Glutamatergic projection to RVLM mediates suppression of reflex bradycardia by parabrachial nucleus

1999 ◽  
Vol 276 (5) ◽  
pp. H1482-H1492 ◽  
Author(s):  
Wen-Bin Len ◽  
Julie Y. H. Chan
Keyword(s):  
Nmda Receptor ◽  
Receptor Antagonist ◽  
Nmda Receptor Antagonist ◽  
Systemic Arterial Pressure ◽  
Parabrachial Nucleus ◽  
Ventrolateral Medulla ◽  
Sprague Dawley ◽  
Reflex Bradycardia ◽  
Sprague Dawley Rats

We investigated the role of glutamatergic projection from the parabrachial nucleus (PBN) complex to the rostral ventrolateral medulla (RVLM) in the PBN-induced suppression of reflex bradycardia in adult Sprague-Dawley rats that were maintained under pentobarbital anesthesia. Under stimulus conditions that did not appreciably alter the baseline systemic arterial pressure and heart rate, electrical (10-s train of 0.5-ms pulses, at 10–20 μA and 10–20 Hz) or chemical (l-glutamate, 1 nmol) stimulation of the ventrolateral regions and Köelliker-Fuse (KF) subnucleus of the PBN complex significantly suppressed the reflex bradycardia in response to transient hypertension evoked by phenylephrine (5 μg/kg iv). The PBN-induced suppression of reflex bradycardia was appreciably reversed by bilateral microinjection into the RVLM of the N-methyl-d-aspartate (NMDA)-receptor antagonist MK-801 (500 pmol) or the non-NMDA-receptor antagonist 6-cyano-7-nitroquinoxaline-2,3-dione (50 pmol). Anatomically, most of the retrogradely labeled neurons in the ventrolateral regions and KF subnucleus of the ipsilateral PBN complex after microinjection of fast blue into the RVLM were also immunoreactive to anti-glutamate antiserum. These results suggest that a direct glutamatergic projection to the RVLM from topographically distinct regions of the PBN complex may participate in the suppression of reflex bradycardia via activation of both NMDA and non-NMDA receptors at the RVLM.

Role of AMPA/kainate receptors in transmission of the sympathetic baroreflex in rat CVLM

1997 ◽  
Vol 272 (3) ◽  
pp. R800-R812 ◽  
Author(s):  
T. Miyawaki ◽  
S. Suzuki ◽  
J. Minson ◽  
L. Arnolda ◽  
J. Chalmers ◽  
...  
Keyword(s):  
Nmda Receptor ◽  
Receptor Antagonist ◽  
Nmda Receptor Antagonist ◽  
Baroreceptor Reflex ◽  
Significant Inhibition ◽  
Kainate Receptors ◽  
Ventrolateral Medulla ◽  
Mk 801 ◽  
Aortic Nerve

We examined the role of alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA)/kainate receptors within the caudal ventrolateral medulla (CVLM) in mediating the sympathetic baroreceptor reflex in anesthetized and paralyzed rats. Bilateral microinjection into CVLM of either DL-2-amino-5-phosphonovaleric acid [APV; a selective N-methyl-D-aspartic acid (NMDA) receptor antagonist, 20 mM, 100 nl] or 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX; a selective AMPA/kainate receptor antagonist, 2 mM, 100 nl) alone failed to eliminate the aortic nerve stimulation-evoked hypotension and inhibition of splanchnic sympathetic nerve activity (SNA) or the cardiac-related rhythmicity of SNA. All components of the sympathetic-baroreceptor reflex were abolished when kynurenate (100 mM, 30 nl) or mixtures of APV and CNQX (10 and 1 mM, respectively, 100 or 30 nl) were injected into CVLM. Injection of APV or CNQX into CVLM reduced aortic nerve-evoked inhibitory responses of bulbospinal sympathoexcitatory neurons in rostral ventrolateral medulla (RVLM). The extent of this reduction was variable. Usually, significant inhibition was preserved. In seven RVLM neurons, intravenous injection of MK-801 (NMDA receptor antagonist, 2 mg/kg) failed to eliminate aortic nerve-evoked inhibitory responses. However, inhibitory responses were abolished when CNQX was injected into CVLM after intravenous MK-801. We conclude that both NMDA and AMPA/kainate receptors in CVLM transmit baroreceptor information.

