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At least 19 recordsLinked to original sources
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↗
PubMed1998

Nitric oxide-producing islet cells modulate the release of sensory neuropeptides in the rat substantia gelatinosa.

The substantia gelatinosa of the spinal cord (lamina II) is the major site of integration for nociceptive information. Activation of NMDA glutamate receptor, production of nitric oxide (NO), and enhanced release of substance P and calcitonin gene-related peptide (CGRP) from primary afferents are key events in pain perception and central hyperexcitability. By combining reduced nicotinamide adenine dinucleotide phosphate (NADPH) diaphorase histochemistry for NO-producing neurons with immunogold labeling for substance P, CGRP, and glutamate, we show that (1) NO-producing neurons in lamina IIi are islet cells; (2) these neurons rarely form synapses onto peptide-immunoreactive profiles; and (3) NADPH diaphorase-positive dendrites are often in close spatial relationship with peptide-containing terminals and are observed at the periphery of type II glomeruli showing glutamate-immunoreactive central endings. By means of confocal fluorescent microscopy in acute spinal cord slices loaded with the Ca2+ indicator Indo-1, we also demonstrate that (1) NMDA evokes a substantial [Ca2+]i increase in a subpopulation of neurons in laminae I-II, with morphological features similar to those of islet cells; (2) a different neuronal population in laminae I-IIo, unresponsive to NMDA, displays a significant [Ca2+]i increase after slice perfusion with either substance P and the NO donor 3morpholinosydnonimine (SIN-1); and (3) the responses to both substance P and SIN-1 are either abolished or significantly inhibited by the NK1 receptor antagonist sendide. These results provide compelling evidence that glutamate released at type II glomeruli triggers the production of NO in islet cells within lamina IIi after NMDA receptor activation. The release of substance P from primary afferents triggered by newly synthesized NO may play a crucial role in the cellular mechanism leading to spinal hyperexcitability and increased pain perception.

Animals↗
PubMed1983

Actions of morphine and met-enkephalin-amide on nociceptor driven neurones in substantia gelatinosa and deeper dorsal horn.

Simultaneous recordings of responses of substantia gelatinosa and deep dorsal horn neurones to thermal noxious cutaneous stimulation were made in spinalized cats anaesthetized with urethane/chloralose. Morphine, whether applied iontophoretically in the substantia gelatinosa (50-200 nA) or injected intravenously (1.0-1.5 mg/kg), enhanced the responses of the substantia gelatinosa cells while depressing those of deep cells. Met-enkephalin-amide (50-200 nA) also had similar reciprocal actions. Naloxone counteracted these effects of the agonists. The results support our previous proposal that the opiates facilitate the activity of a substantia gelatinosa system that controls the responses of deep dorsal horn neurones to pain.

Action Potentials↗
PubMed2006

Changes in properties of substantia gelatinosa neurons after surgical incision in the rat: in vivo patch-clamp analysis.

BACKGROUND: Noxious information through A delta and C afferent fibers is transmitted to substantia gelatinosa, a process that plays an important role in plastic changes of nociceptive processing in pathophysiological conditions. In this study, changes in properties of substantia gelatinosa neurons and their sensitivity to systemic administration of lidocaine after surgical incision were investigated using the in vivo patch-clamp technique. METHODS: Under urethane anesthesia, in the current clamp mode, spontaneous activities and responses of substantia gelatinosa neurons to nonnoxious air-puff stimuli and noxious pinch stimuli were recorded before and after 1-cm-long incisions had been made in hairy skin of the hindquarters of rats. Systemic administration of lidocaine (2 mg/kg) was applied at 30 min after the incision. RESULTS: Stable recordings for 30 min or more after the incision were obtained from 18 substantia gelatinosa neurons that were classified as multireceptive (n = 8), nociceptive (n = 5), and subthreshold (n = 5) neurons. Action potential firing disappeared immediately after completion of the wound closure in most multireceptive and nociceptive neurons, and sustained spontaneous action potential firing was observed in 23% of these substantia gelatinosa neurons. Responsiveness of these substantia gelatinosa neurons, but not that of subthreshold neurons, increased after the incision. Systemic administration of lidocaine suppressed spontaneous firings of action potentials of the substantia gelatinosa neurons and reversed the increased responsiveness of the neurons. CONCLUSIONS: The results suggest that (1) changes in properties of substantia gelatinosa neurons after incision vary depending on the classification of substantia gelatinosa neurons and (2) systemic administration of lidocaine can reverse increased responsiveness of substantia gelatinosa neurons after incision injury.

