Neurotransmission in the medulla mediating insular cortical and lateral hypothalamic sympathetic responses

1998 ◽  
Vol 76 (7-8) ◽  
pp. 737-746 ◽  
Author(s):  
Kenneth S Butcher ◽  
David F Cechetto
Keyword(s):  
Receptor Antagonist ◽  
Sympathetic Nerve ◽  
Pressor Response ◽  
Ventrolateral Medulla ◽  
Bipolar Electrode ◽  
Hypothalamic Area ◽  
Renal Nerve ◽  
Lateral Hypothalamic ◽  
Baseline Activity ◽  
Sympathetic Responses

Previous evidence has shown sympathetic nerve responses to insular cortical (IC) stimulation are mediated by synapses within the lateral hypothalamic area (LHA) and ventrolateral medulla (VLM). The present study was aimed at determining the neurotransmitter(s) and receptor(s) involved at the synapse in the VLM. Twenty male Wistar rats were instrumented for renal nerve, arterial pressure, and heart rate recording. The IC or the LHA was stimulated with a bipolar electrode (200-1000 µA; 2 ms; 0.8 Hz) to elicit sympathetic nerve responses. Antagonists were then pressure-injected into the VLM (300 nL). Bilateral and unilateral kynurenate (25 mM) resulted in 100% block of IC- and LHA-stimulated sympathetic nerve responses. Bilateral injection of the non-NMDA (N-methyl-D-aspartate) receptor antagonist 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX; 200 µM) also resulted in up to 100% block of IC and LHA sympathetic responses. In addition, unilateral injections of CNQX were made in two animals, resulting in 100 and 83% block of LHA sympathetic responses. Bilateral injection of the NMDA receptor antagonist DL-2-amino-5-phosphonopentanoic acid (AP5; 200µM) did not affect the response to IC or LHA stimulation. Kynurenate, CNQX, and AP5 all resulted in an elevation of baseline sympathetic nerve activity and a pressor response. Kynurenate resulted in a 263 ± 79% increase in baseline activity, while CNQX and AP5 resulted in 83 ± 19% and 91 ± 21% increases, respectively. Bilateral injections of antagonists for GABAA (bicuculline; 0.1 µM), acetylcholine (atropine; 0.1 µM) and catecholaminergic alpha and beta receptors (phentolamine and propranolol: 0.1 µM) had no effect on LHA sympathetic responses. Thus, sympathetic responses originating in the IC and LHA are mediated by a non-NMDA receptors in the VLM, which are likely AMPA receptors.Key words: insular cortex, ventrolateral medulla, glutamate, sympathetic activity.

Receptors in lateral hypothalamic area involved in insular cortex sympathetic responses

1998 ◽  
Vol 275 (2) ◽  
pp. H689-H696 ◽  
Author(s):  
Kenneth S. Butcher ◽  
David F. Cechetto
Keyword(s):  
Heart Rate ◽  
Arterial Pressure ◽  
Sympathetic Nerve ◽  
Lateral Hypothalamic Area ◽  
Ventrolateral Medulla ◽  
Bipolar Electrode ◽  
Hypothalamic Area ◽  
Renal Nerve ◽  
Lateral Hypothalamic ◽  
Sympathetic Responses

Previous evidence has shown that sympathetic nerve responses to insular cortical (IC) stimulation are mediated by synapses within the lateral hypothalamic area (LHA) and ventrolateral medulla. The present study determined the receptor(s) involved at the synapse in the LHA associated with stimulation-evoked IC sympathetic responses. Twenty-seven male Wistar rats were instrumented for renal nerve activity, arterial pressure, and heart rate recording. The right IC was stimulated with a bipolar electrode (200–1,000 μA, 2 ms, 0.8 Hz) resulting in sympathetic nerve responses. Antagonists were then pressure injected into the ipsilateral LHA (300–500 nl). Kynurenate (250 mM) injections resulted in 51 ± 8% (range 0–100%) block of IC-stimulated sympathetic nerve responses. Similarly, the N-methyl-d-aspartic acid (NMDA)-receptor antagonistdl-2-amino-5-phosphonopentanoic acid (200 μM) resulted in an inhibition (82 ± 8%; range 51–100%) of IC-stimulated sympathetic responses. Injection of the non-NMDA antagonist 6-cyano-7-nitroquinoxaline-2,3-dione (200 μM) had no effect on IC sympathetic responses. Injection of antagonists to GABA, acetylcholine, and adrenergic receptors was also without effect. No antagonist injections had any effects on baseline sympathetic nerve discharge, arterial pressure, or heart rate. These results suggest that the IC autonomic efferents projecting to the LHA utilize NMDA glutamatergic receptors.

