Activation by Cutaneous or Visceral Noxious Stimulation of Spinal Neurons Projecting to the Medullary Dorsal Reticular Nucleus in the Rat: Ac-fosStudy

1997 ◽  
Vol 9 (4) ◽  
pp. 686-695 ◽  
Author(s):  
Armando Almeida ◽  
Deolinda Lima
Keyword(s):  
Reticular Nucleus ◽  
Noxious Stimulation ◽  
Spinal Neurons ◽  
Stimulation Of

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.

Anatomy and physiology of a nociceptive modulatory system

1985 ◽  
Vol 308 (1136) ◽  
pp. 361-374 ◽  
Keyword(s):  
Spinal Cord ◽  
Electrical Stimulation ◽  
Tail Flick ◽  
Noxious Stimulation ◽  
Spinal Neurons ◽  
Nociceptive Transmission ◽  
Anatomy And Physiology ◽  
Negative Feedback Circuit ◽  
Clinically Significant ◽  
Stimulation Of

Although efferent control of sensory transmission is a well-established concept, a specific network for nociceptive modulation has only recently been discovered. This network includes interconnected components at midbrain, medullary and spinal levels. At the midbrain level, electrical stimulation of the periaqueductal grey (p.a.g.) inhibits spinal neurons that respond to noxious stimuli as well as nociceptor-induced reflexes and escape behaviour in a variety of species. Midbrain stimulation also produces analgesia in patients with clinically significant pain. The rostral ventral medulla (r.v.m.) has similar behavioural and physiological effects and mediates midbrain antinociceptive actions at the level of the spinal cord. Endorphins are present at all levels of this nociceptive modulating network. Opiate microinjections at p.a.g., r.v.m. or spinal levels produce analgesia, presumably by mimicking the actions of the endorphins. The nociceptive modulatory system is diffusely organized, highly interconnected and appears to act as a unit whether activated by opiates or electrical stimulation. There are two classes of r.v.m. neurons the activity of which is correlated with the occurrence of reflexes induced by noxious stimulation. One class (the on-cell) accelerates, the other class (the off-cell) pauses just before tail flick. Both classes project to the spinal cord and are excited by electrical stimulation of the midbrain. However, when morphine is injected either systemically or into the p.a.g., the off-cell is excited and the on-cell stops firing. The off-cell is probably the r.v.m. output cell that inhibits nociceptive transmission at the level of the spinal cord. The function of the on-cell is not clear. The nociceptive modulatory system can be activated by a variety of stressful environmental factors, which are often, but not necessarily, noxious. The idea that the system acts as a simple negative feedback circuit is not consistent with its known properties.

Sympathetic activation of cat spinal neurons responsive to noxious stimulation of deep tissues in the low back

Pain ◽  
1994 ◽  
Vol 56 (1) ◽  
pp. 31-42 ◽  
Author(s):  
Richard G. Gillette ◽  
Ronald C. Kramis ◽  
William J. Roberts
Keyword(s):  
Noxious Stimulation ◽  
Low Back ◽  
Sympathetic Activation ◽  
Spinal Neurons ◽  
Stimulation Of

scholarly journals Synaptic properties of the feedback connections from the thalamic reticular nucleus to the dorsal lateral geniculate nucleus

2020 ◽  
Vol 124 (2) ◽  
pp. 404-417 ◽  
Author(s):  
Peter W. Campbell ◽  
Gubbi Govindaiah ◽  
Sean P. Masterson ◽  
Martha E. Bickford ◽  
William Guido
Keyword(s):  
Lateral Geniculate Nucleus ◽  
Dorsal Lateral Geniculate Nucleus ◽  
Thalamic Reticular Nucleus ◽  
Reticular Nucleus ◽  
Lateral Geniculate ◽  
Dependent Form ◽  
Dorsal Lateral Geniculate ◽  
Feedback Connections ◽  
Spike Firing ◽  
Stimulation Of

The thalamic reticular nucleus (TRN) modulates thalamocortical transmission through inhibition. In mouse, TRN terminals in the dorsal lateral geniculate nucleus (dLGN) form synapses with relay neurons but not interneurons. Stimulation of TRN terminals in dLGN leads to a frequency-dependent form of inhibition, with higher rates of stimulation leading to a greater suppression of spike firing. Thus, TRN inhibition appears more dynamic than previously recognized, having a graded rather than an all-or-none impact on thalamocortical transmission.

Drastic Decrease in Isoflurane Minimum Alveolar Concentration and Limb Movement Forces after Thoracic Spinal Cooling and Chronic Spinal Transection in Rats

2005 ◽  
Vol 102 (3) ◽  
pp. 624-632 ◽  
Author(s):  
Steven L. Jinks ◽  
Carmen L. Dominguez ◽  
Joseph F. Antognini
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Minimum Alveolar Concentration ◽  
Tail Flick ◽  
Noxious Stimulation ◽  
Partial Recovery ◽  
Spinal Transection ◽  
Thoracic Spinal ◽  
Cord Injury ◽  
Stimulation Of

