Fictive locomotion and scratching inhibit dorsal horn neurons receiving thin fiber afferent input

2000 ◽  
Vol 279 (2) ◽  
pp. R394-R403 ◽  
Author(s):  
A. M. Degtyarenko ◽  
M. P. Kaufman

In decerebrate paralyzed cats, we examined the effects of two central motor commands (fictive locomotion and scratching) on the discharge of dorsal horn neurons receiving input from group III and IV tibial nerve afferents. We recorded the impulse activity of 74 dorsal horn neurons, each of which received group III input from the tibial nerve. Electrical stimulation of the mesencephalic locomotor region (MLR), which evoked fictive static contraction or fictive locomotion, inhibited the discharge of 44 of the 64 dorsal horn neurons tested. The mean depth from the dorsal surface of the spinal cord of the 44 neurons whose discharge was inhibited by MLR stimulation was 1.77 ± 0.04 mm. Fictive scratching, evoked by topical application of bicuculline to the cervical spinal cord and irritation of the ear, inhibited the discharge of 22 of the 29 dorsal horn neurons tested. Fourteen of the twenty-two neurons whose discharge was inhibited by fictive scratching were found to be inhibited by MLR stimulation as well. The mean depth from the dorsal surface of the cord of the 22 neurons whose discharge was inhibited by fictive scratching was 1.77 ± 0.06 mm. Stimulation of the MLR or the elicitation of fictive scratching had no effect on the activity of 22 dorsal horn neurons receiving input from group III and IV tibial nerve afferents. The mean depth from the dorsal surface of the cord was 1.17 ± 0.07 mm, a value that was significantly ( P < 0.05) less than that for the neurons whose discharge was inhibited by either MLR stimulation or fictive scratching. We conclude that centrally evoked motor commands can inhibit the discharge of dorsal horn neurons receiving thin fiber input from the periphery.

1993 ◽  
Vol 69 (6) ◽  
pp. 2072-2085 ◽  
Author(s):  
J. M. Laird ◽  
G. J. Bennett

1. Extracellular single-unit recordings have been made from 295 dorsal horn neurons in the lumbar enlargement of rat spinal cord; 191 neurons in 20 rats with an experimental peripheral neuropathy, and 104 in 10 sham-operated rats. Recordings were made 9-11 days after inducing the neuropathy by tying four loose ligatures around the sciatic nerve in the nerve-injured rats or performing a sham procedure in the sham-operated rats. 2. A survey of the general properties of all neurons encountered was made in the 10 sham-operated rats (104 neurons) and compared with those seen in 17 of the nerve-injured animals (180 neurons). The vast majority (87%; 156/180) of neurons recorded in the nerve-injured animals showed abnormal characteristics; these included responses to very gentle mechanical stimulation of the nerve-injury site and to manipulations that resulted in movement of this site such as extension of the leg and probing of the skin and muscle of the thigh (53%), absence of detectable peripheral receptive fields (RFs; 56%), and very high spontaneous activity (7%). In the sham-operated rats none of the neurons recorded could be activated by gentle mechanical stimulation of the sciatic nerve, and only 6% had no detectable peripheral RF. 3. In the nerve-injured animals, 31% (55/180) of cells had both a peripheral RF, and a response to gentle mechanical stimulation of the nerve-injury site. All cells of this type tested (n = 5) showed very prolonged responses (up to 10 min long) to 15 s pinch stimuli applied to the RF and to 15 s gentle tapping of the injury site. The majority of cells in this group were excited by noxious stimuli (71%; 39/55) and had C-fiber inputs (60%; 33/55). 4. The mean threshold temperatures for evoking responses to heat stimuli in cells tested in nerve-injured rats and in sham-operated animals were not different. However, there was a group of neurons in the nerve-injured rats that had low thresholds, failed to encode stimulus intensity, and did not have a C-fiber input. 5. There were significantly fewer neurons excited by low-intensity stimulation of the skin in the nerve-injured (24%; 43/180) than in the sham-operated rats (71%; 74/104). Measurements of mechanical threshold with von Frey hairs showed that, although the mean threshold did not change, none of the cells tested in the nerve-injured animals had thresholds < 12 mN, whereas the lowest threshold recorded in the sham-operated animals was 0.2 mN.(ABSTRACT TRUNCATED AT 400 WORDS)


2007 ◽  
Vol 97 (1) ◽  
pp. 871-882 ◽  
Author(s):  
Hong-Yi Zhou ◽  
Hong-Mei Zhang ◽  
Shao-Rui Chen ◽  
Hui-Lin Pan