Nociceptin in rVLM mediates electroacupuncture inhibition of cardiovascular reflex excitatory response in rats

2005 ◽  
Vol 98 (6) ◽  
pp. 2056-2063 ◽  
Author(s):  
Melissa M. Crisostomo ◽  
Peng Li ◽  
Stephanie C. Tjen-A-Looi ◽  
John C. Longhurst
Keyword(s):  
Blood Pressure ◽  
Receptor Antagonist ◽  
Opioid Receptor ◽  
Pressor Response ◽  
Inhibitory Effect ◽  
Reflex Response ◽  
Ventrolateral Medulla ◽  
Gastric Distension ◽  
Sprague Dawley ◽  
Nociceptin Receptor

Electroacupuncture (EA) at Neiguan-Jianshi acupoints through an opioid mechanism inhibits the cardiovascular pressor response induced by mechanical stimulation of the stomach. Because nociceptin also may regulate cardiovascular activity through its action in the brain stem, we hypothesized that this neuromodulator serves a role in the EA-related inhibitory effect. Blood pressure in ventilated male Sprague-Dawley rats (400–600 g) anesthetized by ketamine and α-chloralose was measured during balloon inflation of the stomach. Gastric distension with 6–8 ml of air induced consistent pressor reflexes of 26 ± 1 mmHg that could be repeated every 10 min for 100 min. When nociceptin (10 nM) was microinjected into the rostral ventrolateral medulla (rVLM), the pressor response induced by gastric distension was inhibited by 68 ± 6%. Thirty minutes of EA also decreased the reflex response by 75 ± 11%; microinjection of saline into the rVLM did not alter the inhibitory effect of EA. In contrast, microinjection of a nociceptin receptor antagonist into the rVLM promptly reversed the EA response. Pretreatment with the opioid receptor antagonist naloxone did not influence the EA-like inhibitory effect of nociceptin on the distension-induced pressor reflex (22 ± 1 to 8 ± 2 mmHg). Furthermore, a μ-opioid receptor agonist microinjected into the rVLM after microinjection of a nociceptin receptor antagonist during EA promptly reversed the nociceptin receptor antagonist-related inhibition of the EA effect. Thus, in addition to the classical opioid system, nociceptin, through opioid receptor-like-1 receptor stimulation in the rVLM, participates in the modulatory influence of EA on reflex-induced increases in blood pressure.

Effects of hypoxia, hyperoxia and hypercapnia on graded cerebral ischemic responses in rabbits

1992 ◽  
Vol 263 (6) ◽  
pp. H1839-H1846
Author(s):  
T. Takeuchi ◽  
J. Horiuchi ◽  
N. Terada ◽  
M. Nagao ◽  
H. Terajima
Keyword(s):  
Blood Flow ◽  
Cerebral Ischemia ◽  
Arterial Pressure ◽  
Internal Carotid ◽  
Pressor Response ◽  
Ventrolateral Medulla ◽  
Left Internal Carotid Artery ◽  
Renal Nerve ◽  
Tissue Po2 ◽  
Cerebral Ischemic

This study was designed to determine how several factors interact to modify the cerebral ischemic pressor response (CIR) in anesthetized rabbits. After the carotid sinus and aortic nerves were bilaterally sectioned, blood flow through the left internal carotid artery (ICF), which was surgically restricted as the sole route of blood supply to the brain, was reduced by a servo-controller during ventilation with room air, and 8% and 90% O2 and 2 and 5% CO2 gas mixtures. Blood flow (MBF), tissue PO2, PCO2, and interstitial pH were measured in the rostral ventrolateral medulla. Internal carotid arterial pressure, tissue PO2, and MBF decreased proportionately as ICF decreased in the range from 4 to 0 ml/min. Hypoxia significantly increased the rise in renal nerve activity (RNA) and CIR caused by cerebral ischemia, while hyperoxia significantly decreased them. Hypercapnia had almost no influence on the increases in RNA and mean arterial pressure produced by cerebral ischemia. CIR showed a much higher correlation with changes in tissue PO2 than with the other factors. We examined how these factors interact to modify CIR and found that central hypoxia is the main factor in producing CIR.