Influence of memantine on nociceptive responses of the trigeminocervical complex after formalin injection

Cephalalgia ◽  
2012 ◽  
Vol 32 (4) ◽  
pp. 308-316 ◽  
Author(s):  
Jeong Wook Park ◽  
Gyoung Im Suh ◽  
Hae Eun Shin ◽  
Go Eun Park
Keyword(s):  
Nmda Receptor ◽  
Receptor Antagonist ◽  
Nmda Receptor Antagonist ◽  
Pain Behavior ◽  
Formalin Injection ◽  
Sensory Threshold ◽  
Sprague Dawley ◽  
Pain Pathways ◽  
Sprague Dawley Rats ◽  
Nociceptive Responses

Background: Glutamate receptors are implicated in central nervous system (CNS) pain pathways, including trigeminovascular activation, central sensitization, and cortical spreading depression. Methods: We investigated the influence of the N-methyl-d-aspartate (NMDA) receptor antagonist memantine on pain pathways involving trigeminocervical complex (TCC) using a formalin injection model. In Sprague Dawley rats, formalin was delivered into the left periorbital area. Memantine (10 mg/kg) or vehicle was injected intraperitoneally 30 min before the formalin injection. The sensory threshold for mechanical stimulation, assessed by the von Frey monofilament threshold (VFMF), was measured 1 h and 2 h after formalin injection. Formalin-induced pain behavior was measured by monitoring the time spent rubbing the injected area during 60 min after formalin injection. The brainstem was then removed, and sections that spanned the TCC were cut, and stained with a Fos antibody. Results: Pretreatment with memantine significantly attenuated formalin-induced pain behavior (p < 0.01) and the sensory threshold for VFMF (p < 0.001). In the TCC, the increase in formalin-induced Fos immunoreactivity was significantly attenuated in the memantine group (p < 0.01). Conclusion: The present study demonstrated that the NMDA receptor antagonist memantine inhibits the nociceptive process from trigemino-ophthalmic nerve endings to the TCC.

Cardiovascular and renal sympathetic activation by blood-borne TNF-α in rat: the role of central prostaglandins

2003 ◽  
Vol 284 (4) ◽  
pp. R916-R927 ◽  
Author(s):  
Zhi-Hua Zhang ◽  
Shun-Guang Wei ◽  
Joseph Francis ◽  
Robert B. Felder
Keyword(s):  
Lateral Ventricle ◽  
Biological Effects ◽  
Brain Regions ◽  
Ventrolateral Medulla ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
Tnf Α ◽  
Hypothalamic Level ◽  
Renal Sympathetic

In pathophysiological conditions, increased blood-borne TNF-α induces a broad range of biological effects, including activation of the hypothalamic-pituitary-adrenal axis and sympathetic drive. In urethane-anesthetized adult Sprague-Dawley rats, we examined the mechanisms by which blood-borne TNF-α activates neurons in paraventricular nucleus (PVN) of hypothalamus and rostral ventrolateral medulla (RVLM), two critical brain regions regulating sympathetic drive in normal and pathophysiological conditions. TNF-α (0.5 μg/kg), administered intravenously or into ipsilateral carotid artery (ICA), activated PVN and RLVM neurons and increased sympathetic nerve activity, arterial pressure, and heart rate. Responses to intravenous TNF-α were not affected by vagotomy but were reduced by mid-collicular decerebration. Responses to ICA TNF-α were substantially reduced by injection of the cyclooxygenase inhibitor ketorolac (150 μg) into lateral ventricle. Injection of PGE2 (50 ng) into lateral ventricle or directly into PVN increased PVN or RVLM activity, respectively, and sympathetic drive, with shorter onset latency than blood-borne TNF-α. These findings suggest that blood-borne cytokines stimulate cardiovascular and renal sympathetic responses via a prostaglandin-dependent mechanism operating at the hypothalamic level.

