Somatostatin directly inhibits substantia gelatinosa neurons in adult rat spinal dorsal horn in vitro

Nan Jiang, Hidemasa Furue, Toshihiko Katafuchi, Megumu Yoshimura

Research output: Contribution to journalArticle

35 Citations (Scopus)

Abstract

Effects of somatostatin (SST) on the synaptic transmission to substantia gelatinosa (SG) neurons of adult spinal cord slices were investigated using intracellular recording and blind whole-cell patch-clamp technique. Bath application of SST (1 μM) induced the membrane hyperpolarization that was accompanied by a decrease in input resistance and had the reversal potential of -92±3 mV (n=5) in the intracellular recording experiment. In patch-clamp experiment, SST (1 μM) induced an outward current with amplitude of 14±2 pA (n=60) at the holding potential of -60 mV, and was not affected by TTX (n=3). The effect was dose-dependent with EC50 value of 0.82 μM (Hill coefficient: 0.89). The outward current was suppressed when the patch-pipette solution containing potassium channel blockers, Cs+ and tetraethylammonium (TEA), and was inhibited by Ba2+ (200 μM) to 15±6% of the control (n=3). In addition, the SST current reversed its polarity at potential close to the equilibrium potential of K+ channel calculated by the Nernst equation. No significant changes were found in amplitude and frequency of miniature excitatory postsynaptic currents (mEPSCs) and dorsal root evoked EPSC (eEPSC) by SST. Also, SST did not affect both of the miniature inhibitory postsynaptic currents (mIPSCs) and evoked inhibitory postsynaptic currents (eIPSCs), mediated by either the GABA or glycine receptor. We conclude that SST activates the K+ channel resulting in postsynaptic hyperpolarization in adult rat SG neurons without affecting presynaptic component of the transmission, which are considered to account, at least a part, for the analgesic effects of SST reported previously.

Original languageEnglish
Pages (from-to)97-107
Number of pages11
JournalNeuroscience Research
Volume47
Issue number1
DOIs
Publication statusPublished - Sep 1 2003

Fingerprint

Substantia Gelatinosa
Somatostatin
Neurons
Inhibitory Postsynaptic Potentials
Patch-Clamp Techniques
Potassium Channel Blockers
Glycine Receptors
Tetraethylammonium
GABA Receptors
Spinal Cord Dorsal Horn
In Vitro Techniques
Spinal Nerve Roots
Excitatory Postsynaptic Potentials
Baths
Synaptic Transmission
Analgesics
Spinal Cord

All Science Journal Classification (ASJC) codes

  • Neuroscience(all)

Cite this

Somatostatin directly inhibits substantia gelatinosa neurons in adult rat spinal dorsal horn in vitro. / Jiang, Nan; Furue, Hidemasa; Katafuchi, Toshihiko; Yoshimura, Megumu.

In: Neuroscience Research, Vol. 47, No. 1, 01.09.2003, p. 97-107.

Research output: Contribution to journalArticle

Jiang, Nan ; Furue, Hidemasa ; Katafuchi, Toshihiko ; Yoshimura, Megumu. / Somatostatin directly inhibits substantia gelatinosa neurons in adult rat spinal dorsal horn in vitro. In: Neuroscience Research. 2003 ; Vol. 47, No. 1. pp. 97-107.
@article{f52781caa7a44f2a826724cd599d8993,
title = "Somatostatin directly inhibits substantia gelatinosa neurons in adult rat spinal dorsal horn in vitro",
abstract = "Effects of somatostatin (SST) on the synaptic transmission to substantia gelatinosa (SG) neurons of adult spinal cord slices were investigated using intracellular recording and blind whole-cell patch-clamp technique. Bath application of SST (1 μM) induced the membrane hyperpolarization that was accompanied by a decrease in input resistance and had the reversal potential of -92±3 mV (n=5) in the intracellular recording experiment. In patch-clamp experiment, SST (1 μM) induced an outward current with amplitude of 14±2 pA (n=60) at the holding potential of -60 mV, and was not affected by TTX (n=3). The effect was dose-dependent with EC50 value of 0.82 μM (Hill coefficient: 0.89). The outward current was suppressed when the patch-pipette solution containing potassium channel blockers, Cs+ and tetraethylammonium (TEA), and was inhibited by Ba2+ (200 μM) to 15±6{\%} of the control (n=3). In addition, the SST current reversed its polarity at potential close to the equilibrium potential of K+ channel calculated by the Nernst equation. No significant changes were found in amplitude and frequency of miniature excitatory postsynaptic currents (mEPSCs) and dorsal root evoked EPSC (eEPSC) by SST. Also, SST did not affect both of the miniature inhibitory postsynaptic currents (mIPSCs) and evoked inhibitory postsynaptic currents (eIPSCs), mediated by either the GABA or glycine receptor. We conclude that SST activates the K+ channel resulting in postsynaptic hyperpolarization in adult rat SG neurons without affecting presynaptic component of the transmission, which are considered to account, at least a part, for the analgesic effects of SST reported previously.",
author = "Nan Jiang and Hidemasa Furue and Toshihiko Katafuchi and Megumu Yoshimura",
year = "2003",
month = "9",
day = "1",
doi = "10.1016/S0168-0102(03)00183-4",
language = "English",
volume = "47",
pages = "97--107",
journal = "Neuroscience Research",
issn = "0168-0102",
publisher = "Elsevier Ireland Ltd",
number = "1",

