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PubMed1992

Responses of spinothalamic tract neurons to mechanical and thermal stimuli in an experimental model of peripheral neuropathy in primates.

1. An experimental peripheral neuropathy (EPN) was induced in three monkeys (Macaca fascicularis) by ligation of spinal nerve L7. Behavioral responses to innocuous mechanical stimuli were tested before and after the surgery. Two weeks after the nerve ligation, the activity of spinothalamic tract (STT) neurons was recorded on both sides of the spinal cord with the animal under general anesthesia. Responses of the STT neurons to the following stimuli applied to the skin were recorded: graded mechanical stimuli (brush, press, pinch and squeeze), von Frey filaments of different bending forces (0.077-19.05 g), 5-s heat stimuli ranging from 39 to 53 degrees C, and 15 s cold stimuli (32-8 degrees C). 2. Innocuous mechanical stimulation of the foot did not evoke hindlimb withdrawal in the animals before surgery. Within 24-48 h after nerve ligation, the animals showed hindlimb withdrawal to the same innocuous stimuli. This behavior was more pronounced on the side of the ligation than on the sham-operated side and more frequent during the second week after the surgery. 3. Responses of 51 STT neurons recorded on the side of the ligation (EPN all group) were compared with responses of 33 STT cells recorded on the sham-operated side (control group) and with records from STT neurons in unoperated animals obtained earlier (reference group). Neurons from the EPN all group were divided into two sets according to their rostrocaudal location (EPN R, rostral to L6/7 border, n = 40; EPN C, caudal to L6/7 border, n = 11). 4. Neurons from the EPN all and EPN R groups had significantly higher background frequencies than those from the control and reference groups. Innocuous brush stimuli evoked mean discharge frequencies of approximately 35 Hz in EPN R neurons and only approximately 15 Hz in both control and reference groups. Increased responsiveness of EPN R neurons to innocuous stimuli was also demonstrated by lower thresholds and higher discharge frequencies to von Frey filament stimulation and by discriminative analysis of the responses evoked by graded mechanical stimuli. 5. The responses of the EPN R neurons to heat stimulation of the skin showed decreased thresholds and increased responses to suprathreshold stimuli, resulting in a significant leftward shift of the stimulus-response curve compared with both reference and control groups. The neurons from the control group showed responses comparable to reference group values. 6. Neurons from the reference group tested with the cooling stimuli showed no evoked response above background.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

PubMed1978

Spinothalamic tract neurons in the substantia gelatinosa.

The substantia gelatinosa of the mammalian spinal cord is generally believed to be a closed system; that is its neurons are thought to project only to the substantia gelatinosa of the same or the contralateral side. Experiments in monkeys, using injections of the marker enzyme horseradish peroxidase, show that at least some neurons of the substantia gelatinosa project to the thalamus and thus belong to the spinothalamic tract. Such neurons include two cell types intrinsic to the gelatinosa, the central cells and the limitrophe cells of Cajal.

Animals↗

PubMed2002

Role of protein kinase A in phosphorylation of NMDA receptor 1 subunits in dorsal horn and spinothalamic tract neurons after intradermal injection of capsaicin in rats.

Protein phosphorylation is a major mechanism for regulation of N-methyl-D-aspartate (NMDA) receptor function. The NMDA receptor 1 subunit (NR1) is phosphorylated by protein kinase A (PKA) on serine 890 and 897. We have recently reported that there is enhanced phosphorylation of NR1 on serine 897 in dorsal horn and spinothalamic tract (STT) neurons after intradermal injection of capsaicin (CAP) in rats [Zou et al. (2000) J. Neurosci. 20, 6989-6997]. Whether or not this phosphorylation, which develops during central sensitization following CAP injection, is mediated by PKA remains to be determined. In this study, western blots and immunofluorescence staining were employed to observe if pretreatment with a PKA inhibitor, N-[2-((p-bromocinnamyl)amino)ethyl]-5-isoquinolinesulfonamide, HCl (H89), blocks the enhanced phosphorylation of NR1 on serine 897 following injection of CAP into the glabrous skin of one hind paw of anesthetized rats. Western blots showed that pretreatment with H89 caused a decrease in CAP-induced phosphorylation of NR1 protein in spinal cord segments L(4)-S(1). In experiments using immunofluorescence staining, the numbers of phospho-NR1-like immunoreactive (p-NR1-LI) neurons seen after CAP injection were significantly decreased in the dorsal horn of the L(4)-L(5) segments on the side ipsilateral to the injection after PKA was inhibited. When STT cells were labeled by microinjection of the retrograde tracer, fluorogold, we found that the proportion of p-NR1-LI STT cells on the side ipsilateral to the injection in the superficial laminae of spinal cord segments L(4)-L(5) was markedly reduced when H89 was administered intrathecally before CAP injection. However, the proportion of p-NR1-LI STT cells in deep laminae was unchanged unless the PKC inhibitor, chelerythrine chloride, was co-administered with H89. Combined with our previous findings, the present results indicate that NR1 in spinal dorsal horn neurons, including the superficial dorsal horn STT cells, is phosphorylated following CAP injection and that this phosphorylation is due to the action of PKA. However, the phosphorylation of deep STT cells involves both PKA and PKC.