Action Potentials↗
PubMed1994

mu-Opioid agonists inhibit spinal trigeminal substantia gelatinosa neurons in guinea pig and rat.

The actions of opioid agonists in the substantia gelatinosa are important for their antinociceptive effects. In order to identify possible mechanisms underlying opioid actions in the substantia gelatinosa, the pre- and postsynaptic effects of opioid agonists on neurons of the substantia gelatinosa were examined using a brain slice preparation. Intracellular recordings were made from neurons of the substantia gelatinosa of the spinal trigeminal nucleus pars caudalis in guinea pig and rat. To correlate morphology and electrophysiology, neurons were filled with biocytin and visualized using HRP. The majority of neurons (86%) were hyperpolarized by [Met]5enkephalin (ME), and this was mimicked by the mu-opioid agonist (D-Ala2,N-Me-Phe4,Gly5-ol)enkephalin (DAMGO) but not the delta-opioid agonist (D-Pen2,5)enkephalin (DPDPE). Naloxone (300 nM) shifted the DAMGO dose-response 213-fold to the right, giving an estimated KD of 1.4 nM. Under voltage clamp, the ME current reversed polarity at the potassium equilibrium potential, indicating the hyperpolarization was due to an increase in potassium conductance. EPSPs mediated by glutamate were evoked by stimulating the spinal trigeminal tract, which contains the primary afferent fibers that synapse in the spinal trigeminal nucleus. The excitation produced by stimulating the spinal trigeminal tract was greatly enhanced in the presence of glycine and GABAA receptor antagonists, indicating that local inhibitory circuitry is activated by exciting the primary afferents. The EPSPs were reduced by mu- but not delta-opioid receptor activation. The degree of inhibition varied from 0 to 100%. These results indicate that opioid agonists cause inhibition in the substantia gelatinosa by both pre- and postsynaptic actions.

Animals↗
PubMedDate not supplied

Substantia gelatinosa neurones hyperpolarized in vitro by enkephalin.

The sensation of pain is carried to the central nervous system by small-diameter fibres which terminate in the superficial layers of the spinal grey matter, particularly the substantia gelatinosa. Opiate drugs administered into the substantia gelatinosa inhibit the excitation of deeper dorsal horn neurones by noxious peripheral stimuli while sparing the responses to other sensations such as touch. It has been suggested that opiates impair the release of the transmitter from the small-diameter nociceptive fibres, but it is also possible that opiates directly depress the responses of cells in the substantia gelatinosa which serve as interneurones in the pain pathway. We have made intracellular recordings from substantia gelatinosa neurones in a slice of rat spinal cord, and report here that morphine and enkephalin directly hyperpolarize substantia gelatinosa cells by opening membrane K+ channels. This inhibitory action of exogenous morphine provides a likely cellular mechanism for its analgesic properties. Moreover, enkephalin is an endogenous constituent of some cells of the substantia gelatinosa, where it is concentrated within terminals making synaptic contacts with other cell bodies and dendrites. The present findings thus strongly suggest that enkephalin serves as an inhibitory neurotransmitter within the substantia gelatinosa.

Animals↗
PubMed2005

Action of neuropeptide Y on nociceptive transmission in substantia gelatinosa of the adult rat spinal dorsal horn.

