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

Nakatsuka, Terumasa; Ataka, Toyofumi; Kumamoto, Eiichi; Tamaki, Toru; Yoshimura, Michihiro

doi:10.1016/s0306-4522(00)00224-4

Cited by 125 publications

(139 citation statements)

References 39 publications

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“…The methods used for obtaining adult rat spinal cord slice preparations have been described previously (Nakatsuka et al, 2000). In brief, male adult Sprague Dawley rats (6 -8 weeks of age, 200 -300 g) were deeply anesthetized with urethane (1.2 g/kg, i.p.)…”

Section: Methodsmentioning

confidence: 99%

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Activation of TRPA1 Channel Facilitates Excitatory Synaptic Transmission in Substantia Gelatinosa Neurons of the Adult Rat Spinal Cord

Kosugi

Nakatsuka²,

Fujita³

et al. 2007

J. Neurosci.

134

109

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TRPA1 is expressed in primary sensory neurons and hair cells, and it is proposed to be activated by cold stimuli, mechanical stimuli, or pungent ingredients. However, its role in regulating synaptic transmission has never been documented yet. In the present study, we examined whether activation of the TRPA1 channels affects synaptic transmission in substantia gelatinosa (SG) neurons of adult rat spinal cord slices by using the whole-cell patch-clamp technique. A chief ingredient of mustard oil, allyl isothiocyanate (AITC), superfused for 2 min markedly increased the frequency and amplitude of spontaneous EPSCs (sEPSCs), which was accompanied by an inward current. Similar actions were produced by cinnamaldehyde and allicin. The AITC-induced increases in sEPSC frequency and amplitude were resistant to tetrodotoxin (TTX) and La 3ϩ , whereas being significantly reduced in extent in a Ca 2ϩ -free bath solution. In the presence of glutamate receptor antagonists CNQX and AP5, AITC did not generate any synaptic activities. The AITC-induced increases in sEPSC frequency and amplitude were reduced by ruthenium red, whereas being unaffected by capsazepine. AITC also increased the frequency and amplitude of spontaneous inhibitory postsynaptic currents; this AITC action was abolished in the presence of TTX or glutamate receptor antagonists. These results indicate that TRPA1 appears to be localized not only at presynaptic terminals on SG neurons to enhance glutamate release, but also in terminals of primary afferents innervating onto spinal inhibitory interneurons, which make synapses with SG neurons. This central modulation of sensory signals may be associated with physiological and pathological pain sensations.

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Section: Methodsmentioning

confidence: 99%

“…Blind whole-cell patch-clamp recordings were made from SG neurons with patch-pipette electrodes having a resistance of 5-10 M⍀ (Nakatsuka et al, 2000). The patchpipette solution used to record EPSCs was composed of the following (in mM): 135 potassium gluconate, 5 KCl, 0.5 CaCl 2 , 2 MgCl 2 , 5 EGTA, 5 HEPES, and 5 ATP-Mg, pH 7.2.…”

Section: Methodsmentioning

confidence: 99%

Activation of TRPA1 Channel Facilitates Excitatory Synaptic Transmission in Substantia Gelatinosa Neurons of the Adult Rat Spinal Cord

Kosugi

Nakatsuka²,

Fujita³

et al. 2007

J. Neurosci.

134

109

View full text Add to dashboard Cite

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“…Upon electrical stimulation with an Aβ fiber intensity (8-26 pA) (Nakatsuka et al, 2000;Torsney and MacDermott, 2006) Figures 3D-F).…”

Section: Ret+ Ddh Neurons Receive Excitatory Inputs From Aβ Mechanosementioning

confidence: 99%

Identification of Early RET+ Deep Dorsal Spinal Cord Interneurons in Gating Pain

Cui¹,

Miao²,

Liang³

et al. 2016

Neuron

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The gate control theory (GCT) of pain proposes that pain-and touch-sensing neurons antagonize each other through spinal cord dorsal horn (DH) gating neurons. However, the exact neural circuits underlying the GCT remain largely elusive. Here, we identified a new population of deep layer DH (dDH) inhibitory interneurons that express the receptor tyrosine kinase Ret neonatally. These early RET+ dDH neurons receive excitatory as well as polysynaptic inhibitory inputs from touch-and/or pain-sensing afferents. In addition, they negatively regulate DH pain and touch pathways through both pre-and postsynaptic inhibition. Finally, specific ablation of early RET+ dDH neurons increases basal and chronic pain, whereas their acute activation reduces basal pain perception and relieves inflammatory and neuropathic pain. Taken together, our findings uncover a novel spinal circuit that mediates crosstalk between touch and pain pathways and suggest that some early RET + dDH neurons could function as pain "gating" neurons.

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“…Whole-cell recordings were performed if they matched all of the following criteria: Ͼ1 G⍀ seal resistance before "breakthrough" with additional suction; a resting potential of Ϫ55 mV or more negative; and Ͼ100 M⍀ input resistance after whole-cell mode was established. Data were collected using an EPC-9 patch-clamp amplifier and the Pulse software (version 8.31 (Nakatsuka et al, 2000). Stimulus intensity was adjusted to 1.5 times the threshold for evoking detectable EPSCs in the C-afferent fibers.…”

Section: Animals and Drugsmentioning

confidence: 99%

“…After blockade of GABA A receptor-and glycine receptor-mediated IPSCs with 20 M bicuculline and 2 M strychnine, the monosynaptic glutamate-mediated EPSCs of afferent C-fibers were evoked by 0.2 Hz stimulation (100 s duration; 350 -380 A strength) of the dorsal root (Nakatsuka et al, 2000). Such evoked EPSCs could be inhibited by following perfusion of BNP (200 ng/ml) ( p Ͻ 0.05; n ϭ 5 of 8 recorded lamina II neurons) (Fig.…”

Section: Intrathecally Applied Bnp Reduces Inflammatory Painmentioning

confidence: 99%

Inhibition of Inflammatory Pain by Activating B-Type Natriuretic Peptide Signal Pathway in Nociceptive Sensory Neurons

Zhang¹,

Liu²,

Gong³

et al. 2010

J. Neurosci.

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B-type natriuretic peptide (BNP) has been known to be secreted from cardiac myocytes and activate its receptor, natriuretic peptide receptor-A (NPR-A), to reduce ventricular fibrosis. However, the function of BNP/NPR-A pathway in the somatic sensory system has been unknown. In the present study, we report a novel function of BNP in pain modulation. Using microarray and immunoblot analyses, we found that BNP and NPR-A were expressed in the dorsal root ganglion (

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

Cited by 125 publications

References 39 publications

Activation of TRPA1 Channel Facilitates Excitatory Synaptic Transmission in Substantia Gelatinosa Neurons of the Adult Rat Spinal Cord

Activation of TRPA1 Channel Facilitates Excitatory Synaptic Transmission in Substantia Gelatinosa Neurons of the Adult Rat Spinal Cord

Identification of Early RET+ Deep Dorsal Spinal Cord Interneurons in Gating Pain

Inhibition of Inflammatory Pain by Activating B-Type Natriuretic Peptide Signal Pathway in Nociceptive Sensory Neurons

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