Subcortical sites mediating sympathetic responses from insular cortex in rats

1990 ◽  
Vol 258 (1) ◽  
pp. R245-R255 ◽  
Author(s):  
D. F. Cechetto ◽  
S. J. Chen
Keyword(s):  
Insular Cortex ◽  
Lateral Hypothalamic Area ◽  
Parabrachial Nucleus ◽  
Solitary Tract ◽  
Nerve Activity ◽  
Hypothalamic Area ◽  
Renal Nerve ◽  
Lateral Hypothalamic ◽  
Nerve Response ◽  
Renal Nerve Activity

Stimulation of the insular cortex elicits a number of autonomic responses. The insular cortex projects directly to the lateral hypothalamic area, the parabrachial nucleus, and the nucleus of the solitary tract, which in turn project directly to sympathetic preganglionic areas. To determine which of these subcortical sites mediates sympathetic responses evoked from the insular cortex, changes in renal nerve activity were recorded before and after injection of the synaptic blocking agent cobalt into each of these regions. Blood pressure, heart rate, and renal nerve activity were continuously monitored in chloralose or urethan-anesthetized rats. Single-pulse electrical stimulation (200 microA, 1 ms) elicited either an early increase or decrease in renal nerve activity from pressor and depressor sites, respectively, in the insular cortex. Cobalt injections (500 nl) into the lateral hypothalamic area attenuated the nerve response 10-100%. Cobalt injections into the nucleus of the solitary tract significantly enhanced the initial increase in the nerve response obtained from pressor sites in the insular cortex. Injections into the parabrachial nucleus did not affect the nerve responses. These results suggest that there is a mandatory synapse in the lateral hypothalamic area in the pathway from the insular cortex to the sympathetic nervous system.

Medullary lateral tegmental field: an important source of basal sympathetic nerve discharge in the cat

2000 ◽  
Vol 278 (4) ◽  
pp. R995-R1004 ◽  
Author(s):  
Susan M. Barman ◽  
Gerard L. Gebber ◽  
Hakan S. Orer
Keyword(s):  
Nmda Receptor ◽  
Receptor Antagonist ◽  
Sympathetic Nerve ◽  
Excitatory Amino Acid ◽  
Nmda Receptor Antagonist ◽  
Ventrolateral Medulla ◽  
Cardiac Sympathetic Nerve ◽  
Significant Component ◽  
Synaptic Drive ◽  
Nerve Discharge

We used blockade of excitatory amino acid (EAA) neurotransmission in the medullary lateral tegmental field (LTF) and rostral ventrolateral medulla (RVLM) to assess the roles of these regions in the control of inferior cardiac sympathetic nerve discharge (SND) and mean arterial pressure (MAP) in urethan-anesthetized, baroreceptor-denervated cats. Bilateral microinjection of a non- N-methyl-d-aspartate (NMDA)-receptor antagonist [1,2,3,4-tetrahydro-6-nitro-2,3-dioxobenzo-[f]quinoxaline-7-sulfonamide (NBQX)] into the LTF significantly decreased SND to 46 ± 4% of control (as demonstrated with power-density spectral analysis) and MAP by 16 ± 6 mmHg. In contrast, bilateral microinjection of an NMDA-receptor antagonist [d(−)-2-amino-5-phosphonopentanoic acid (d-AP5)] into the LTF did not decrease SND or MAP. These results demonstrate that the LTF is an important synaptic relay in the pathway responsible for basal SND in the cat. Bilateral microinjection of NBQX or d-AP5 into the RVLM significantly decreased power in SND to 48 ± 5 or 61 ± 5% of control, respectively, and reduced MAP by 15 ± 2 or 8 ± 4 mmHg, respectively. These data indicate that EAA-mediated synaptic drive to RVLM-spinal sympathoexcitatory neurons accounts for a significant component of their basal activity.

scholarly journals Glucoprivation in the ventrolateral medulla decreases brown adipose tissue sympathetic nerve activity by decreasing the activity of neurons in raphé pallidus

