Fluoride-resistant acid phosphatase (FRAP)-reactive terminals making contact with interneuronal soma are found in the substantia gelatinosa of the mouse spinal dorsal horn. About one half of the interneuronal somata receive FRAP-positive boutons. By electron microscopy, these FRAP-positive terminals appear small, dark, slender, roundish, cap-like, ellipsoid or sinuous and electron-dense, scalloped (fan-like) contours with clear spherical synaptic vesicles of variable size, some large dense-core vesicles and mitochondria. All these features are very similar to those of capsaicin-sensitive terminals. Thus they are considered to be nociceptive primary afferent endings. Therefore, some of the FRAP-positive terminals are suggested to have a modulatory role in the nociceptive circuit in the substantia gelatinosa.
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http://dx.doi.org/10.2535/ofaj1936.74.2-3_109 | DOI Listing |
Neurosci Lett
January 2025
Division of Anesthesiology, Niigata University Graduate School of Medical and Dental Sciences, 1-757 Asahimachi Dori, Chuo-Ku, Niigata City, Niigata 951-8510, Japan. Electronic address:
Spinal cord injuries (SCIs) can lead to severe neuropathic pain and increased risk of myocardial infarction and heart failure; therefore, the use of analgesics against SCI-induced pain should be minimized because of their adverse effects on the cardiovascular system. Ivabradine, a blocker of hyperpolarization-activated cyclic nucleotide-gated cation (HCN) channels, is used as a bradycardic agent, but recent studies focused on it as an analgesic agent for peripheral neuropathic pain. However, the analgesic effects of ivabradine on central neuropathic pain, such as SCI-induced pain, have not been examined.
View Article and Find Full Text PDFFront Neurosci
February 2024
Division of Anesthesiology, Niigata University Graduate School of Medical and Dental Sciences, Niigata, Japan.
Spinal cord injury (SCI) leads to the development of neuropathic pain. Although a multitude of pathological processes contribute to SCI-induced pain, excessive intracellular calcium accumulation and voltage-gated calcium-channel upregulation play critical roles in SCI-induced pain. However, the role of calcium-channel blockers in SCI-induced pain is unknown.
View Article and Find Full Text PDFNeurosci Lett
February 2024
Department of Physiology, Zunyi Medical University, Zunyi 563000, China. Electronic address:
Previous studies have shown that the hyperpolarized cyclic nucleotide gated (HCN) ion channels in the spinal dorsal horn (SDH) might be involved in the development of diabetic neuropathic pain (DNP). Additionally, other studies have shown that the decreased potassium-chloride cotransporter 2 (KCC2) expression in the SDH promotes pain hypersensitivity. Both HCN channels and KCC2 were highly expressed in spinal substantia gelatinosa neurons.
View Article and Find Full Text PDFKorean J Physiol Pharmacol
January 2024
Department of Oral Physiology, School of Dentistry & Institute of Oral Bioscience, Jeonbuk National University, Jeonju 54896, Korea.
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