Hypothalamic projections to cardiovascular centers of the medulla

Hardy, Sandro

doi:10.1016/s0006-8993(01)02053-4

Cited by 91 publications

(69 citation statements)

References 43 publications

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“…The hypothalamic PVN is a heterogenous structure that contains magnocellular neuroendocrine neurons as well as parvocellular sympathetic premotor neurons (Swanson and Sawchenko, 1983;Ranson et al, 1998;Yang and Coote, 1998;Pyner and Coote, 2000;Hardy, 2001). Although the PVN sympathetic premotor neurons send projections to both the RVLM and IML, the relative functional importance of these two pathways in autonomic regulation remains to be established.…”

Section: Discussionmentioning

confidence: 99%

“…In addition to the projection to sympathetic preganglionic neurons located in the intermediolateral cell column (IML) of the spinal cord, the PVN neurons also project to neurons within the rostral ventrolateral medulla (RVLM) (Shafton et al, 1998;Yang and Coote, 1998;Pyner and Coote, 2000;Hardy, 2001). The RVLM is a pivotal structure in maintaining tonic sympathetic nerve activity and basal blood pressure through projections to the IML.…”

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confidence: 99%

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Angiotensin II Attenuates Synaptic GABA Release and Excites Paraventricular-Rostral Ventrolateral Medulla Output Neurons

Pan²

2005

J Pharmacol Exp Ther

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The hypothalamic paraventricular nucleus (PVN) neurons regulate sympathetic outflow through projections to the spinal cord and rostral ventrolateral medulla (RVLM). Although the PVN-RVLM pathway is important for the action of brain angiotensin II (Ang II) on autonomic control, the cellular mechanisms involved are not fully known. In this study, we examined the effect of Ang II on the excitability and synaptic inputs to RVLMprojecting PVN neurons. PVN neurons were retrogradely labeled by FluoSpheres injected into the RVLM of rats. Wholecell patch-clamp recordings were performed on labeled PVN neurons in brain slices. Ang II significantly increased the firing rate of PVN neurons from 3.63 Ϯ 0.65 to 6.10 Ϯ 0.75 Hz (P Ͻ 0.05, n ϭ 9), and such an effect was eliminated by an AT 1 receptor antagonist, losartan. Furthermore, inclusion of a G protein inhibitor, guanosine 5Ј-O-(2-thiodiphosphate, in the pipette internal solution did not alter the excitatory effect of Ang II on labeled PVN neurons. Application of 0.5 to 5 M Ang II significantly decreased the amplitude of evoked GABAergic inhibitory postsynaptic currents (IPSCs) in a dose-dependent manner. Also, 2 M Ang II significantly decreased the frequency of miniature IPSCs (mIPSCs) from 3.89 Ϯ 0.84 to 2.06 Ϯ 0.45 Hz (P Ͻ 0.05, n ϭ 11), but did not change the amplitude and decay time constant of mIPSCs. By contrast, Ang II had no significant effect on glutamatergic excitatory postsynaptic currents at the concentrations that inhibited IPSCs. In addition, Ang II failed to excite PVN neurons in the presence of bicuculline. Collectively, this study provides important new information that Ang II excites RVLM-projecting PVN neurons through attenuation of GABAergic synaptic inputs.

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Angiotensin II Attenuates Synaptic GABA Release and Excites Paraventricular-Rostral Ventrolateral Medulla Output Neurons

Pan²

2005

J Pharmacol Exp Ther

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“…Because PVN neurons terminate over a large rostralto-caudal portion of the ventrolateral medulla, including the caudal ventrolateral medulla (CVLM) (Hardy 2001;Krukoff et al 1997), we were careful to place antidromic stimulating electrodes in the RVLM at sites from which large-amplitude increases of ABP were elicited by injection of L-glutamate (see Fig. 1A).…”

Section: Technical Considerationsmentioning

confidence: 99%

In Vivo Discharge Properties of Hypothalamic Paraventricular Nucleus Neurons With Axonal Projections to the Rostral Ventrolateral Medulla