Animals↗

PubMed2002

Hypersensitivity of spinothalamic tract neurons associated with diabetic neuropathic pain in rats.

Diabetic neuropathic pain is often considered to be caused by peripheral neuropathy. The involvement of the CNS in this pathological condition has not been well documented. Development of hypersensitivity of spinal dorsal horn neurons is involved in neuropathic pain induced by traumatic nerve injury. In the present study, we determined the functional changes of identified spinothalamic tract (STT) neurons and their correlation to diabetic neuropathic pain. Diabetes was induced in rats by intraperitoneal injection of streptozotocin. Hyperalgesia and allodynia were assessed by the withdrawal responses to pressure, radiant heat, and von Frey filaments applied to the hindpaw. Single-unit activity of STT neurons was recorded from the lumbar spinal cord in anesthetized rats. The responses of STT neurons to mechanical and thermal stimuli and the sensitivity to intravenous morphine were determined in diabetic and normal rats. In 12 diabetic rats, mechanical allodynia and hyperalgesia, but not thermal hyperalgesia, developed within 2 wk after streptozotocin injection and lasted for >/=7 wk. Compared to the 32 STT neurons recorded in normal animals, the 37 STT neurons in diabetic rats displayed a higher spontaneous discharge activity and enlarged receptive fields. Also, the STT neurons in diabetic rats exhibited lower thresholds and augmented responses to mechanical stimulation. Intravenous injection of 2.5 mg/kg of morphine suppressed significantly the responses of STT neurons to noxious stimuli in 12 nondiabetic rats. However, such an inhibitory effect of morphine on the evoked response of STT neurons was diminished in 14 diabetic animals. This electrophysiological study provides new information that development of hypersensitivity of spinal dorsal horn projection neurons may be closely related to neuropathic pain symptoms caused by diabetes. Furthermore, the attenuated inhibitory effects of morphine on evoked responses of STT neurons in diabetes likely accounts for its reduced analgesic efficacy in this clinical form of neuropathic pain.

Analgesics, Opioid↗

PubMed1996

Inhibition of primate spinothalamic tract neurons by spinal glycine and GABA is reduced during central sensitization.

1. In our previous work, we demonstrated that the glycinergic and GABAergic mechanisms that help mediate the descending inhibition from the periaqueductal gray exert a tonic modulation of nociceptive inputs through spinal glycine and gamma-aminobutyric acid (GABA) receptors. This study was designed to examine further possible changes in the inhibition of the activity of spinothalamic tract (STT) neurons mediated by spinal glycine and GABA receptors when STT cells are sensitized by intradermal injection of capsaicin, and to investigate the role of the protein kinase C (PKC) system in the functional modulation of these receptors. 2. Although the responses of STT cells to cutaneous mechanical stimuli were sensitized by intradermal injection of capsaicin, the inhibition of the responses of all STT cells tested to noxious cutaneous stimuli produced by iontophoretic release of glycine and GABA was significantly attenuated. The inhibition elicited by iontophoretic application of a GABAA agonist, muscimol, was reduced in some of the cells tested. 3. When the spinal cord dorsal horn was pretreated with a selective PKC inhibitor, 2,6-diamino-N-([1-oxotridecyl-2-piperidinyl]- methyl)hexanamide, by microdialysis, sensitization of STT cells by capsaicin injection and the accompanying attenuation of glycine- and GABA-induced inhibition were prevented. 4. Sensitization of STT cells to cutaneous mechanical stimuli was also induced by administration of the PKC activator, 12-O-tetradecanoylphorbol-13-acetate, into the spinal dorsal horn. The inhibition produced by iontophoretic release of glycine, GABA, and muscimol was found to be reduced in most cells examined when this phorbol ester was used. An inactive phorbol ester, 4 alpha-phorbol 12,13-didecanoate, did not produce significant effects on cellular activity. 5. These results suggest that there is an activation of PKC in the spinal cord when STT neurons are sensitized after intradermal injection of capsaicin or administration of phorbol ester. This sensitization is likely to be involved in the development of allodynia and secondary hyperalgesia not only by enhancing the responses of excitatory amino acid receptors but also by desensitizing glycine and GABA receptors.

