scholarly journals Systemically administered tempol reduces neuronal activity in paraventricular nucleus of hypothalamus and rostral ventrolateral medulla in rats

2009 ◽  
Vol 27 (3) ◽  
pp. 543-550 ◽  
Author(s):  
Shun-Guang Wei ◽  
Zhi-Hua Zhang ◽  
Yang Yu ◽  
Robert B Felder
Keyword(s):  
Neuronal Activity ◽  
Paraventricular Nucleus ◽  
Rostral Ventrolateral Medulla ◽  
Ventrolateral Medulla ◽  
Paraventricular Nucleus Of Hypothalamus

scholarly journals Activation of corticotropin-releasing factor receptors in the rostral ventrolateral medulla is required for glucose-induced sympathoexcitation

2014 ◽  
Vol 307 (10) ◽  
pp. E944-E953 ◽  
Author(s):  
Megan E. Bardgett ◽  
Amanda L. Sharpe ◽  
Glenn M. Toney
Keyword(s):  
Energy Expenditure ◽  
Neuronal Activity ◽  
Rostral Ventrolateral Medulla ◽  
Corticotropin Releasing Factor ◽  
Glucose Infusion ◽  
Neural Mechanisms ◽  
Male Rats ◽  
Ventrolateral Medulla ◽  
Sympathetic Activation ◽  
Gaba A

Energy expenditure is determined by metabolic rate and diet-induced thermogenesis. Normally, energy expenditure increases due to neural mechanisms that sense plasma levels of ingested nutrients/hormones and reflexively increase sympathetic nerve activity (SNA). Here, we investigated neural mechanisms of glucose-driven sympathetic activation by determining contributions of neuronal activity in the hypothalamic paraventricular nucleus (PVN) and activation of corticotropin-releasing factor (CRF) receptors in the rostral ventrolateral medulla (RVLM). Glucose was infused intravenously (150 mg/kg, 10 min) in male rats to raise plasma glucose concentration to a physiological postprandial level. In conscious rats, glucose infusion activated CRF-containing PVN neurons and TH-containing RVLM neurons, as indexed by c-Fos immunofluorescence. In α-chloralose/urethane-anesthetized rats, glucose infusion increased lumbar and splanchnic SNA, which was nearly prevented by prior RVLM injection of the CRF receptor antagonist astressin (10 pmol/50 nl). This cannot be attributed to a nonspecific effect, as sciatic afferent stimulation increased SNA and ABP equivalently in astressin- and aCSF-injected rats. Glucose-stimulated sympathoexcitation was largely reversed during inhibition of PVN neuronal activity with the GABA-A receptor agonist muscimol (100 pmol/50 nl). The effects of astressin to prevent glucose-stimulated sympathetic activation appear to be specific to interruption of PVN drive to RVLM because RVLM injection of astressin prior to glucose infusion effectively prevented SNA from rising and prevented any fall of SNA in response to acute PVN inhibition with muscimol. These findings suggest that activation of SNA, and thus energy expenditure, by glucose is initiated by activation of CRF receptors in RVLM by descending inputs from PVN.

scholarly journals Angiotensin II Excites Paraventricular Nucleus Neurons That Innervate the Rostral Ventrolateral Medulla: An In Vitro Patch-Clamp Study in Brain Slices

2005 ◽  
Vol 93 (1) ◽  
pp. 403-413 ◽  
Author(s):  
Matthew J. Cato ◽  
Glenn M. Toney
Keyword(s):  
Membrane Potential ◽  
Angiotensin Ii ◽  
Patch Clamp ◽  
Paraventricular Nucleus ◽  
Rostral Ventrolateral Medulla ◽  
Ventrolateral Medulla ◽  
Ang Ii ◽  
At1 Receptors ◽  
Inward Current

Neurons of the hypothalamic paraventricular nucleus (PVN) are key controllers of sympathetic nerve activity and receive input from angiotensin II (ANG II)–containing neurons in the forebrain. This study determined the effect of ANG II on PVN neurons that innervate in the rostral ventrolateral medulla (RVLM)—a brain stem site critical for maintaining sympathetic outflow and arterial pressure. Using an in vitro brain slice preparation, whole cell patch-clamp recordings were made from PVN neurons retrogradely labeled from the ipsilateral RVLM of rats. Of 71 neurons tested, 62 (87%) responded to ANG II. In current-clamp mode, bath-applied ANG II (2 μM) significantly ( P < 0.05) depolarized membrane potential from −58.5 ± 2.5 to −54.5 ± 2.0 mV and increased the frequency of action potential discharge from 0.7 ± 0.3 to 2.8 ± 0.8 Hz ( n = 4). Local application of ANG II by low-pressure ejection from a glass pipette (2 pmol, 0.4 nl, 5 s) also elicited rapid and reproducible excitation in 17 of 20 cells. In this group, membrane potential depolarization averaged 21.5 ± 4.1 mV, and spike activity increased from 0.7 ± 0.4 to 21.3 ± 3.3 Hz. In voltage-clamp mode, 41 of 47 neurons responded to pressure-ejected ANG II with a dose-dependent inward current that averaged -54.7 ± 3.9 pA at a maximally effective dose of 2.0 pmol. Blockade of ANG II AT1 receptors significantly reduced discharge ( P < 0.001, n = 5), depolarization ( P < 0.05, n = 3), and inward current ( P < 0.01, n = 11) responses to locally applied ANG II. In six of six cells tested, membrane input conductance increased ( P < 0.001) during local application of ANG II (2 pmol), suggesting influx of cations. The ANG II current reversed polarity at +2.2 ± 2.2 mV ( n = 9) and was blocked ( P < 0.01) by bath perfusion with gadolinium (Gd3+, 100 μM, n = 8), suggesting that ANG II activates membrane channels that are nonselectively permeable to cations. These findings indicate that ANG II excites PVN neurons that innervate the ipsilateral RVLM by a mechanism that depends on activation of AT1 receptors and gating of one or more classes of ion channels that result in a mixed cation current.

Sign in / Sign up

Export Citation Format

Share Document