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.

Neurons of rostral ventrolateral medulla mediate somatic pressor reflex

1989 ◽  
Vol 256 (2) ◽  
pp. R448-R462 ◽  
Author(s):  
R. L. Stornetta ◽  
S. F. Morrison ◽  
D. A. Ruggiero ◽  
D. J. Reis
Keyword(s):  
Spinal Cord ◽  
Kainic Acid ◽  
Rostral Ventrolateral Medulla ◽  
Ventrolateral Medulla ◽  
Reticular Nucleus ◽  
Lumbar Spinal Cord ◽  
Afferent Nerves ◽  
Electrolytic Lesions ◽  
Pressor Reflex ◽  
Stimulation Of

The somatic pressor reflex (SPR) elicited in anesthetized paralyzed rats by electrical stimulation of the sciatic or sural cutaneous afferent nerves produced an increase in arterial pressure ranging from 5 to 40 mmHg. Stimulation of femoral or tibial afferent nerves from muscle produced a depressor response. The SPR was not affected by midpontine transection but was eliminated either by hemisection of the lumbar spinal cord contralateral, but not ipsilateral, to the stimulated nerve or by electrolytic or kainic acid lesion of the contralateral, but not ipsilateral, rostral ventrolateral medulla (RVL). Stimulation of the brachial plexus elicited an SPR that was not eliminated by contralateral lumbar hemisection but was abolished by RVL lesion. RVL lesions consistently overlapped areas containing phenylethanolamine N-methyltransferase-labeled C1 adrenergic neurons. Kainic acid injections into the lateral reticular nucleus (LRN) did not affect the SPR. Neither contralateral nor ipsilateral electrolytic lesions of other autonomic areas including parabrachial nucleus, the nucleus tractus solitarii, the A5 region, or the inferior cerebellar peduncle (output pathway of the LRN) affected the reflex. In axonal transport studies using horseradish peroxidase, afferent terminals of the sciatic nerve were shown to overlap spinoreticular neurons in the dorsal horn retrogradely labeled from tracer injections in the RVL. We conclude that the SPR can be elicited in rats, that it is mediated by spinoreticular afferents traveling in the contralateral spinal cord, and that the C1 adrenergic area of the RVL is a critical region for the integration of the somatic pressor reflex.

Renal and somatic input to spinal neurons antidromically activated from the ventrolateral medulla

1988 ◽  
Vol 60 (6) ◽  
pp. 1967-1981 ◽  
Author(s):  
W. S. Ammons
Keyword(s):  
Reticular Formation ◽  
Receptive Fields ◽  
Ventrolateral Medulla ◽  
Reticular Nucleus ◽  
Lateral Reticular Nucleus ◽  
Spinal Neurons ◽  
C Fiber ◽  
Somatic Input ◽  
Fiber Stimulation ◽  
Stimulation Of

1. Studies were done to characterize responses of spinal neurons backfired from the ventrolateral medulla to renal and somatic stimuli. Experiments were performed on 31 cats that were anesthetized with alpha-chloralose. Sixty-six spinal neurons were antidromically activated from the area of the lateral reticular nucleus or the ventrolateral reticular formation just rostral to the lateral reticular nucleus contralateral to the recording site. These cells could not be backfired from the medial reticular formation or from the spinothalamic tract just caudal to the thalamus. 2. Cells were located in laminae I, V, and VII of the T12-L2 segments. Antidromic conduction velocities averaged 35.9 +/- 7.2 m/s. Conduction velocities were unrelated to the projection site or laminar location of the cells. Termination sites of 21 cells were located in antidromic mapping experiments. Terminals were localized to the ventrolateral reticular formation, including the lateral reticular nucleus. 3. Responses to electrical stimulation of the renal nerves were always excitatory. Stimulation of renal A-delta-fibers excited 33 cells. These cells failed to respond to stimulation of renal C-fibers. The other 33 cells responded to both A-delta- and C-fiber stimulation. Latencies to A-delta-fiber stimulation averaged 9 +/- 2 ms, whereas latencies to C-fiber stimulation averaged 57 +/- 10 ms. 4. Renal mechanoreceptors were activated by occlusion of the renal vein or upper portion of the ureter. Renal vein occlusion excited 14 of 32 cells tested. Activity increased from 6 +/- 2 to 14 +/- 4 spike/s. Ureteral occlusion increased activity of 19 of 32 cells from 7 +/- 2 to 16 +/- 5 spikes/s. Cells responding to one of the mechanical stimuli were significantly more likely to receive A-delta-and C-fiber input compared with nonresponding cells. Nonresponders were more likely than responders to receive only A-delta input. 5. All cells received somatic input in addition to renal input. Twelve cells were classified as wide dynamic range, 46 as high threshold, and 8 as Deep. Somatic receptive fields most often included skin and muscle of the left flank and abdomen. Thirty-two cells had bilateral receptive fields, and 22 had inhibitory fields in addition to excitatory fields. 6. These data show that spinal neurons projecting to the ventrolateral medulla receive convergent inputs from the kidney and somatic structures. These cells may participate in a variety of functions including autonomic reflexes of renal origin.

scholarly journals Effects of lateral reticular nucleus lesions on the exercise pressor reflex in cats.