Animals↗

PubMed1992

Enhanced responses of spinothalamic tract neurons to excitatory amino acids accompany capsaicin-induced sensitization in the monkey.

Sensitization of the responses of dorsal horn neurons to mechanical stimulation may play a role in the generation of hyperalgesia. Intradermal injection of capsaicin (CAP) provides a model of experimental hyperalgesia that possesses a component of allodynia. This hyperalgesia is produced by chemical stimulation of C-fibers, leading to sensitization of dorsal horn neurons, including spinothalamic tract (STT) cells. The changes in the physiological responses of STT neurons following intradermal CAP in monkeys parallel the acute pain and hyperalgesia produced by intradermal CAP in humans. The present study addresses the role that excitatory amino acids (EAAs) may play in the sensitization of STT neurons by intradermal CAP. Our results show that the background discharge rate and the responses of STT cells to mechanical stimulation increase following intradermal CAP. In addition, the responses of the sensitized cells to one or more iontophoretically released EAA agonists, including NMDA, glutamate, aspartate, kainate, DL-alpha-amino-3-hydroxy-5-methyl-isoxazoleproprionic acid, and/or quisqualate, increase following intradermal CAP. It is proposed that an increase in the responses of STT neurons to EAAs contributes to the hyperalgesia produced by this noxious chemical stimulus.

Amino Acids↗

PubMed1997

Capsaicin-induced sensitization of primate spinothalamic tract cells is prevented by a protein kinase C inhibitor.

Protein kinase C (PKC) has been shown to be involved in nociceptive transmission in the spinal cord. This study tested the hypothesis that induction of central sensitization in the dorsal horn by an intradermal capsaicin injection involves activation of PKC. A PKC inhibitor (NPC15437) was infused through a microdialysis fiber into the spinal cord prior to capsaicin injection. The responses of spinothalamic tract (STT) cells were recorded before and after infusion of NPC15437, and after injection of capsaicin. STT cells show an increased background activity and increased responses to innocuous stimuli following capsaicin injection while responses to heat are decreased. Spinal infusion of the PKC inhibitor, NPC15437, had no effect on background activity or responses to peripherally applied stimuli prior to capsaicin injection. However, NPC15437 prevented the sensitization of cells to weak mechanical stimuli (brush and pressure) that occurs following capsaicin injection. NPC15437 had no effect on the increased background activity or decreased responses to heat stimuli induced by capsaicin injection, suggesting alternative mechanisms for these responses. These data suggest that PKC is important for the development of central sensitization to peripheral mechanical stimuli.

Animals↗

PubMed1996

Possible role of protein kinase C in the sensitization of primate spinothalamic tract neurons.

The responsiveness of spinal cord nociceptive neurons to innocuous mechanical stimuli can be increased by the release of excitatory amino acids (EAAs) and peptides attributable to an injury-induced barrage of impulses. This sensitization of spinal dorsal horn neurons can also result from administration of phorbol ester by microdialysis, presumably by direct activation of protein kinase C (PKC). This study was designed to examine the effects of central sensitization of spinothalamic tract (STT) neurons produced by intradermal injection of capsaicin on the descending inhibition driven from the periaqueductal gray (PAG) and the possible role of PKC in this process in anesthetized monkeys. Sensitization of responses of STT cells to mechanical stimuli was induced by intradermal injection of capsaicin. PAG inhibition was significantly attenuated when sensitization of responses to mechanical stimuli occurred. However, perfusion of the spinal cord with NPC15437 (a selective PKC inhibitor) by microdialysis could prevent the sensitization of the responses to mechanical stimuli and the reduction in PAG inhibition of these responses induced by capsaicin injection. Results similar to those produced by capsaicin injection were observed when a PKC activator, phorbol ester (12-O-tetradecanoylphorbol-13-acetate), was infused within the dorsal horn by microdialysis. An inactive phorbol ester (4 alpha-phorbol 12,13-didecanoate) had no effect. These results provide evidence that the activation of PKC contributes to the development of central sensitization in dorsal horn neurons produced by chemical stimulation with capsaicin. Attenuation of the effectiveness of PAG inhibition takes place when the sensitization of dorsal horn cells develops, and PKC may play a significant role in this process.