Background Individuals with spinal cord injury may undergo multiple surgical procedures; however, it is not clear how spinal cord injury affects anesthetic requirements and movement force under anesthesia during both acute and chronic stages of the injury. Methods The authors determined the isoflurane minimum alveolar concentration (MAC) necessary to block movement in response to supramaximal noxious stimulation, as well as tail-flick and hind paw withdrawal latencies, before and up to 28 days after thoracic spinal transection. Tail-flick and hind paw withdrawal latencies were measured in the awake state to test for the presence of spinal shock or hyperreflexia. The authors measured limb forces elicited by noxious mechanical stimulation of a paw or the tail at 28 days after transection. Limb force experiments were also conducted in other animals that received a reversible spinal conduction block by cooling the spinal cord at the level of the eighth thoracic vertebra. Results A large decrease in MAC (to </= 40% of pretransection values) occurred after spinal transection, with partial recovery (to approximately 60% of control) at 14-28 days after transection. Awake tail-flick and hind paw withdrawal latencies were facilitated or unchanged, whereas reflex latencies under isoflurane were depressed or absent. However, at 80-90% of MAC, noxious stimulation of the hind paw elicited ipsilateral limb withdrawals in all animals. Hind limb forces were reduced (by >/= 90%) in both chronic and acute cold-block spinal animals. Conclusions The immobilizing potency of isoflurane increases substantially after spinal transection, despite the absence of a baseline motor depression, or "spinal shock." Therefore, isoflurane MAC is determined by a spinal depressant action, possibly counteracted by a supraspinal facilitatory action. The partial recovery in MAC at later time points suggests that neuronal plasticity after spinal cord injury influences anesthetic requirements.

scholarly journals Focal Stimulation of the Thalamic Reticular Nucleus Induces Focal Gamma Waves in Cortex

1998 ◽  
Vol 79 (1) ◽  
pp. 474-477 ◽  
Author(s):  
Kurt D. Macdonald ◽  
Eva Fifkova ◽  
Michael S. Jones ◽  
Daniel S. Barth
Keyword(s):  
Electrical Stimulation ◽  
Internal Capsule ◽  
Thalamic Reticular Nucleus ◽  
Gamma Activity ◽  
Reticular Nucleus ◽  
Cortical Arousal ◽  
Electrical Potentials ◽  
Gamma Frequency ◽  
Slow Potentials ◽  
Stimulation Of

MacDonald, Kurt D., Eva Fifkova, Michael S. Jones, and Daniel S. Barth. Focal stimulation of the thalamic reticular nucleus induces focal gamma waves in cortex. J. Neurophysiol. 79: 474–477, 1998. Electrical stimulation of the thalamic reticular nucleus (TRN; 0.5-s trains of 500-Hz 0.5-ms pulses at 5–10 μA) evokes focal oscillations of cortical electrical potentials in the gamma frequency band (∼35–55 Hz). These evoked oscillations are specific to either the somatosensory or auditory cortex and to subregions of the cortical receptotopic map, depending on what part of the TRN is stimulated. Focal stimulation of the internal capsule, however, evokes focal slow potentials, without gamma activity. Our results suggest that the TRN's role extends beyond that of general cortical arousal to include specific modality and submodality activation of the forebrain.

scholarly journals An objective approach to assess colonic pain in mice using colonometry

PLoS ONE ◽  
2021 ◽  
Vol 16 (3) ◽  
pp. e0245410
Author(s):  
Liya Y. Qiao ◽  
Jonathan Madar
Keyword(s):  
Neurological Disorders ◽  
Stretch Reflex ◽  
Distal Colon ◽  
Saline Infusion ◽  
Noxious Stimulation ◽  
Trinitrobenzene Sulfonic Acid ◽  
Primary Afferent ◽  
Reflex Pathways ◽  
Constant Rate ◽  
Stimulation Of

The present study presents a non-surgical approach to assess colonic mechanical sensitivity in mice using colonometry, a technique in which colonic stretch-reflex contractions are measured by recording intracolonic pressures during saline infusion into the distal colon in a constant rate. Colonometrical recording has been used to assess colonic function in healthy individuals and patients with neurological disorders. Here we found that colonometry can also be implemented in mice, with an optimal saline infusion rate of 1.2 mL/h. Colonometrograms showed intermittent pressure rises that was caused by periodical colonic contractions. In the sceneries of colonic hypersensitivity that was generated post 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced colonic inflammation, following chemogenetic activation of primary afferent neurons, or immediately after noxious stimulation of the colon by colorectal distension (CRD), the amplitude of intracolonic pressure (AICP) was markedly elevated which was accompanied by a faster pressure rising (ΔP/Δt). Colonic hypersensitivity-associated AICP elevation was a result of the enhanced strength of colonic stretch-reflex contraction which reflected the heightened activity of the colonic sensory reflex pathways. The increased value of ΔP/Δt in colonic hypersensitivity indicated a lower threshold of colonic mechanical sensation by which colonic stretch-reflex contraction was elicited by a smaller saline infusion volume during a shorter period of infusion time. Chemogenetic inhibition of primary afferent pathway that was governed by Nav1.8-expressing cells attenuated TNBS-induced up-regulations of AICP, ΔP/Δt, and colonic pain behavior in response to CRD. These findings support that colonometrograms can be used for analysis of colonic pain in mice.

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