Chen

Toney

2010

Journal of Neurophysiology

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Chen Q-H, Toney GM. In vivo discharge properties of hypothalamic paraventricular nucleus neurons with axonal projections to the rostral ventrolateral medulla. J Neurophysiol 103: 4 -15, 2010. First published November 4, 2009 doi:10.1152/jn.00094.2009. The hypothalamic paraventricular nucleus (PVN) and rostral ventrolateral medulla (RVLM) are key components of a neural network that generates and regulates sympathetic nerve activity (SNA). Although each region has been extensively studied, little is presently known about the in vivo discharge properties of individual PVN neurons that directly innervate the RVLM. Here extracellular recording was performed in anesthetized rats, and antidromic stimulation was used to identify single PVN neurons with axonal projections to the RVLM (n ϭ 94). Neurons were divided into two groups that had either unbranched axons terminating in the RVLM (i.e., PVN-RVLM neurons, n ϭ 65) or collateralized axons targeting both the RVLM and spinal cord [i.e., PVN-RVLM/ intermediolateral cell column (IML) neurons, n ϭ 29]. Many PVN-RVLM (32/65, 49%) and PVN-RVLM/IML (17/29, 59%) neurons were spontaneously active. The average firing frequency was not different across groups. Spike-triggered averaging revealed that spontaneous discharge of most neurons was temporally correlated with renal SNA (PVN-RVLM: 12/21, 57%; PVN-RVLM/IML: 6/9, 67%). Time histograms triggered by the electrocardiogram (ECG) R-wave indicated that discharge of most cells was also cardiac rhythmic (PVN-RVLM: 25/32, 78%; PVN-RVLM/IML: 10/17, 59%). Raising and lowering arterial blood pressure to increase and decrease arterial baroreceptor input caused a corresponding decrease and increase in firing frequency among cells of both groups (PVN-RVLM: 9/13, 69%; PVN-RVLM/IML: 4/4, 100%). These results indicate that PVN-RVLM and PVN-RVLM/IML neurons are both capable of contributing to basal sympathetic activity and its baroreflex modulation.

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“…12A, in the context of sympathetic regulation. PVN neurons directly innervate preganglionic sympathetic neurons in the IML, as well as presympathetic neurons in the RVLM and neurons in the nucleus of the solitary tract (NTS), the site of first termination for cardiovascular afferent nerve fibers (31,74,96,158,163).…”

Section: Sympathetic Drive In Heart Failure: a Hypothetical Constructmentioning

confidence: 99%

Heart failure and the brain: new perspectives

Felder¹,

Francis²,

Zhang³

et al. 2003

American Journal of Physiology-Regulatory, Integrative and Comp

109

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Heart failure and the brain: new perspectives. Am J Physiol Regul Integr Comp Physiol 284: R259-R276, 2003; 10.1152/ajpregu.00317.2002.-Despite recent therapeutic advances, the prognosis for patients with heart failure remains dismal. Unchecked neurohumoral excitation is a critical element in the progressive clinical deterioration associated with the heart failure syndrome, and its peripheral manifestations have become the principal targets for intervention. The link between peripheral systems activated in heart failure and the central nervous system as a source of neurohumoral drive has therefore come under close scrutiny. In this context, the forebrain and particularly the paraventricular nucleus of the hypothalamus have emerged as sites that sense humoral signals generated peripherally in response to the stresses of heart failure and contribute to the altered volume regulation and augmented sympathetic drive that characterize the heart failure syndrome. This brief review summarizes recent studies from our laboratory supporting the concept that the forebrain plays a critical role in the pathogenesis of ischemiainduced heart failure and suggesting that the forebrain contribution must be considered in designing therapeutic strategies. Forebrain signaling by neuroactive products of the renin-angiotensin system and the immune system are emphasized.angiotensin; aldosterone; cytokines; tumor necrosis factor; immune system; renin; vasopressin; sympathetic; extracellular fluid volume; baroreflex THE IMPORTANCE OF AUTONOMIC dysfunction to the progression of heart failure is firmly established (55,113,120,152). The most effective treatments for heart failure specifically target the peripheral manifestations of neurohumoral activation (86,113). Yet the understanding of the mechanisms leading to neurohumoral excitation in heart failure is still quite limited.Over the last several decades, substantial evidence has been amassed to support the concept that peripheral afferent systems innervating the heart and vascular tree are altered in heart failure. Dysfunction has been described in all components of the reflexes mediated by these cardiovascular afferent systems-the afferent fibers themselves, the central processing of the afferent signals, the efferent innervation of the end organs, and the end organs themselves. In general, the influence of low-and high-pressure baroreceptors (40,42,191) that normally restrain sympathetic drive and vasopressin release is diminished, whereas the excitatory influences of arterial chemoreceptors (161) and cardiac sympathetic afferent fibers (100) are enhanced.Central nervous system (CNS) neurons affecting cardiovascular regulation respond to humoral as well neural signals. Blood-borne neuroactive peptides, too large to readily cross the blood-brain barrier, may influence the brain by activating sensory neurons at specific sites in hindbrain and forebrain that lack a blood-brain barrier (15,18) or by inducing the release of mediators that do penetrate the barrier (135). These neuroactive s...

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Hypothalamic projections to cardiovascular centers of the medulla

Cited by 91 publications

References 43 publications

Angiotensin II Attenuates Synaptic GABA Release and Excites Paraventricular-Rostral Ventrolateral Medulla Output Neurons

Angiotensin II Attenuates Synaptic GABA Release and Excites Paraventricular-Rostral Ventrolateral Medulla Output Neurons

In Vivo Discharge Properties of Hypothalamic Paraventricular Nucleus Neurons With Axonal Projections to the Rostral Ventrolateral Medulla

Heart failure and the brain: new perspectives

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