Animals↗

PubMed2004

Effect of protein kinase C blockade on phosphorylation of NR1 in dorsal horn and spinothalamic tract cells caused by intradermal capsaicin injection in rats.

We have previously reported that protein kinase A (PKA) is involved in the phosphorylation of NR1 subunits of N-methyl-d-aspartate (NMDA) receptors in dorsal horn neurons after intradermal injection of capsaicin (CAP). To see if protein kinase C (PKC) also participates in the phosphorylation of NR1, we used electron microscopic techniques to determine further where the phosphorylated NR1 subunits (pNR1) are expressed in the spinothalamic tract (STT) cells and immunohistochemistry to examine whether a PKC inhibitor, chelerythrine chloride, blocks the enhanced phosphorylation of NR1 on serine 896. The pNR1 subunits were in the soma and dendrites of STT cells and in presynaptic endings. Western blots showed that pretreatment with the PKC inhibitor caused a decrease in CAP-induced phosphorylation of NR1 protein. In immunofluorescence staining, the number of pNR1-like immunoreactive neurons was significantly decreased on the side ipsilateral to the injection when chelerythrine chloride was administered intrathecally before CAP injection. In addition, when STT cells were labeled by microinjection of the retrograde tracer, fluorogold (FG), into the thalamus, we found that the proportion of p-NR1-LI STT cells was markedly reduced after PKC inhibition. Combined with our previous findings, these results strongly suggest that NR1 subunits in spinal dorsal horn neurons are phosphorylated following CAP injection, and this phosphorylation is catalyzed by PKC, as well as by PKA.

Alkaloids↗

PubMed2002

Increased expression of metabotropic glutamate receptor subtype 1 on spinothalamic tract neurons following spinal cord injury in the rat.

Spinal cord injury (SCI) leads to an increase in metabotropic glutamate receptor subtype 1 (mGluR1) immunoreactivity in the peri-lesion area. The increased expression of mGluR1 parallels the development of thermal hyperalgesia and mechanical allodynia and has been suggested to contribute to the development and maintenance of chronic central pain (CCP) syndromes resulting from SCI. However, expression of mGluR1 has not been directly shown to increase on cells in the pain pathway. Therefore, the expression of mGluR1 on spinothalamic tract (STT) neurons was quantified using confocal imaging and densiometric analysis in normal, sham, and SCI rats. Contusion SCI produced an increase in mGluR1 expression on STT cells in both the cervical enlargement and the spinal section just rostral to contusion SCI. These results suggest that mGluR1 is expressed on neurons that modulate pain transmission and expression on these cells increases following injury, supporting the hypothesis that mGluR1 contributes to CCP following SCI.

Animals↗

PubMed2005

TrkB expression and phospho-ERK activation by brain-derived neurotrophic factor in rat spinothalamic tract neurons.

Brain-derived neurotrophic factor (BDNF) is a neurotrophin implicated in the phenomena of synaptic plasticity in the adult. It is found in terminals of nociceptive primary afferents. Following a pain-related stimulus, it is released in the spinal cord, where it activates its high-affinity receptor TrkB, leading to the phosphorylation of the mitogen-activated protein kinase (MAPK) extracellular signal-regulated kinase (ERK). A large body of evidence suggests that BDNF has a positive neuromodulatory effect on glutamate transmission in the spinal cord. However, none of these studies examined anatomically whether projection neurons known to be involved in transmission of nociceptive inputs express BDNF's receptor. Because the spinothalamic tract (STT) is a well-characterized pathway for its role in the transfer and integration of sensory and nociceptive informations, this study in rats aimed to 1) determine whether neurons of the STT pathway express the TrkB receptor, 2) establish the rostrocaudal and laminar distribution of STT-TrkB neurons in the whole spinal cord, and 3) test the potential functionality of TrkB expression in these cells by investigating the ability of BDNF to activate the MAP kinase ERK. Using tract tracing coupled to immunofluorescent labeling for TrkB, we observed that in all levels of the spinal cord most STT neurons were immunoreactive for TrkB. Furthermore, microinjections of BDNF into the spinal cord or release of endogenous BDNF by intraplantar injection of capsaicin activated ERK phosphorylation in TrkB-containing STT neurons. These data suggest an important role for BDNF in nociception as an activator of spinothalamic projection neurons.