}

TY - JOUR

T1 - Somatostatin directly inhibits substantia gelatinosa neurons in adult rat spinal dorsal horn in vitro

AU - Jiang, Nan

AU - Furue, Hidemasa

AU - Katafuchi, Toshihiko

AU - Yoshimura, Megumu

PY - 2003/9/1

Y1 - 2003/9/1

N2 - Effects of somatostatin (SST) on the synaptic transmission to substantia gelatinosa (SG) neurons of adult spinal cord slices were investigated using intracellular recording and blind whole-cell patch-clamp technique. Bath application of SST (1 μM) induced the membrane hyperpolarization that was accompanied by a decrease in input resistance and had the reversal potential of -92±3 mV (n=5) in the intracellular recording experiment. In patch-clamp experiment, SST (1 μM) induced an outward current with amplitude of 14±2 pA (n=60) at the holding potential of -60 mV, and was not affected by TTX (n=3). The effect was dose-dependent with EC50 value of 0.82 μM (Hill coefficient: 0.89). The outward current was suppressed when the patch-pipette solution containing potassium channel blockers, Cs+ and tetraethylammonium (TEA), and was inhibited by Ba2+ (200 μM) to 15±6% of the control (n=3). In addition, the SST current reversed its polarity at potential close to the equilibrium potential of K+ channel calculated by the Nernst equation. No significant changes were found in amplitude and frequency of miniature excitatory postsynaptic currents (mEPSCs) and dorsal root evoked EPSC (eEPSC) by SST. Also, SST did not affect both of the miniature inhibitory postsynaptic currents (mIPSCs) and evoked inhibitory postsynaptic currents (eIPSCs), mediated by either the GABA or glycine receptor. We conclude that SST activates the K+ channel resulting in postsynaptic hyperpolarization in adult rat SG neurons without affecting presynaptic component of the transmission, which are considered to account, at least a part, for the analgesic effects of SST reported previously.

AB - Effects of somatostatin (SST) on the synaptic transmission to substantia gelatinosa (SG) neurons of adult spinal cord slices were investigated using intracellular recording and blind whole-cell patch-clamp technique. Bath application of SST (1 μM) induced the membrane hyperpolarization that was accompanied by a decrease in input resistance and had the reversal potential of -92±3 mV (n=5) in the intracellular recording experiment. In patch-clamp experiment, SST (1 μM) induced an outward current with amplitude of 14±2 pA (n=60) at the holding potential of -60 mV, and was not affected by TTX (n=3). The effect was dose-dependent with EC50 value of 0.82 μM (Hill coefficient: 0.89). The outward current was suppressed when the patch-pipette solution containing potassium channel blockers, Cs+ and tetraethylammonium (TEA), and was inhibited by Ba2+ (200 μM) to 15±6% of the control (n=3). In addition, the SST current reversed its polarity at potential close to the equilibrium potential of K+ channel calculated by the Nernst equation. No significant changes were found in amplitude and frequency of miniature excitatory postsynaptic currents (mEPSCs) and dorsal root evoked EPSC (eEPSC) by SST. Also, SST did not affect both of the miniature inhibitory postsynaptic currents (mIPSCs) and evoked inhibitory postsynaptic currents (eIPSCs), mediated by either the GABA or glycine receptor. We conclude that SST activates the K+ channel resulting in postsynaptic hyperpolarization in adult rat SG neurons without affecting presynaptic component of the transmission, which are considered to account, at least a part, for the analgesic effects of SST reported previously.

UR - http://www.scopus.com/inward/record.url?scp=0043163768&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0043163768&partnerID=8YFLogxK

U2 - 10.1016/S0168-0102(03)00183-4

DO - 10.1016/S0168-0102(03)00183-4

M3 - Article

VL - 47

SP - 97

EP - 107

JO - Neuroscience Research

JF - Neuroscience Research

SN - 0168-0102

IS - 1

ER -