Stimulation of nociceptive primary afferents elicits pain by promoting glutamatergic transmission in the spinal cord. Little is known about how increased nociceptive input controls GABAergic tone in the spinal dorsal horn. In this study, we determined how increased nociceptive inflow affects GABAergic spontaneous inhibitory postsynaptic currents (sIPSCs) of lamina II neurons by using whole cell recordings in rat spinal cord slices. Bath application of capsaicin for 3 min induced a long-lasting inhibition of sIPSCs in 50% of the neurons tested. In the other half of the neurons, capsaicin either increased the frequency of sIPSCs (34.6%) or had no effect on sIPSCs (15.4%). The GABAA current elicited by puff application of GABA was not altered by capsaicin. Capsaicin did not inhibit sIPSCs in rats treated with intrathecal pertussis toxin. Also, capsaicin failed to inhibit sIPSCs in the presence of ionotropic glutamate receptor antagonists or in the presence of both LY341495 and CPPG (group II and group III metabotropic glutamate receptor antagonists, respectively). However, when LY341495 or CPPG was used alone, capsaicin still decreased the frequency of sIPSCs in some neurons. Additionally, bradykinin significantly inhibited sIPSCs in a population of lamina II neurons and this inhibitory effect was also abolished by LY341495 and CPPG. Our study provides novel information that stimulation of nociceptive primary afferents rapidly suppresses GABAergic input to many dorsal horn neurons through endogenous glutamate and activation of presynaptic group II and group III metabotropic glutamate receptors. These findings extend our understanding of the microcircuitry of the spinal dorsal horn involved in nociception.


2005 ◽  
Vol 94 (1) ◽  
pp. 845-851 ◽  
Author(s):  
Arun K. Senapati ◽  
Stacey C. Lagraize ◽  
Paula J. Huntington ◽  
Hilary D. Wilson ◽  
Perry N. Fuchs ◽  
...  

The anterior cingulate cortex (ACC) is involved in the affective and motivational aspect of pain perception. Behavioral studies show a decreased avoidance behavior to noxious stimuli without change in mechanical threshold after stimulation of the ACC. However, as part of the neural circuitry of behavioral reflexes, there is no evidence showing that ACC stimulation alters dorsal horn neuronal responses. We hypothesize that ACC stimulation has two phases: a short-term phase in which stimulation elicits antinociception and a long-term phase that follows stimulation to change the affective response to noxious input. To begin testing this hypothesis, the purpose of this study was to examine the response of spinal cord dorsal horn neurons during stimulation of the ACC. Fifty-eight wide dynamic range spinal cord dorsal horn neurons from adult Sprague-Dawley rats were recorded in response to graded mechanical stimuli (brush, pressure, and pinch) at their respective receptive fields, while simultaneous stepwise electrical stimulations (300 Hz, 0.1 ms, at 10, 20, and 30 V) were applied in the ACC. The responses to brush at control, 10, 20, and 30 V, and recovery were 14.2 ± 1.4, 12.3 ± 1.2, 10.9 ± 1.2, 10.3 ± 1.1, and 14.1 ± 1.4 spikes/s, respectively. The responses to pressure at control, 10, 20, and 30 V, and recovery were 39.8 ± 4.7, 25.6 ± 3.0, 25.0 ± 3.0, 21.6 ± 2.4, and 34.2 ± 3.7 spikes/s, respectively. The responses to pinch at control, 10, 20, and 30 V, and recovery were 40.7 ± 3.8, 30.6 ± 3.1, 27.8 ± 2.8, 27.2 ± 3.2, and 37.4 ± 3.9 spikes/s, respectively. We conclude that electrical stimulation of the ACC induces significant inhibition of the responses of spinal cord dorsal horn neurons to noxious mechanical stimuli. The stimulation-induced inhibition begins to recover as soon as the stimulation is terminated. These results suggest differential short-term and long-term modulatory effects of the ACC stimulation on nociceptive circuits.


2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Rebecca Rani Das Gupta ◽  
Louis Scheurer ◽  
Pawel Pelczar ◽  
Hendrik Wildner ◽  
Hanns Ulrich Zeilhofer

AbstractThe spinal dorsal horn harbors a sophisticated and heterogeneous network of excitatory and inhibitory neurons that process peripheral signals encoding different sensory modalities. Although it has long been recognized that this network is crucial both for the separation and the integration of sensory signals of different modalities, a systematic unbiased approach to the use of specific neuromodulatory systems is still missing. Here, we have used the translating ribosome affinity purification (TRAP) technique to map the translatomes of excitatory glutamatergic (vGluT2+) and inhibitory GABA and/or glycinergic (vGAT+ or Gad67+) neurons of the mouse spinal cord. Our analyses demonstrate that inhibitory and excitatory neurons are not only set apart, as expected, by the expression of genes related to the production, release or re-uptake of their principal neurotransmitters and by genes encoding for transcription factors, but also by a differential engagement of neuromodulator, especially neuropeptide, signaling pathways. Subsequent multiplex in situ hybridization revealed eleven neuropeptide genes that are strongly enriched in excitatory dorsal horn neurons and display largely non-overlapping expression patterns closely adhering to the laminar and presumably also functional organization of the spinal cord grey matter.


2004 ◽  
Vol 48 (2) ◽  
pp. 175-184
Author(s):  
M Björklund ◽  
S Radovanovic ◽  
M Ljubisavljevic ◽  
U Windhorst ◽  
H Johansson

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