Animals↗

PubMedDate not supplied

Upregulation of the phosphorylated form of CREB in spinothalamic tract cells following spinal cord injury: relation to central neuropathic pain.

Spinal cord injury (SCI) often leads to the generation of chronic intractable neuropathic pain. The mechanisms that lead to chronic central neuropathic pain (CNP) following SCI are not well understood, resulting in ineffective treatments for pain relief. Studies have demonstrated persistent hyperexcitability of dorsal horn neurons which may provide a substrate for CNP. We propose a number of similarities between CNP mechanisms and mechanisms that occur in long-term potentiation, in which hippocampal neurons are hyperexcitable. One biochemical similarity may be activation of the transcription factor, cyclic AMP response element-binding protein (CREB), via phosphorylation (pCREB). The current study was designed to examine whether tactile allodynia that develops in segments rostral to SCI (at-level pain) correlates with an increase in CREB phosphorylation in specific neurons known to be involved in allodynia, the spinothalamic tract (STT) cells. This study determined that, in animals experiencing at-level allodynia 35 days after SCI, pCREB was upregulated in the spinal cord segment rostral to the injury. In addition, pCREB was found to be upregulated specifically in STT cells in the rostral segment 35 days after SCI. These findings suggest one mechanism of maintained central neuropathic pain following SCI involves persistent upregulation of pCREB expression within STT cells.

Analysis of Variance↗

PubMed1991

Effects of vagal afferent stimulation on cervical spinothalamic tract neurons in monkeys.

The purpose of this study was to determine if electrical stimulation of vagal afferents inhibited activity of primate spinothalamic tract (STT) neurons located in cervical segments of the spinal cord. Previous studies show vagal inhibition of STT neurons in more caudal segments of the cord, which receive visceral spinal inputs and somatic inputs from proximal body regions. We hypothesized that activation of vagal afferents would inhibit cervical STT neurons that were excited by cardiopulmonary sympathetic afferents and not inhibit those cells inhibited or unaffected by this visceral input. Because visceral pain is referred to proximal somatic fields, we also hypothesized that STT neurons with excitatory somatic fields confined to distal areas would not be inhibited by vagal stimulation. In 42 cervical STT neurons, we found no difference in effects of vagal stimulation between cells excited or not excited by stimulation of cardiopulmonary sympathetic afferents. Responses to vagal stimulation also were the same for cervical STT cells with proximal or distal somatic fields. Furthermore, there was no difference in the inhibitory effects of vagal stimulation in cervical as compared to thoracic STT neurons. We concluded that vagal afferent stimulation causes a general inhibitory effect at all levels of the spinal cord on neurons which transmit nociceptive information.

Animals↗

PubMed1991

Inhibitory effects of phrenic afferent fibers on primate lumbosacral spinothalamic tract neurons.

Studies were conducted to determine if electrical or mechanical stimulation of phrenic afferent fibers (PHR) would inhibit the activity of lumbosacral spinothalamic tract (STT) neurons. Twelve monkeys were anesthetized, paralyzed, and artificially ventilated. Extracellular action potentials were recorded from 78 STT neurons located in L2-S3 spinal segments. Electrical stimulation of PHR reduced the activity of 65%, did not affect 33%, and excited 1% of STT neurons. Mechanical stimulation of the diaphragm reduced the activity of 63%, did not effect 34%, and excited 1% of lumbosacral STT neurons. Distention of the urinary bladder (UBD) inhibited 52%, did not affect 23%, excited 23%, and elicited a biphasic response in 1% of STT neurons. However, there was no correlation between the effect of PHR and UBD or somatic classification of the neurons. We conclude that electrical or mechanical stimulation of PHR can produce a generalized inhibition of lumbosacral STT neurons. This inhibitory effect of PHR is similar to inhibitory effects reported for a variety of other afferent systems.

Action Potentials↗

PubMed1991

Effects of electrical stimulation of vagal afferents on spinothalamic tract cells in the rat.

