Difference in distribution of glutamate-immunoreactive neurons projecting into the subretrofacial nucleus in the rostral ventrolateral medulla of SHR and WKY: a double-labeling study

1992 ◽  
Vol 570 (1-2) ◽  
pp. 259-266 ◽  
Author(s):  
Kiyoshige Takayama ◽  
Mitsuhiko Miura
Keyword(s):  
Rostral Ventrolateral Medulla ◽  
Ventrolateral Medulla ◽  
Double Labeling

Role of glutamate in a visceral sympathoexcitatory reflex in rostral ventrolateral medulla of cats

2006 ◽  
Vol 291 (3) ◽  
pp. H1309-H1318 ◽  
Author(s):  
Wei Zhou ◽  
Liang-Wu Fu ◽  
Stephanie C. Tjen-A-Looi ◽  
Zhi-ling Guo ◽  
John C. Longhurst
Keyword(s):  
Receptor Antagonist ◽  
Ampa Receptors ◽  
Glutamate Transporter ◽  
Rostral Ventrolateral Medulla ◽  
Visceral Afferents ◽  
Ventrolateral Medulla ◽  
Double Labeling ◽  
Excitatory Neurotransmitter ◽  
Reflex Responses ◽  
Arterial Blood

The rostral ventrolateral medulla (rVLM) is involved in processing visceral sympathetic reflexes. However, there is little information on specific neurotransmitters in this brain stem region involved in this reflex. The present study investigated the importance of glutamate and glutamatergic receptors in the rVLM during gallbladder stimulation with bradykinin (BK), because glutamate is thought to function as an excitatory neurotransmitter in this region. Stimulation of visceral afferents activated glutamatergic neurons in the rVLM, as noted by double-labeling with c-Fos and the cellular vesicular glutamate transporter 3 (VGLUT3). Visceral reflex activation significantly increased arterial blood pressure as well as extracellular glutamate concentrations in the rVLM as determined by microdialysis. Barodenervation did not alter the release of glutamate in the rVLM evoked by visceral reflex stimulation. Iontophoresis of glutamate into the rVLM enhanced the activity of sympathetic premotor cardiovascular rVLM neurons. Also, the responses of these neurons to visceral afferent stimulation with BK were attenuated significantly (70%) by blockade of glutamatergic receptors with kynurenic acid. Microinjection of either an N-methyl-d-aspartate (NMDA) receptor antagonist 2-amino-5-phosphonopentanate (25 mM, 30 nl) or an dl-α-amino-3-hydroxy-5-methylisoxazole-4-propionate (AMPA) receptor antagonist 6-cyano-7-nitroquinoxaline-2,3-dione (2 mM, 30 nl) into the rVLM significantly attenuated the visceral sympathoexcitatory reflex responses. These results suggest that glutamate in the rVLM serves as an excitatory neurotransmitter through a baroreflex-independent mechanism and that both NMDA and AMPA receptors mediate the visceral sympathoexcitatory reflex responses.

c-Fos expression in the medulla induced by static muscle contraction in cats

1997 ◽  
Vol 272 (1) ◽  
pp. H48-H56 ◽  
Author(s):  
J. Li ◽  
G. A. Hand ◽  
J. T. Potts ◽  
L. B. Wilson ◽  
J. H. Mitchell
Keyword(s):  
Muscle Contraction ◽  
Vestibular Nucleus ◽  
Rostral Ventrolateral Medulla ◽  
Ventrolateral Medulla ◽  
Reticular Nucleus ◽  
Lateral Reticular Nucleus ◽  
Double Labeling ◽  
Exercise Pressor Reflex ◽  
Pressor Reflex ◽  
Stimulation Of

