCN to the DMN and PVN. Stimulation of ARCN results in the release of α-MSH and glutamate in the DMN and PVN which, in turn, cause increases in IBATSNA and TBAT.

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

Cited by 8 publications

References 49 publications

Neurotransmission to parasympathetic cardiac vagal neurons in the brain stem is altered with left ventricular hypertrophy-induced heart failure

Neurotransmission to parasympathetic cardiac vagal neurons in the brain stem is altered with left ventricular hypertrophy-induced heart failure

Challenges and opportunities for brainstem neuroimaging with ultrahigh field MRI

Stimulation of the hypothalamic arcuate nucleus increases brown adipose tissue nerve activity via hypothalamic paraventricular and dorsomedial nuclei

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