2012 ◽  
Vol 302 (2) ◽  
pp. R224-R232 ◽  
Author(s):  
C. J. Madden
Keyword(s):  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Cold Exposure ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Ventrolateral Medulla ◽  
Nerve Activity ◽  
Hypothalamic Area ◽  
Brown Adipose ◽  
Raphe Pallidus

In urethane/α-chloralose anesthetized rats, cold exposure increased brown adipose tissue sympathetic nerve activity (BAT SNA: +699 ± 104% control). Intravenous administration of 2-deoxy-d-glucose (2-DG; 200 mg·ml−1·kg−1) reversed the cold-evoked activation of BAT SNA (nadir: 139 ± 36% of control) and decreased BAT temperature (−1.1 ± 0.2°C), expired CO2 (−0.4 ± 0.1%), and core temperature (−0.5 ± 0.0). Similarly, unilateral nanoinjection of the glucoprivic agent 5-thioglucose (5-TG; 12 μg/100 nl) in the ventrolateral medulla (VLM) completely reversed the cold-evoked increase in BAT SNA (nadir: 104 ± 7% of control), and decreased TBAT (−1.4 ± 0.3°C), expired CO2 (−0.2 ± 0.0%), and heart rate (−35 ± 10 beats/min). The percentage of rostral raphé pallidus (RPa)-projecting neurons in the dorsal hypothalamic area/dorsomedial hypothalamus that expressed Fos in response to cold exposure (ambient temperature: 4–10°C) did not differ between saline (28 ± 6%) and 2-DG (30 ± 5%) pretreated rats, whereas the percentage of spinally projecting neurons in the RPa/raphé magnus that expressed Fos in response to cold exposure was lower in 2-DG- compared with saline-pretreated rats (22 ± 6% vs. 42 ± 5%, respectively). The increases in BAT SNA evoked by nanoinjection of bicuculline in the RPa or by transection of the neuraxis at the pontomedullary border were resistant to inhibition by glucoprivation. These results suggest that neurons within the VLM play a role in the glucoprivic inhibition of BAT SNA and metabolism, that this inhibition requires neural structures rostral to the pontomedullary border, and that this inhibition is mediated by a GABAergic input to the RPa.

Sympathoinhibition from ventrolateral periaqueductal gray mediated by 5-HT1A receptors in the RVLM

2001 ◽  
Vol 280 (4) ◽  
pp. R976-R984 ◽  
Author(s):  
M. Bago ◽  
C. Dean
Keyword(s):  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Pressor Response ◽  
Periaqueductal Gray ◽  
Ventrolateral Medulla ◽  
Nerve Activity ◽  
Pentobarbital Sodium ◽  
Arterial Blood ◽  
Way 100635

The role of 5-hydroxytryptamine 1A (5-HT1A) receptors located in the rostral ventrolateral medulla (RVLM) in the mediation of a sympathoinhibitory and depressor response elicited from the ventrolateral periaqueductal gray (vlPAG) matter of the midbrain was examined in pentobarbital sodium-anesthetized rats. Activation of neurons in the vlPAG evoked a decrease in renal and lumbar sympathetic nerve activities and a decrease in arterial blood pressure. After microinjection of the specific 5-HT1A-receptor antagonist WAY-100635 into the pressor area of the RVLM, the vlPAG-evoked sympathoinhibition and hypotension was attenuated to control levels (7 of 15 animals) or converted into a sympathoexcitation and pressor response (8 of 15 animals). Baroreflex inhibition of sympathetic nerve activity was not impaired by microinjection of WAY into the sympathoexcitatory region of the RVLM. These data suggest that sympathoinhibition and hypotension elicited by activation of neurons in the vlPAG are mediated by 5-HT1A receptors in the RVLM.

Different cardiac and renal inhibitory and excitatory areas in rabbit hypothalamus

1983 ◽  
Vol 244 (6) ◽  
pp. H832-H838 ◽  
Author(s):  
Y. Okada ◽  
I. Ninomiya
Keyword(s):  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
New Method ◽  
Cardiac Sympathetic Nerve ◽  
Nerve Activity ◽  
Hypothalamic Area ◽  
Renal Nerve ◽  
Cardiac Sympathetic Nerve Activity ◽  
Renal Nerve Activity ◽  
The Right

The hypothalamic area was stimulated in anesthetized rabbits at a large number of selected points, and the effects on the simultaneously recorded right cardiac sympathetic nerve activity (CSNA) and renal nerve activity (RNA) were analyzed quantitatively. Four characteristic patterns of CSNA and RNA responses could be observed. The most striking finding was the presence of opposite responses of CSNA and RNA at many hypothalamic stimulus points, in addition to the conventionally observed CSNA and RNA responses in the same direction. By a new method, we drew hypothalamic maps for CSNA and RNA response magnitudes. These maps show that the excitatory areas of CSNA and RNA are surrounded by respective inhibitory areas. Although the excitatory areas of CSNA and RNA correspond with each other on the right side, they are not identical on the left side. These data suggest that the heart and kidney are controlled by sympathetic nerve activities originating from different hypothalamic neural groups in the rabbit.