Effects of neuropeptide Y (NPY) on substantia gelatinosa neurons were investigated in adult rat spinal cord slices using blind whole-cell patch-clamp technique. Bath application of NPY (1 microM) induced a membrane hyperpolarization, resulting in a suppression of the dorsal root stimulation-induced action potentials in 24% of the substantia gelatinosa neurons tested. In voltage clamp mode, NPY produced an outward current dose-dependently in about one third of substantia gelatinosa neurons at the holding potential of -60 mV, which was not affected by tetrodotoxin (1 microM). The NPY-induced current was suppressed by perfusion with a Ba2+-containing external solution and a Cs2SO4 or tetraethylammonium-containing pipette solution. In addition, The NPY-induced outward currents reversed its polarity near the equilibrium potential of K+ ions (-93 mV). The response to NPY recorded with guanosine-5'-O-(2-thiodiphosphate)-beta-S (GDP-beta-S) containing pipette solution was abolished 30 min after patch formation, suggesting that the response was mediated by the G-protein-coupled receptors. Application of an NPY-Y1 selective agonist, [Leu(31), Pro(-34)]-NPY (1 microM), for 30 s also induced an outward current with a similar time course and amplitude to that induced by NPY. On the other hand, the NPY response was blocked by a simultaneous application of NPY-Y1 selective antagonist, BIBP 3226 (1 microM). No significant changes were found in amplitude and frequency of miniature excitatory postsynaptic currents and dorsal root evoked excitatory postsynaptic currents by NPY. In addition, NPY did not affect both of the miniature inhibitory postsynaptic currents and evoked inhibitory postsynaptic currents, mediated by either the GABA or glycine receptor. These findings, taken together, suggest that NPY produces an outward current in substantia gelatinosa neurons through G-protein coupled, and NPY-Y1 receptor-mediated activation of K+ channels without affecting presynaptic components. The inhibition of the synaptic transmission from the primary fibers to the substantia gelatinosa neurons is considered to contribute to the antinociceptive effects of NPY.

Animals↗
PubMed2004

AM404 enhances the spontaneous release of L-glutamate in a manner sensitive to capsazepine in adult rat substantia gelatinosa neurones.

In 84% of substantia gelatinosa (SG) neurones examined in adult rat spinal cord slices, an anandamide transport inhibitor, AM404, increased the frequency of spontaneous excitatory postsynaptic currents in a manner similar to that of capsaicin. AM404 was without actions in the presence of a vanilloid TRPV1 receptor antagonist, capsazepine. We conclude that AM404 enhances the spontaneous release of L-glutamate by activating TRPV1 receptors in the SG.

Anesthetics, Local↗
PubMed1976

Afferent fibers in the substantia gelatinosa of the adult monkey (Macaca mulatta): a Golgi study.

In horizontally and sagittally sectioned Golgi preparations of the adult monkey spinal cord the afferent fibers in the substantia gelatinosa (laminae II and III of Rexed, '52) were studied with the hope of finding clues that would make it possible to correlate them with the afferent fibers that Ramón y Cajal ('09) traced from the white matter into the substantia gelatinosa in Golgi preparations of the newborn cat. Throughout the substantia gelatinosa there are fibers with fine terminal branches, bearing small "bouton en passant" endings. These fine terminal branches and the collaterals of the axons of the neurons in the substantia gelatinosa are similar; hence, the fine terminal branches are interpreted as the terminals of the proprius bundles generated by the axons of the neurons in the substantia gelatinosa. Also, there are fibers in lamina II that can be followed for relatively long distances (900 microns) before they are cut off in section. They have collaterals bearing large irregular endings, which usually consist of several or more elongated swelling connected by constricted regions. Some of these endings have holes within them and their surfaces have prominent indentations. The fibers with fine terminal branches and the fibers with large irregular endings are interpreted here as the two varieties of fine or superficial collaterals of the substance of Rolando described by Ramóm y Cajal ('09). The most elaborate afferent formations in the present material are found in horizontal sections. They are designated "confined ansiform axonal complexes" and are confined to elongated, oblong blocks of substantia gelatinosa that approximate each other in length, width and depth. Their branches, running rostrally and caudally, loop back and forth, interweave in and intricate pattern and bear large synaptic endings. Because these formations are elaborate and because their parent fibers and initial branches are thicker in lamina III than they are in lamina II, these complexes are interpreted here as the large or deep collaterals of the substance of Rolando described by Ramón y Cajal ('09). Considering their shapes, sizes and surface contours, it is probable that the large endings on the ansiform axonal complexes and the large irregular endings on the long fibers in lamina II are the central terminals in the glomeruli of the substanta gelatinosa that have been revealed by electron microscopy. Finally, there are fine collaterals from fibers in Lissauer's fasciculus which distribute exclusively to the marginal zone (lamina I) of the dorsal horn. Their endings are ovoid or bulbous and are almost uniformly approximately 2 microns in diameter. Undoubtedly, these collaterals are the marginal collaterals Ramón y Cajal ('09) demonstrated in Ehrlich's methylene blue preparations of the 8-day old cat.

