Blocking interactions between brain-stem reflex facilitation and sympathetic reflex enhancement

1959 ◽  
Vol 196 (3) ◽  
pp. 669-673 ◽  
Author(s):  
H. B. Kelly ◽  
L. M. N. Bach

In cats anesthetized with Nembutal the integrity of the lumbar sympathetic chain is necessary for the maintenance of the normal basal height of the patellar reflex. The centrally activated sympathetic component of brain stem enhancement of the patellar reflex is consistently and totally abolished by either surgical or chemical interference with the sympathetic supply to the hind leg. Although the use of sympatholytic drugs does not affect (presumably) synaptic facilitation of reflex activity resulting from brain stem reticular stimulation, mechanical stimulation of either the lumbar sympathetic or splanchnic nerves will cause a temporary but marked depression of this facilitation. Simultaneous stimulation of either the lumbar sympathetic or splanchnic nerves completely and consistently blocks the facilitatory effects of brain stem reticular stimulation. Conversely, simultaneous stimulation of the brain stem reticular formation consistently and totally blocks the enchancement of the patellar reflex which results from stimulation of the peripheral lumbar sympathetic or splanchnic nerves. The former phenomenon does not result from any peripheral locus of interaction between adrenaline and the innervation of the quadriceps muscle. Cross perfusion experiments indicate that the locus of interaction may involve the brain stem reticular formation.

1984 ◽  
Vol 246 (3) ◽  
pp. R389-R395 ◽  
Author(s):  
P. A. Femano ◽  
S. Schwartz-Giblin ◽  
D. W. Pfaff

Lumbar axial muscle responses to electrical stimulation of the brain stem reticular formation were used to characterize reticular influences on these muscles. Electromyographic recordings were obtained from the transversospinalis, medial longissimus, and lateral longissimus systems in the urethan-anesthetized rat. Ipsilateral stimulation of the pontomedullary reticular formation evoked excitatory responses in these muscles. Trains of pulses were required, but currents as low as 15 microA were effective. Contralateral reticular stimulation with currents similar to those that elicited activation during ipsilateral stimulation at the same brain stem levels could inhibit lumbar electromyographic activity. The results suggest that the motoneurons innervating the lumbar axial musculature in the rat receive strong reticulospinal influences that could be important for postural maintenance and the expression of certain behaviors.


1983 ◽  
Vol 50 (4) ◽  
pp. 743-769 ◽  
Author(s):  
P. Rudomin ◽  
I. Jimenez ◽  
M. Solodkin ◽  
S. Duenas

The present series of investigations was aimed to disclose the possible sites of action of excitatory and inhibitory inputs on tho-interneuron pathway mediating the primary afferent depolarization (PAD) of group I afferents of extensor muscles in the cat spinal cord. To this end we compared the effects produced by stimulation of segmental and descending pathways on the PAD generated either by stimulation of group I fibers of flexor muscles or by intraspinal microstimulation. It was assumed that under the appropriate conditions the PAD produced by intraspinal microstimulation results from the activation of the last-order interneurons in the PAD pathway and may, therefore, allow detection pathway. The PAD of single group I afferent fibers was determined in barbiturate-anesthetized preparations by measuring the test stimulus current required to maintain a constant probability of antidromic firing. This was achieved by means of a feedback system that continuously adjusted the test stimulus current to the required values. The PAD of individual group Ia gastrocnemius soleus (GS) fibers that is produced by activation of the low-threshold afferents of the posterior biceps and semitendinosus nerve was found to be inhibited by conditioning stimulation of the relatively low-threshold cutaneous fibers and also by stimulation of supraspinal structures such as the ipsilateral brain stem reticular formation, the contralateral red nucleus, and the contralateral pyramidal tract. In contrast, the PAD of group Ia fibers produced by microstimulation applied in the intermediate nucleus could be inhibited only by stimulation of the brain stem reticular formation but not by stimulation of the other descending inputs presently tested or by stimulation of cutaneous nerves. PAD of group Ia fibers was produced also by microstimulation applied within the motor nucleus. However, in most fibers the resulting PAD could not be inhibited either by stimulation of the brain stem reticular formation, the red nucleus, the pyramidal tract, or cutaneous nerves. Stimulation of cutaneous and of flexor muscle nerves of the brain stem reticular formation, the red nucleus, and the pyramidal tract all produced PAD of the group Ib GS fibers.(ABSTRACT TRUNCATED AT 400 WORDS)


2000 ◽  
Vol 84 (4) ◽  
pp. 1942-1948 ◽  
Author(s):  
T. Hajnik ◽  
Y. Y. Lai ◽  
J. M. Siegel

Electrical stimulation of circumscribed areas of the pontine and medullary reticular formation inhibits muscle tone in cats. In this report, we present an analysis of the anatomical distribution of atonia-inducing stimulation sites in the brain stem of the rat. Muscle atonia could be elicited by electrical stimulation of the nuclei reticularis pontis oralis and caudalis in the pons as well as the nuclei gigantocellularis, gigantocellularis alpha, gigantocellularis ventralis, and paragigantocellularis dorsalis in the medulla of decerebrate rats. This inhibitory effect on muscle tone was a function of the intensity and frequency of the electrical stimulation. Average latencies of muscle-tone suppressions elicited by electrical stimulation of the pontine reticular formation were 11.02 ± 2.54 and 20.49 ± 3.39 (SD) ms in the neck and in the hindlimb muscles, respectively. Following medullary stimulation, these latencies were 11.29 ± 2.44 ms in the neck and 18.87 ± 2.64 ms in the hindlimb muscles. Microinjection of N-methyl-d-aspartate (NMDA, 7 mM/0.1 μl) agonists into the pontine and medullary inhibitory sites produced muscle-tone facilitation, whereas quisqualate (10 mM/0.1 μl) injection induced an inhibition of muscle tone. NMDA-induced muscle tone change had a latency of 31.8 ± 35.3 s from the pons and 10.5 ± 0.7 s from the medulla and a duration of 146.7 ± 95.2 s from the pons and 55.5 ± 40.4 s from the medulla. The latency of quisqualate (QU)-induced reduction of neck muscle tone was 30.1 ± 37.9 s after pontine and 39.5 ± 21.8 s after medullary injection. The duration of muscle-tone suppression induced by QU injection into the pons and medulla was 111.5 ± 119.2 and 169.2 ± 145.3 s. Smaller rats (8 wk old) had a higher percentage of sites producing muscle-tone inhibition than larger rats (16 wk old), indicating an age-related change in the function of brain stem inhibitory systems. The anatomical distribution of atonia-related sites in the rat has both similarities and differences with the distribution found in the cat, which can be explained by the distinct anatomical organization of the brain stem in these two species.


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