Lateral hypothalamic injection of 2-deoxy-D-glucose suppresses sympathetic activity

1989 ◽  
Vol 257 (6) ◽  
pp. R1386-R1392 ◽  
Author(s):  
M. Egawa ◽  
H. Yoshimatsu ◽  
G. A. Bray
Keyword(s):  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Hypothalamic Nucleus ◽  
High Dose ◽  
Base Line ◽  
Nerve Activity ◽  
Hypothalamic Area ◽  
Interscapular Brown Adipose Tissue ◽  
Lateral Hypothalamic ◽  
Brown Adipose

To investigate the effects of glucoprivation on sympathetic nerve activity to interscapular brown adipose tissue (IBAT), 2-deoxy-D-glucose (2-DG) was injected into the third cerebral ventricle (icv), lateral hypothalamic area (LHA), and ventromedial hypothalamic nucleus (VMN) of rats. The multiunit discharges of sympathetic nerves to IBAT were recorded electrophysiologically. The icv injection of high and low doses of 2-DG (5.0 and 2.5 mg/rat) suppressed sympathetic nerve activity by 76.9 and 49.8% respectively, 30 min after injection compared with preinjected base line. After the low dose of 2-DG, there was a gradual recovery, but after the high dose recovery did not occur. The unilateral microinjection of 2-DG (0.25 mg/rat) into the LHA induced a similar suppression of sympathetic nerve activity to that observed after icv injection of 10 times as much 2-DG (-25.3%). The injection of vehicle or sucrose into the LHA did not suppress sympathetic nerve activity. The microinjection into the VMN either unilaterally or bilaterally did not suppress sympathetic nerve activity to IBAT. We conclude that the LHA but not the VMH is one site of action of 2-DG. The data are consistent with the hypothesis that the brain senses glucoprivation in the LHA and reduces sympathetic drive to thermogenic tissues such as IBAT.

Hypothalamic and cortical sympathetic responses relay in the medulla of the rat

1992 ◽  
Vol 263 (3) ◽  
pp. R544-R552 ◽  
Author(s):  
D. F. Cechetto ◽  
S. J. Chen
Keyword(s):  
Spinal Cord ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Ventrolateral Medulla ◽  
Nerve Activity ◽  
Thoracic Spinal Cord ◽  
Efferent Pathway ◽  
Arterial Blood ◽  
Sympathetic Responses ◽  
Stimulation Of

Previously, investigations have indicated that the efferent pathway for sympathetic responses originating in the insular cortex (IC) must initially synapse in the lateral hypothalamic area (LHA). The LHA projects to both the ventrolateral medulla (VLM) and directly to the thoracic spinal cord. To determine the role of the VLM in mediating sympathetic responses from the IC and the LHA, in alpha-chloralose-anesthetized rats, renal nerve responses were recorded following electrical stimulation of these two forebrain sites before and after bilateral injection (300 nl) of cobalt (a synaptic blocking agent) into the VLM. The results demonstrated that a complete block of the increase in sympathetic nerve activity following stimulation of the IC or the LHA could be obtained with cobalt injections into the VLM. The most effective injection sites were located in the rostral ventrolateral medulla at the rostrocaudal middle and posterior regions of the C1 group of neurons. Chemical stimulation with DL-homocysteic acid, in the LHA, to activate cell bodies only evoked a decrease in arterial blood pressure and sympathetic nerve activity. These responses were also blocked by cobalt injection into the VLM. Injections of cobalt into the nucleus of the solitary tract did not block sympathetic responses elicited from the LHA. These results indicate that the efferent pathway for sympathetic responses from the IC through the LHA goes to the preganglionic region of the spinal cord via a mandatory synapse in the VLM.

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