Animals↗
PubMed2002

Postsynaptic action mechanism of somatostatin on the membrane excitability in spinal substantia gelatinosa neurons of juvenile rats.

We used tight-seal, whole-cell recording in juvenile rat spinal slices to investigate the action of somatostatin on substantia gelatinosa neurons. Bath application of somatostatin caused a robust and repeatable hyperpolarization or outward current in substantia gelatinosa neurons. Somatostatin inhibited spontaneous action potentials in subpopulation of substantia gelatinosa neurons. The amplitude of dorsal root-evoked excitatory postsynaptic currents and the frequency of spontaneous excitatory postsynaptic currents were not affected by somatostatin. The current induced by somatostatin developed almost instantaneously and did not show any time-dependent inactivation. The current-voltage relationship exhibited inward rectification. The conductance of somatostatin-sensitive current increased with the concentration of external K(+). The reversal potentials in different external K(+) concentrations were close to the K(+) equilibrium potentials. The effect of somatostatin was dose-dependent, with an EC(50) of 113 nM. The somatostatin-sensitive current was blocked by low concentration of extracellular Ba(2+) but not by glibenclamide, an inhibitor of ATP-sensitive K(+) channels. Hyperpolarization-activated cation current in a subpopulation of substantia gelatinosa neurons was not affected by somatostatin. In neurons recorded with an internal solution containing GTPgammaS, somatostatin induced outward current and hyperpolarization that did not reverse on washing. When the spontaneous induction of outward current with GTPgammaS was greatest, somatostatin did not induce any outward currents. Furthermore, intracellular dialysis of GDPbetaS, a G-protein antagonist, abolished the effect of somatostatin. In addition, SST-sensitive neurons were fewer in slices incubated with pertussis toxin than in adjacent control slices incubated without pertussis toxin. These results suggest that somatostatin decreases the postsynaptic membrane excitability of substantia gelatinosa neurons by a pertussis toxin-sensitive G-protein-mediated activation of an inwardly rectifying K(+) conductance.

Age Factors↗
PubMed2000

Alteration in synaptic inputs through C-afferent fibers to substantia gelatinosa neurons of the rat spinal dorsal horn during postnatal development.

The change in synaptic inputs through primary afferent C- and A-fibers during postnatal development was examined in substantia gelatinosa neurons of a rat spinal cord slice with an attached L5 dorsal root by use of the blind whole-cell patch-clamp technique; the synaptic responses were compared between the slices obtained from immature (postnatal days 21-23) and mature (postnatal days 56-60) male rats. The mono- and/or polysynaptic afferent inputs were monitored by recording glutamatergic excitatory postsynaptic currents and potentials evoked by stimulating C- and A-fibers, the identification of which was based on the values of threshold stimulus intensity and of the conduction velocity of the fibers, determined by intracellular recordings from dorsal root ganglion neurons. Immature substantia gelatinosa neurons received synaptic inputs through Abeta-, Adelta- and C-afferents, with proportions of 51%, 46% and 36%, respectively. In mature substantia gelatinosa neurons, C- and Adelta-afferent inputs were increased in number (to 84% and 86%, respectively), while Abeta-inputs were decreased to 9%. In both immature and mature rats, repetitive stimulation of C-afferents did not elicit any slow responses, which are longer in duration than the monosynaptic excitatory postsynaptic currents, although C-fibers are known to contain not only excitatory amino acids, but also neuropeptides such as substance P, which is thought to be involved in the production of slow responses. These results indicate that both C- and Adelta-afferents innervating substantia gelatinosa neurons are reorganized following maturation, accompanied by a withdrawal or elimination of Abeta-fibers from the substantia gelatinosa, probably due to a competition among the fibers during development. In spite of the developmental increase in C-fiber inputs, mature as well as immature substantia gelatinosa neurons did not display any slow synaptic responses, which appear to be mediated by transmitters other than excitatory amino acids.