In this study, we examined Fos-like immunoreactivity (FLI) in the medulla after static muscle contraction induced by stimulation of L7 and S1 ventral roots of the spinal cord in anesthetized cats. The results show that FLI increases in the lateral reticular nucleus, nucleus of the solitary tract, lateral tegmental field, vestibular nucleus, subretrofacial nucleus, and A1 region of the medulla in comparison with these same areas in sham-operated animals (P < 0.05 in each region). In the rostral ventrolateral medulla, FLI distribution in neurons containing phenylethanolamine-N-methyltransferase (PNMT, the synthetic enzyme for epinephrine) was also observed utilizing double-labeling methods. The majority of neurons with PNMT also expressed FLI (66 +/- 4%). These data are in contrast to the results from sham-operated animals showing that 24 +/- 3% of the neurons costained with PNMT (P < 0.05). Our findings indicate that expression of FLI can be used to identify neurons activated during static muscle contraction and support previous studies implicating the ventrolateral medulla as a critical region for expression of the exercise pressor reflex. Furthermore, neurons in the rostral ventrolateral medulla containing PNMT were activated during static muscle contraction.

B�tzinger neurons project towards bulbospinal neurons in the rostral ventrolateral medulla of the rat

1997 ◽  
Vol 388 (1) ◽  
pp. 23-31 ◽  
Author(s):  
Qi-Jian Sun ◽  
Jane Minson ◽  
Ida J. Llewellyn-Smith ◽  
Leonard Arnolda ◽  
John Chalmers ◽  
...  
Keyword(s):  
Rostral Ventrolateral Medulla ◽  
Ventrolateral Medulla

Role of Nitric Oxide Synthase Uncoupling at Rostral Ventrolateral Medulla in Redox-Sensitive Hypertension Associated With Metabolic Syndrome

Hypertension ◽  
2014 ◽  
Vol 64 (4) ◽  
pp. 815-824 ◽  
Author(s):  
Kay L.H. Wu ◽  
Yung-Mei Chao ◽  
Shiow-Jen Tsay ◽  
Chen Hsiu Chen ◽  
Samuel H.H. Chan ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Metabolic Syndrome ◽  
Nitric Oxide Synthase ◽  
Rostral Ventrolateral Medulla ◽  
Ventrolateral Medulla ◽  
Oxide Synthase

Cardiovascular effects of opioid antagonist naloxone in rostral ventrolateral medulla of rabbits

1990 ◽  
Vol 258 (2) ◽  
pp. R325-R331 ◽  
Author(s):  
D. A. Morilak ◽  
G. Drolet ◽  
J. Chalmers
Keyword(s):  
Pressor Response ◽  
Cardiovascular Effects ◽  
Rostral Ventrolateral Medulla ◽  
Endogenous Opioids ◽  
Opioid Antagonist ◽  
Ventrolateral Medulla ◽  
Inhibitory Influence ◽  
Beneficial Effects ◽  
Arterial Blood ◽  
Depressor Effect

We have examined the influence of endogenous opioids on the basal and reflex control of arterial blood pressure in the pressor region of the rostral ventrolateral medulla (RVLM) of chloralose-anesthetized rabbits. We tested basal effects both in intact animals and after hypotensive hemorrhage. Bilateral administration of the opiod antagonist naloxone (20 nmol, 100 nl) directly into the RVLM induced a gradual and prolonged increase in mean arterial pressure (MAP) (+17 +/- 2 mmHg). This was preceded by a brief and mild depressor effect (-9 +/- 3 mmHg), which was attributable to a transient reduction in excitability immediately after naloxone injection. When naloxone was administered into the RVLM after hemorrhage (20 ml/kg), it improved recovery of MAP relative to saline controls, again producing a gradual, prolonged pressor response (+29 +/- 5 mmHg). The effect of naloxone on a baroreflex in intact animals was only transient, with a brief, nonsignificant attenuation of the reflex depressor response to aortic nerve stimulation. We conclude that endogenous opioids exert a tonic inhibitory influence on RVLM pressor neurons and that this input remains active after hemorrhage. The RVLM may thus be one site for the beneficial effects of naloxone in preventing circulatory decompensation after hemorrhage. In contrast, opioid neurons are not an essential component of baroreflex-mediated sympathoinhibition in the RVLM.

Sign in / Sign up

Export Citation Format

Share Document