The effects of electrical stimulation of cervical vagal afferents (VAS) on the background activity and on the responses of 25 spinothalamic tract (STT) neurons to noxious stimuli were studied in anesthetized rats. Background (spontaneous) activity of 9 (36%) STT neurons was inhibited by all intensities of VAS. 6 (24%) units were facilitated at lesser and inhibited at greater intensities of VAS, 5 (20%) units were only facilitated by all intensities of VAS, and 5 (20%) units were not affected by VAS. Responses of 8 (36%) STT neurons to noxious stimuli were only inhibited by VAS, 9 (41%) were facilitated at lesser and inhibited at greater intensities of VAS, and 5 units (23%) were only facilitated by VAS. There were no significant differences in VAS-produced modulatory effects between STT neurons and 16 unidentified lumbar spinal dorsal horn neurons studied under the same conditions. These results reveal that descending facilitatory and inhibitory pathways engaged by activation of vagal afferents modulate rostrally projecting nociceptive transmission neurons in the spinal cord, constituting an important regulatory network for nociception.

Anesthesia↗

PubMed1991

Short-latency excitatory postsynaptic potentials are evoked in primate spinothalamic tract neurons by corticospinal tract volleys.

The responses of 8 wide-dynamic-range (WDR) STT neurons to electrical stimulation of the sensorimotor cortex or the cerebral peduncle were recorded intracellularly in anesthetized monkeys. EPSPs and spikes were evoked in STT neurons with short latencies ranging from 0.4 to 5.3 msec after the corticospinal volley, indicating a monosynaptic connection in at least some STT neurons. Spatial and temporal summation seem necessary for the cortex to maintain an effective excitatory influence on STT neurons. It is postulated that the cortical facilitation of STT neurons helps them to acquire more nociceptive signals during behavioral tasks such as exploring a new object so that the brain can make decisions about whether to continue or to abandon a certain task. Possible implications for central pain states are discussed.

Animals↗

PubMed1993

Thalamic neuronal hyperactivity following transection of the spinothalamic tract in the cat: involvement of N-methyl-D-aspartate receptor.

Single neuron activities responding to peripheral stimuli with short latencies were recorded within the thalamic nucleus ventralis posterolateralis (VPL) after transection of the spinothalamic tract (STT) in the cat under alpha-chloralose anesthesia. The VPL neurons showed spontaneous and evoked hyperactivity after STT transection, which was revealed at 1-2 weeks. The spontaneous hyperactivity further progressed until 3-4 weeks. These hyperactivities were observed in core-area neurons as well as neurons found in the shell area, suggesting that some, if not many, of the N-methyl-D-aspartate (NMDA) receptor antagonist (MK-801, 4-16 mg; i.v.) attenuated both the spontaneous and evoked hyperactivity observed after STT transection. No such effects were demonstrated in sham-operated animals. These findings suggest that VPL neurons become hyperactive after STT transection through recruitment of NMDA receptors. The hyperactivity of VPL neurons may represent an important background process in the production of deafferentation pain induced by lesions involving the STT.

Amino Acids↗

PubMed1994

Glycine and GABAA antagonists reduce the inhibition of primate spinothalamic tract neurons produced by stimulation in periaqueductal gray.

Amino acids are demonstrated to be important neurotransmitters mediating the inhibitory transmission from nucleus raphe magnus to spinal nociceptive dorsal horn neurons. In this study, the role of glycine and GABA in the inhibitory processes evoked by stimulation in periaqueductal gray (PAG) of responses of primate spinothalamic tract (STT) neurons to cutaneous mechanical and thermal stimuli was investigated by examining the effects of strychnine and bicuculline, antagonists of glycine and GABAA receptors, respectively, introduced into the dorsal horn through a microdialysis fiber. The inhibitory effects of iontophoretic application of glycine and GABAA agonists on STT cell activity evoked by noxious mechanical stimulation of the skin were selectively blocked by their specific antagonist, strychnine or bicuculline, infused into the dorsal horn. Similarly, intra-spinal application of strychnine or bicuculline resulted in a significant reduction in the PAG stimulation-induced inhibition of responses of STT cells to cutaneous stimuli. This reduction was mainly on the PAG-induced inhibition of the responses to noxious mechanical stimuli. Our results suggest that glycinergic and GABAergic inhibitory interneurons in the spinal cord dorsal horn synapsing on STT cells are activated during stimulation in PAG and contribute to descending antinociceptive actions.

Animals↗