Action Potentials↗
PubMed1983

Morphine blocks the increase in acid phosphatase in the substantia gelatinosa during pain.

Acid phosphatase activity in the rat substantia gelatinosa has been shown to increase in response to a formalin-induced painful stimulus. In the rat the substantia gelatinosa is the location of the first synapse in the pain pathway. One site of morphine's analgesic effect is at this first synapse. The present study shows that morphine blocks the previously observed increase in acid phosphatase activity during a painful stimulus. Naloxone antagonizes the morphine effect. These results point to a possible functional role of acid phosphatase in the afferent transmission of pain signals.

Acid Phosphatase↗
PubMed1999

Second messengers, the substantia gelatinosa and injury-induced persistent pain.

Although there is now unequivocal evidence that the circuitry within the substantia gelatinosa is a major contributor to the transmission and control of nociceptive messages, this was not known 35 years ago, when Pat Wall first focussed attention on this region. In addition to being the target of neurochemically distinct nociceptors, this region contains a heterogeneous population of excitatory and inhibitory interneurons. This review focuses on the contribution of second messenger systems that are found in the substantia gelatinosa. In particular the review highlights their critical contribution to the development of persistent pain conditions in the setting of tissue and nerve injury. Several of the studies used animals with deletions of genes that encode major second messenger molecules, including protein kinase A, C and nitric oxide synthase. Our laboratory has shown that mice with a deletion of the gene that encodes the gamma isoform of protein kinase C (which is almost exclusively expressed in a population of interneurons of the inner part of the substantia gelatinosa) have completely normal acute pain responses. However, the allodynia that characteristically develops after injury does not occur in these mice, particularly when it is generated by partial sciatic nerve injury. By contrast, deletion of genes that encode protein kinase A subunits only show deficits in the development of tissue inflammation-induced pain. These differences highlight the selectivity that characterizes the contribution of different second messenger molecules. Because of the restricted distribution of these molecules, it is likely that they are activated by different populations of primary afferent nociceptor and under very different conditions of injury. Understanding the circuitry within the substantia gelatinosa is thus critical to elucidating the mechanisms through which these second messenger molecules contribute to the development of persistent pain in the setting of injury.

Animals↗
PubMed2005

Altered long-term synaptic plasticity and kainate-induced Ca2+ transients in the substantia gelatinosa neurons in GLU(K6)-deficient mice.

Functional kainate receptors are expressed in the spinal cord substantia gelatinosa region, and their activation contributes to bi-directional regulation of excitatory synaptic transmission at primary afferent synapses with spinal cord substantia gelatinosa neurons. However, no study has reported a role(s) for kainate receptor subtypes in long-term synaptic plasticity phenomena in this region. Using gene-targeted mice lacking glutamate receptor 5 (GLU(K5)) or GLU(K6) subunit, we here show that GLU(K6) subunit, but not GLU(K5) subunit, is involved in the induction of long-term potentiation of excitatory postsynaptic potentials, evoked by two different protocols: (1) high-frequency primary afferent stimulation (100 Hz, 3 s) and (2) low-frequency spike-timing stimulation (1 Hz, 200 pulses). In addition, GLU(K6) subunit plays an important role in the expression of kainate-induced Ca2+ transients in the substantia gelatinosa. On the other hand, genetic deletion of GLU(K5) or GLU(K6) subunit does not prevent the induction of long-term depression. These results indicate that unique expression of kainate receptors subunits is important in regulating spinal synaptic plasticity and thereby processing of sensory information, including pain.

