Sites of action of segmental and descending control of transmission on pathways mediating PAD of Ia- and Ib-afferent fibers in cat spinal cord

1983 ◽  
Vol 50 (4) ◽  
pp. 743-769 ◽  
Author(s):  
P. Rudomin ◽  
I. Jimenez ◽  
M. Solodkin ◽  
S. Duenas
Keyword(s):  
Brain Stem ◽  
Reticular Formation ◽  
Pyramidal Tract ◽  
Red Nucleus ◽  
Intraspinal Microstimulation ◽  
Group I ◽  
Afferent Fibers ◽  
Sites Of Action ◽  
The Brain ◽  
Stimulation Of

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)

Brain stem responses to electrical stimulation of ventral vagal gastric fibers

1989 ◽  
Vol 257 (1) ◽  
pp. G24-G29
Author(s):  
W. D. Barber ◽  
C. S. Yuan
Keyword(s):  
Electrical Stimulation ◽  
Brain Stem ◽  
Time Of Arrival ◽  
Neuronal Responses ◽  
Proximal Stomach ◽  
Afferent Fibers ◽  
Sensory Modalities ◽  
The Mean ◽  
The Brain ◽  
Stimulation Of

The brain stem neuronal responses to electrical stimulation of gastric branches of the ventral vagal trunk serving the proximal stomach were localized and evaluated in anesthetized cats. The responses were equally distributed bilaterally in the region of nucleus solitarius in the caudal brain stem. The mean latency of the response was 289 +/- 46 (SD) ms, which translated into a conduction velocity of less than 1 m/s based on the distance between the stimulating and recording electrodes. The responses consisted of single and multiple spikes that showed slight variability in the latency, indicating orthodromic activation via a synapse in approximately 98% of the responses recorded. Forty two percent of the units tested showed evidence of convergence of input from vagal afferent fibers in different branches of the ventral vagal trunk that served the proximal stomach. The resultant activity pattern of the unitary response appeared to be the product of 1) the gastric sensory input or modality conveyed by the afferent source and 2) the time of arrival and diversity of modalities served by other gastric afferents impinging on the unit. This provides a mechanism capable of responding on the basis of specific sensory modalities that dynamically reflect ongoing events monitored and conveyed by other gastric afferents in the region.

scholarly journals Effects of cholecystokinin-8s in the nucleus tractus solitarius of vagally deafferented rats

2007 ◽  
Vol 292 (3) ◽  
pp. R1092-R1100 ◽  
Author(s):  
V. Baptista ◽  
K. N. Browning ◽  
R. A. Travagli
Keyword(s):  
Brain Stem ◽  
Nucleus Tractus Solitarius ◽  
Glutamate Release ◽  
Intraperitoneal Administration ◽  
Whole Cell Patch Clamp ◽  
Afferent Fibers ◽  
Vagal Afferent ◽  
Sites Of Action ◽  
The Brain ◽  
Brain Stem Slices

We have shown recently that cholecystokinin octapeptide (CCK-8s) increases glutamate release from nerve terminals onto neurons of the nucleus tractus solitarius pars centralis (cNTS). The effects of CCK on gastrointestinal-related functions have, however, been attributed almost exclusively to its paracrine action on vagal afferent fibers. Because it has been reported that systemic or perivagal capsaicin pretreatment abolishes the effects of CCK, the aim of the present work was to investigate the response of cNTS neurons to CCK-8s in vagally deafferented rats. In surgically deafferented rats, intraperitoneal administration of 1 or 3 μg/kg CCK-8s increased c-Fos expression in cNTS neurons (139 and 251% of control, respectively), suggesting that CCK-8s' effects are partially independent of vagal afferent fibers. Using whole cell patch-clamp techniques in thin brain stem slices, we observed that CCK-8s increased the frequency of spontaneous and miniature excitatory postsynaptic currents in 43% of the cNTS neurons via a presynaptic mechanism. In slices from deafferented rats, the percentage of cNTS neurons receiving glutamatergic inputs responding to CCK-8s decreased by ∼50%, further suggesting that central terminals of vagal afferent fibers are not the sole site for the action of CCK-8s in the brain stem. Taken together, our data suggest that the sites of action of CCK-8s include the brain stem, and in cNTS, the actions of CCK-8s are not restricted to vagal central terminals but that nonvagal synapses are also involved.

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
Keyword(s):  
Brain Stem ◽  
Reticular Formation ◽  
Quadriceps Muscle ◽  
Chemical Interference ◽  
Simultaneous Stimulation ◽  
Splanchnic Nerves ◽  
Peripheral Locus ◽  
The Brain ◽  
Brain Stem Reflex ◽  
Stimulation Of

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.

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