The triple function of the capsaicin-sensitive sensory neurons: In memoriam János Szolcsányi

Erika Pintér; Zsuzsanna Helyes; Éva Szőke; Kata Bölcskei; Angéla Kecskés; Gábor Pethő

doi:10.1080/23328940.2022.2147388

The triple function of the capsaicin-sensitive sensory neurons: In memoriam János Szolcsányi

Temperature (Austin). 2022 Nov 21;10(1):13-34. doi: 10.1080/23328940.2022.2147388. eCollection 2023.

Authors

Erika Pintér^{1

2

3}, Zsuzsanna Helyes^{1

2

3}, Éva Szőke^{1

2

3}, Kata Bölcskei¹, Angéla Kecskés¹, Gábor Pethő^{1

4}

Affiliations

¹ Department of Pharmacology and Pharmacotherapy, Medical School, University of Pécs, Szigeti str. 12, H-7624, Pécs, Hungary.
² National Laboratory for Drug Research and Development, Magyar tudósok krt. 2. H-1117 Budapest, Hungary.
³ Eötvös Lorand Research Network, Chronic Pain Research Group, University of Pécs, H7624, Pécs, Hungary.
⁴ Department of Pharmacology, Faculty of Pharmacy, University of Pécs, Rókus Str. 2, H-7624 , Pécs, Hungary.

Abstract

This paper is dedicated to the memory of János Szolcsányi (1938-2018), an outstanding Hungarian scientist. Among analgesics that act on pain receptors, he identified capsaicin as a selective lead molecule. He studied the application of capsaicin and revealed several physiological (pain, thermoregulation) and pathophysiological (inflammation, gastric ulcer) mechanisms. He discovered a new neuroregulatory system without sensory efferent reflex and investigated its pharmacology. The authors of this review are his former Ph.D. students who carried out their doctoral work in Szolcsányi's laboratory between 1985 and 2010 and report on the scientific results obtained under his guidance. His research group provided evidence for the triple function of the peptidergic capsaicin-sensitive sensory neurons including classical afferent function, local efferent responses, and remote, hormone-like anti-inflammatory, and antinociceptive actions. They also proposed somatostatin receptor type 4 as a promising drug target for the treatment of pain and inflammation. They revealed that neonatal capsaicin treatment caused no acute neuronal death but instead long-lasting selective ultrastructural and functional changes in B-type sensory neurons, similar to adult treatment. They described that lipid raft disruption diminished the agonist-induced channel opening of the TRPV1, TRPA1, and TRPM8 receptors in native sensory neurons. Szolcsányi's group has developed new devices for noxious heat threshold measurement: an increasing temperature hot plate and water bath. This novel approach proved suitable for assessing the thermal antinociceptive effects of analgesics as well as for analyzing peripheral mechanisms of thermonociception.

Keywords: Capsaicin-sensitive neuron; TRPV1; lipid raft; neurogenic inflammation; noxious heat threshold; pain; somatostatin; thermonociception.

Publication types

Review

Grants and funding

This work was funded by the Hungarian National Research, Development and Innovation Office K134214, K138046 and K138936. We acknowledge the support of the Governmental Information Technology Development Agency, Hungary. “Project no. RRF-2.3.1-21-202200015 has been implemented with the support provided by the European Union.” A.K was supported by the János Bolyai Research Scholarship of the Hungarian Academy of Sciences. Bolyai Fellowship and Research grant of Medical School, University of Pécs (KA-2021-23; Hungarian Scientific Research FundMagyarország Kormánya [RRF-2.3.1-21-2022-00015];