6-Cyano-7-nitroquinoxaline-2,3-dione↗
PubMed1981

An ultrastructural morphometric study of developing rat substantia gelatinosa.

A morphometric analysis has been done on developing rat substantia gelatinosa of the lower cervical and upper thoracic levels of the spinal cord starting on the 15th day of gestation. The following parameters were measured: cell body diameter, cytoplasmic/nuclear areas, synaptic density, synaptic type and vesicle morphology of the presynaptic terminal in axodendritic synapses. Cell body size and cytoplasmic/nuclear areas of gelatinosal cells increase until the 15th day postnatally and then decrease somewhat to the adult values. The first synapses are seen on gestation day 17. Synaptic density increases linearly until the third day postnatally. Axodendritic synapses are most common throughout development and in the adult, while the proportion of axoaxonic synapses increases and axosomatic synapses decreases during development. Most of the terminals in axodendritic synapses contain clear-spherical vesicles but the occurrence of clear-flat vesicles and dense-cored vesicles in the terminals increases during development. It appears that these morphological parameters provide a stable index of development in the substantia gelatinosa which can be correlated with functional devleopment of the area. Hopefully, they will provide a means to asses subtle anomalies induced by nonteratogenic drugs or other environmental changes.

Animals↗
PubMed1983

Substantia gelatinosa Rolandi neurons: ultrastructure of the cellular somata, synapses and intercellular contacts.

The central cells of substantia gelatinosa are small spindle-shaped neurons with an average perimeter of 26.8 micrometers and an average cross-sectional area of 44.9 micrometers2. No difference has been found between neurons of C1 and those of the lower cervical segments. It was calculated that axo-somatic synapses are about 20 per cell and generally occur in small clusters of 3-4 synapses each. Despite their low number they are probably of functional relevance when compared to the small size of the somata of substantia gelatinosa neurons. Most of the synaptic boutons contain pleomorphic electronlucent vesicles and have symmetrical synaptic junctions. Large granular synaptic vesicles also occur intermingled with the electronlucent ones. Sites of somato-dendritic and somato-somatic membrane apposition are fairly extensive: they over about 8% of the cellular perimeter. The possibility of cellular interactions or material interchanges at these sites of direct membrane apposition is suggested. Somatodendritic synapses were occasionally observed. Although the neuropil is indeed the main target of the different inputs to the substantia gelatinosa and the site of most of the local circuits, the somata may too be involved in synaptic transmission and possibly in intercellular coupling.

Animals↗
PubMed2004

[Effects of etomidate on local synaptic transmission in substantia gelatinosa neurons of the adult rat spinal cord].