Role of the medullary lateral tegmental field in reflex-mediated sympathoexcitation in cats

2004 ◽  
Vol 286 (3) ◽  
pp. R451-R464 ◽  
Author(s):  
Hakan S. Orer ◽  
Gerard L. Gebber ◽  
Shaun W. Phillips ◽  
Susan M. Barman
Keyword(s):  
Nmda Receptor ◽  
Nmda Receptors ◽  
Receptor Antagonist ◽  
Sympathetic Nerve Activity ◽  
Nmda Receptor Antagonist ◽  
Vagal Afferents ◽  
Reflex Pathways ◽  
Excitatory Responses ◽  
Stimulation Of

We tested the hypothesis that blockade of N-methyl-d-aspartate (NMDA) and non-NMDA receptors on medullary lateral tegmental field (LTF) neurons would reduce the sympathoexcitatory responses elicited by electrical stimulation of vagal, trigeminal, and sciatic afferents, posterior hypothalamus, and midbrain periaqueductal gray as well as by activation of arterial chemoreceptors with intravenous NaCN. Bilateral microinjection of a non-NMDA receptor antagonist into LTF of urethane-anesthetized cats significantly decreased vagal afferent-evoked excitatory responses in inferior cardiac and vertebral nerves to 29 ± 8 and 24 ± 6% of control ( n = 7), respectively. Likewise, blockade of non-NMDA receptors significantly reduced chemoreceptor reflex-induced increases in inferior cardiac (from 210 ± 22 to 129 ± 13% of control; n = 4) and vertebral nerves (from 253 ± 41 to 154 ± 20% of control; n = 7) and mean arterial pressure (from 39 ± 7 to 21 ± 5 mmHg; n = 8). Microinjection of muscimol, but not an NMDA receptor antagonist, caused similar attenuation of these excitatory responses. Sympathoexcitatory responses to the other stimuli were not attenuated by microinjection of a non-NMDA receptor antagonist or muscimol into LTF. In fact, excitatory responses elicited by stimulation of trigeminal, and in some cases sciatic, afferents were enhanced. These data reveal two new roles for the LTF in control of sympathetic nerve activity in cats. One, LTF neurons are involved in mediating sympathoexcitation elicited by activation of vagal afferents and arterial chemoreceptors, primarily via activation of non-NMDA receptors. Two, non-NMDA receptor-mediated activation of other LTF neurons tonically suppresses transmission in trigeminal-sympathetic and sciatic-sympathetic reflex pathways.

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.

Both NMDA and non-NMDA receptors in the NTS participate in the baroreceptor reflex in rats

1994 ◽  
Vol 267 (4) ◽  
pp. R1065-R1070 ◽  
Author(s):  
H. Ohta ◽  
W. T. Talman
Keyword(s):  
Single Dose ◽  
Nmda Receptor ◽  
Nmda Receptors ◽  
Receptor Antagonist ◽  
Nmda Receptor Antagonist ◽  
Baroreceptor Reflex ◽  
Simultaneous Administration ◽  
Mk 801 ◽  
Selective Blockade ◽  
Reflex Bradycardia

In this study, we determined whether either N-methyl-D-aspartate (NMDA) receptors or non-NMDA receptors in the nucleus tractus solitarii (NTS) participate in the baroreceptor reflex in rats. Microinjection of an NMDA receptor antagonist, MK-801, and a non-NMDA receptor antagonist, 6,7-dinitroquinoxaline-2,3-dione, into the NTS decreased the sensitivity of the baroreceptor reflex by 51 and 41%, respectively. Simultaneous administration of both agents further reduced the sensitivity of the baroreceptor reflex to 28% of control. A competitive NMDA receptor antagonist, 2-amino-5-phosphonovaleric acid, also attenuated reflex bradycardia or tachycardia elicited by a single dose of phenylephrine or nitroprusside, respectively. Specificity of each antagonist's effects was supported by selective blockade of depressor responses produced by agonists that act at the NMDA and non-NMDA receptors, respectively. Results of this study indicate that both non-NMDA- and NMDA-sensitive receptors are involved in baroreceptor reflex transmission in the NTS.

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