Role of paraventricular nucleus in regulation of  sympathetic nerve frequency components

Kenney, Michael J.; Weiss, Mark L.; Mendes, Tammy; Wang, Yan; Fels, Richard J.

doi:10.1152/ajpheart.00673.2002

Cited by 25 publications

(24 citation statements)

References 34 publications

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“…Conversely, sympathetic or cardiovascular effects seen after microinjection of higher doses of BMI into nearby regions may well be a consequence of exciting neurons in the DMH (see DeNovellis et al, 1995). This would be particularly true in reports that have targeted the PVN with microinjections ranging from 50 pmol to as much as 2 nmol of BMI and assumed that sympathoexcitatory or cardiovascular effects noted were a consequence of disinhibiting neurons in the latter region (Martin et al, 1991;Reynolds et al, 1996;Zhang and Patel, 1998;Kenney et al, 2003;LaGrange et al, 2003;Reddy et al, 2005;Martin et al, 2006). The extent of the region activated by microinjection of 10 pmoles of BMI in this study make it highly plausible that at least some of the changes elicited by microinjection of these larger doses into the nearby PVN may be a consequence of spread or diffusion to the DMH.…”

Section: Discussionmentioning

confidence: 99%

Induction of Fos-immunoreactivity in the rat brain following disinhibition of the dorsomedial hypothalamus

et al. 2008

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Activation of neurons in the dorsomedial hypothalamus (DMH) appears to play an important role in signaling the excitation of brain regions responsible for experimental fever and for many of the physiological and behavioral changes seen in experimental stress or anxiety in rats. Here, we examined the effect of disinhibition of the DMH by unilateral microinjection of bicuculline methiodide (BMI) on Fos expression in selected regions of the brain that have been implicated in anxiety and responses to stress and fever in rats. Disinhibition of the DMH resulted in dramatic increases in local Fos expression and also increased the numbers of Fos-positive neurons in the lateral septal nucleus and in both the parvocellular and magnocellular subdivisions of the paraventricular nucleus, with greater increases ipsilateral to the injection site in the DMH. However, microinjection of BMI had no significant effect on Fos expression in the bed nucleus of the stria terminalis, another forebrain area implicated in stress and anxiety. In the brainstem, disinhibition of the DMH increased Fos expression in the nucleus tractus solitarius and the ventrolateral medulla bilaterally with greater increases again ipsilateral to the site of the microinjection, and also in the midline rostral raphe pallidus. Thus, disinhibition of neurons in the DMH in conscious rats results in increases in Fos expression in selected forebrain and brainstem regions that have been implicated in stress-induced physiological changes, anxiety, and experimental fever.

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Section: Discussionmentioning

confidence: 99%

Induction of Fos-immunoreactivity in the rat brain following disinhibition of the dorsomedial hypothalamus

et al. 2008

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“…In spite of receiving strong tonic inhibitory input (Chen and Toney 2003b;Chen et al 2003;Kenney et al 2003;Li et al 2006;Martin et al 1991), PVN neurons nevertheless do contribute to ongoing SNA. In anesthetized rats, for example, studies have shown that acute inhibition of PVN neuronal activity or blockade of excitatory inputs reduces ongoing renal SNA (RSNA) (Akine et al 2003;Allen 2002;Stocker et al 2004b, lumbar SNA , and ABP (Akine et al 2003;Allen 2002;Freeman and Brooks 2007;Stocker et al 2004b.…”

Section: Introductionmentioning

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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“…The coordinated actions of excitatory and inhibitory neurotransmitters in the PVN determine the neuronal activity of the PVN. There are complex interactions between specific PVN neurotransmitters for altering sympathetic nerve activity (11,12). Either the increased excitatory stimuli or decreased inhibitory stimuli into the PVN would lead to the increased neuronal activity of the PVN, and consequent increased sympathetic outflow (38,39).…”

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confidence: 99%

Blunted nitric oxide-mediated inhibition of sympathetic nerve activity within the paraventricular nucleus in diabetic rats

Zheng

Mayhan²,

Bidasee³

et al. 2006

American Journal of Physiology-Regulatory, Integrative and Comp

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Recent evidence suggests that a central mechanism may be contributing to the sympathetic abnormality in diabetes. Nitric oxide (NO) has been known as a neurotransmitter in the central nervous system. The goal of this study was to examine the role of the endogenous NO system of the paraventricular nucleus (PVN) in regulation of renal sympathetic nerve activity (RSNA) in streptozotocin (STZ)-induced diabetic rats. The change in number of NADPH-diaphorase-positive neurons [a marker for neuronal NO synthase (nNOS) activity] in the PVN was measured. Diabetic rats were found to have significantly fewer nNOS positive cells in the PVN than in the control group (120 +/- 11 vs. 149 +/- 13, P < 0.05). Using RT PCR, Western blotting and immunofluorescent staining, it was also found that nNOS mRNA expression and protein level in the PVN were significantly decreased in the diabetic rats. Furthermore, using an in vivo microdialysis technique, we found that there was a lower NO(x) release from the PVN perfusates in rats with diabetes compared with the control rats (142 +/- 33 nM vs. 228 +/- 29 nM, P < 0.05). In alpha-chloralose- and urethane-anesthetized rats, an inhibitor of NO synthase, l-NMMA, microinjected into the PVN produced a dose-dependent increase in RSNA, mean arterial pressure (MAP), and heart rate (HR) in both control and diabetic rats. These responses were significantly attenuated in rats with diabetes compared with control rats (RSNA: 11 +/- 3% vs. 35 +/- 3%, P < 0.05). On the other hand, an NO donor, sodium nitroprusside (SNP), microinjected into the PVN produced a dose-dependent decrease in RSNA, MAP, and HR in the control and diabetic rats. RSNA (17 +/- 3%, vs. 41 +/- 6%, P < 0.05) and MAP in response to SNP were significantly blunted in the diabetic group compared with the control group. In conclusion, these data indicate an altered NO mechanism in the PVN of diabetic rats. This altered mechanism may contribute to the increased renal sympathetic neural activity observed in diabetes.

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Role of paraventricular nucleus in regulation of sympathetic nerve frequency components

Cited by 25 publications

References 34 publications

Induction of Fos-immunoreactivity in the rat brain following disinhibition of the dorsomedial hypothalamus

Induction of Fos-immunoreactivity in the rat brain following disinhibition of the dorsomedial hypothalamus

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

Blunted nitric oxide-mediated inhibition of sympathetic nerve activity within the paraventricular nucleus in diabetic rats

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