By using blind spinal slice whole-cell patch-clamp technique, we observed the influence of etomidate (ET) on synaptic transmission in substantia gelatinosa neurons of the adult rat spinal cord. Male adult Sprague-Dawley rats (7~8 weeks old) were anaesthetized with urethane (1.2 g/kg, i.p.), and then lumbosacral laminectomy was performed. The lumbosacral spinal cord (L1~S3) was removed and placed in preoxygenated Krebs solution at 1~3 degrees C. After cutting all of the ventral and dorsal roots, the pia-arachnoid membrane was removed. The spinal cord was mounted on a vibrating microslicer and then a 500 microm thick transverse slice was cut. The slice was placed on a nylon mesh in the recording chamber, and then perfused at a rate of 15~20 ml/min with Krebs solution saturated with 95% O2 and 5% CO2, and maintained at 36+/-1 degrees C. Substantia gelatinosa neurons were identified by their location. Under a binocular microscope and with transmitted illumination, the substantia gelatinosa was clearly discernible as a relatively translucent band across the dorsal horn. The resistance of patch clamp electrodes was 8~12 Msigma. Signals were gained by using an Axopatch 200B amplifier with low-passfiltered at 5 kHz, and digitized at 333 kHz with an A/D converter. The results are as follows. (1) To see whether or not ET has any effects on the local miniature excitatory postsynaptic currents (mEPSC), the holding potential was set up at -70 mV. Under such a condition extracellular superfusion was made with 1 micromol/L TTX for 2 min first, which was followed by consistent application of 500 micromol/L ET and 1 micromol/L TTX for 1 min. It was shown that ET did not influence the decay time, frequency and amplitude of mEPSC, when compared to the control. (2) To see whether or not ET has any effects on the local miniature inhibitory postsynaptic currents (mIPSC) mediated by GABA(A) receptor, the holding potential was set up at 0 mV. Under this condition extracellular superfusion was made with 1 micromol/L TTX and 1 micromol/L strychnine, an antagonist of glycine receptor, for 2 min, and then with consistent application of 50 micromol/L ET, 1 micromol/L TTX and 1 micromol/L strychnine for 1 min. ET prolonged the decay time of GABAergic mIPSC by 45.57+/-12.46% (P<0.05), but did not influence the frequency and amplitude of GABAergic mIPSC, when compared with the control. (3) To see whether or not ET has any effects on the local mIPSC mediated by glycine receptor, the holding potential was also set up at 0 mV, and under this condition extracellular superfusion was made with 1 mmol/L TTX and 10 mmol/L bicuculline, an antagonist also set up at 0 mV, and under this condition extracellular superfusion was made with 1 micromol/L TTX and 10 micromol/L bicuculline, an antagonist of GABA(A) receptor, for 2 min, and then with consistent application of 50 micromol/L ET, 1 micromol/L TTX and 10 micromol/L bicuculline for 1 min. ET had no effects on decay time, frequency and amplitude of glycinergic mIPSC. The above-mentioned results show that ET plays anesthetic or analgesic roles by modulating the decay time of GABAergic mIPSC, i.e. by prolonging the mean open time of GABA(A) receptors, however, ET has no direct effect on local excitatory synaptic transmission in substantia gelatinosa neurons of the adult rat spinal cord.

Anesthetics, Intravenous↗
PubMed1988

Adenosine A1 and A2 receptors of the substantia gelatinosa are located predominantly on intrinsic neurons: an autoradiography study.

Tissue autoradiography was used to examine the distribution of A1 and A2 adenosine receptors in the rat spinal cord. The distribution of binding sites for the A1 selective agonist, N6-[3H]-[(R)-1-methyl-2-phenylethyl]adenosine (R-[3H]PIA), was similar to the distribution of binding sites for [3H]-5'-N-ethylcarboxamide adenosine [( 3H]NECA), an agonist that binds to A1 and A2 receptors with nearly equal affinities. Binding site densities were highest in the substantia gelatinosa, followed by lamina 10; the remainder of the spinal cord displayed uniformly low levels of binding sites. In each of these three areas, [3H]NECA bound to more sites than R-[3H]PIA. When the A1-selective agonist, N6-(cyclopentyl)adenosine, was used to block [3H]NECA binding to A1 receptors, the autoradiograms demonstrated a band of A2 receptor density which tended to be localized in the ventral portion of the substantia gelatinosa. Unilateral dorsal rhizotomy, hemitransection and complete transection of the spinal cord failed to alter the [3H]NECA or R-[3H]PIA binding in the substantia gelatinosa. In contrast, unilateral microinjections of kainic acid into the dorsal horn decreased [3H]NECA and R-[3H]PIA binding at the level of the injections by 42 and 37%, respectively. In some areas, kainic acid injection eliminated all R-[3H]PIA and [3H]NECA binding in the substantia gelatinosa. It is therefore concluded that spinal cord A1 and A2 adenosine receptors in the substantia gelatinosa are located predominantly on intrinsic neurons.

Adenosine↗