1982 ◽  
Vol 51 (3) ◽  
pp. 400-403 ◽  
Author(s):  
G A Iwamoto ◽  
M P Kaufmann ◽  
B R Botterman ◽  
J H Mitchell
Keyword(s):  
Reticular Nucleus ◽  
Lateral Reticular Nucleus ◽  
Exercise Pressor Reflex ◽  
Pressor Reflex

Responses of neurons in rostral ventrolateral medulla to activation of cardiac receptors in rats

2000 ◽  
Vol 279 (5) ◽  
pp. H2549-H2557 ◽  
Author(s):  
De-Pei Li ◽  
Hui-Lin Pan
Keyword(s):  
Rostral Ventrolateral Medulla ◽  
Ventrolateral Medulla ◽  
Single Unit Activity ◽  
Afferent Pathways ◽  
Sympathetic Control ◽  
Stellate Ganglia ◽  
Cervical Vagotomy ◽  
The Mean ◽  
Cardiac Receptors ◽  
Stimulation Of

Ischemic stimulation of cardiac receptors reflexly excites the cardiovascular system. However, the supraspinal mechanisms involved in this reflex are not well defined. This study examined the responses of barosensitive neurons in the rostral ventrolateral medulla (RVLM) to stimulation of cardiac receptors and the afferent pathways involved in these responses. Single-unit activity of RVLM neurons was recorded in α-chloralose-anesthetized rats. Cardiac receptors were stimulated by epicardial application of 10 μg/ml of bradykinin (BK). Barosensitive neurons were silenced by stimulation of baroreceptors. Application of BK increased the mean arterial pressure from 65.2 ± 1.9 to 89.3 ± 2.9 mmHg and excited RVLM barosensitive neurons from 6.2 ± 0.7 to 10.7 ± 0.9 impulses/s ( P < 0.05, n = 40). BK had no effect on 21 nonbarosensitive neurons. Blockade of stellate ganglia abolished the response of barosensitive neurons to BK. Cervical vagotomy significantly increased the baseline discharges of RVLM barosensitive neurons but had no effect on their responses to BK. Thus this study indicates that stimulation of cardiac receptors selectively activates RVLM barosensitive neurons through sympathetic afferent pathways. This information suggests that the RVLM barosensitive neurons are likely involved in the sympathetic control of circulation during myocardial ischemia.

Caudolateral areas of medulla-mediating release of ACTH in cats

1986 ◽  
Vol 251 (5) ◽  
pp. R934-R940
Author(s):  
D. A. Bereiter ◽  
D. S. Gann
Keyword(s):  
Brain Stem ◽  
Stimulus Pattern ◽  
Reticular Nucleus ◽  
Lateral Reticular Nucleus ◽  
Plasma Acth ◽  
Acth Stimulation ◽  
Afferent Information ◽  
Burst Pattern ◽  
Stimulation Of ◽  
Acth Release

The effect of electrical stimulation of the caudolateral brain stem on plasma adrenocorticotropin (ACTH) was assessed in cats anesthetized with alpha-chloralose-urethan. To examine the influence of stimulus pattern on ACTH release, an equal number of pulses was presented in a continuous pattern and in a burst pattern at each electrode site. Stimulation of the magnocellular portion (layers 4-6) of trigeminal nucleus caudalis evoked a significant (P less than 0.01) and equal peak change in plasma ACTH after continuous pattern (+121 +/- 32 pg/ml) and after burst pattern stimuli (+126 +/- 30 pg/ml, n = 21). In contrast, stimulation of more ventromedial portions (layers 7-8) of nucleus caudalis had no significant effect on plasma ACTH. Stimulation of the trigeminal lateral cervical region the caudal extent of the A1 noradrenergic cell group, or the lateral reticular nucleus evoked significant peak increases in plasma ACTH regardless of stimulus pattern. Transient changes in arterial pressure accompanied brain stem stimulation and were not correlated with the changes in ACTH. The results indicate that stimulation of trigeminal subnucleus caudalis, a brain stem region that processes nociceptor afferent information, evokes a prompt increase in plasma ACTH. Stimulation of brain stem regions that process autonomic and cardiovascular afferent information (A1 region, lateral reticular nucleus) also facilitate ACTH release. No significant influence of stimulus pattern on brain stem-evoked ACTH release was seen. The results support the hypothesis that the influence of the central nervous system on ACTH release may be processed by parallel pathways at the caudal brain stem level.

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