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Purpose. To test the model of spinal cord lateral hemiexcision in young rats. Materials and methods. Animals ‒ male rats (age about 1 month, body weight about 50 g, inbred derivatives of the Wistar line); the number of experimental groups is: 1) lateral spinal cord hemisection at the level of segments about T12–T13 (Sect; n=11); 2) lateral spinal cord hemiexcision about 1 mm long at the similar level (Exc; n=8). Assessment of motor Function Index (FI) and the Spasticity Index (SI) of the paretic hindlimb was carried out using the Basso–Beattie–Bresnahan (BBB) scale and Ashworth scale, respectively, in our technical modifications. The non-inclusion criteria: the BBB score above 9 points of FI for the ipsilateral hindlimb in a week after injury ‒and / or BBB score less than or equal to 14 points of FI of the contralateral hindlimb during a long follow-up period (in general, 2 animals in the Sect group, 3 animals ‒ in the Exc group). Asymptotic differences in the timing of testing between subgroups and groups were revealed during the first three weeks of follow-up. Interpolation reproduction of individual values of FI and SI was used in exceptional cases. The total follow-up period was 5 months. Statistical analysis was performed using the Mann-Whitney U Test, Wilcoxon Matched Pairs Test, Spearman’s Rank Order Correlation. For pathomorphological study, the method of silver impregnation of the spinal cord longitudinal sections of the Exc group animals obtained in 5 months after the simulation of injury was used. Results. One week after injury, the FI in the Sect group was 5.9±1.1 according to BBB points, a statistically significant increase in the FI lasted for the first 3 weeks (p

Previously, we have characterized the capsaicin-insensitive low pH-sensitive (caps−lpH+) subtype of small-sized nociceptive dorsal root ganglion (DRG) neurons that express acid-sensing ion channels, T-type Ca2+ channels, and have isolectin B4-negative phenotype. These neurons demonstrated increased excitability in a model of long-term diabetes, contributing to chronic pain sensation. Here we studied changes in the excitability of the caps−lpH+ neurons and underlying changes in the functional expression and gating properties of ion channels under complete Freund's adjuvant (CFA)-induced peripheral inflammation. We have found that, under these pathological conditions, the functional expression of the acid-sensing ion channels (ASICs) and voltage-gated Na+ channels, was increased. In addition, T-type Ca2+ current was significantly increased in the neurons at the membrane potentials close to its resting value. Altogether, the observed changes in the channel functioning shifted a pH level evoking an action potential (AP) toward its physiological value and led to an increase of evoked and spontaneous excitability of the caps−lpH+ neurons that may contribute to hyperalgesia and chronic inflammatory pain.

Corrections to the article: https://doi.org/10.25305/unj.234154 In the article by V.V. Medvedev et al., published in UNJ № 3 in 2021, the source number 92 from the reference list does not support the statement given in the appropriate place in the text. Instead, we offer the reader two other works that mention the presence of posterior median spinal artery in the adult rat - D. Mazensky et al. (2017) and O.U. Scremin (G. Paxinos, ed.; 2015, p. 1003, 1005). In most works on this topic (Z. Zhang et al., 2001; Y. Cao et al., 2015; P. Li et al., 2020) the dorsal median vein is considered as the median vessel of the posterior surface of the rat spinal cord, and as in humans, describe 2 parallel dorsal spinal arteries. At the same time, D. Mazensky et al. (2017), sharing the opinion of O.U. Scremin (2015), mention 3 dorsal spinal arteries of the rat, in particular the median one. Taking into account that, from our experience, damage to the median vessel of the posterior surface of the spinal cord is accompanied by its rapid edema and irrepversible deep deficit in the motor function of both hind limbs of the animal, we consider it necessary to draw the reader's attention to this feature of the anatomy of the spinal arteries of an adult rat. Medvediev VV, Abdallah IM, Draguntsova NG, Savosko SI, Vaslovych VV, Tsymbaliuk VI, Voitenko NV. [Model of spinal cord lateral hemi-excision at the lower thoracic level for the tasks of reconstructive and experimental neurosurgery]. Ukr Neurosurg J [Internet]. 2021 Sep 27 [cited 2021 Oct 11];27(3):33-5. Available from: http://theunj.org/article/view/234154 Cao Y, Wu T, Yuan Z, Li D, Ni S, Hu J, Lu H. Three-dimensional imaging of microvasculature in the rat spinal cord following injury. Sci Rep. 2015 Jul 29;5:12643. doi: 10.1038/srep12643. PMID: 26220842; PMCID: PMC4518284. Li P, Xu Y, Cao Y, Wu T. 3D Digital Anatomic Angioarchitecture of the Rat Spinal Cord: A Synchrotron Radiation Micro-CT Study. Front Neuroanat. 2020 Jul 22;14:41. doi: 10.3389/fnana.2020.00041. PMID: 32792915; PMCID: PMC7387706. Mazensky D, Flesarova S, Sulla I. Arterial Blood Supply to the Spinal Cord in Animal Models of Spinal Cord Injury. A Review. Anat Rec (Hoboken). 2017 Dec;300(12):2091-2106. doi: 10.1002/ar.23694. Epub 2017 Oct 13. PMID: 28972696. Paxinos G, editor. The rat nervous system. 4th ed., London: Elsevier; 2015. Scremin OU. Capter 31, Cerebral Vascular System; p. 985‒1011. Zhang Z, Nonaka H, Nagayama T, Hatori T, Ihara F, Zhang L, Akima M. Circulatory disturbance of rat spinal cord induced by occluding ligation of the dorsal spinal vein. Acta Neuropathol. 2001 Oct;102(4):335-8. doi: 10.1007/s004010100377. PMID: 11603808.

T-type Ca2+ channels are known as important participants of nociception and their remodeling contributes to diabetes-induced alterations of pain sensation. In this work we have established that about 30% of rat nonpeptidergic thermal C-type nociceptive (NTCN) neurons of segments L4–L6 express a slow T-type Ca2+ current (T-current) while a fast T-current is expressed in the other 70% of these neurons. Streptozotocin-induced diabetes in young rats resulted in thermal hyperalgesia, hypoalgesia, or normalgesia 5-6 weeks after the induction. Our results show that NTCN neurons obtained from hyperalgesic animals do not express the slow T-current. Meanwhile, the fraction of neurons expressing the slow T-current did not significantly change in the hypo- and normalgesic diabetic groups. Moreover, the peak current density of fast T-current was significantly increased only in the neurons of hyperalgesic group. In contrast, the peak current density of slow T-current was significantly decreased in the hypo- and normalgesic groups. Experimental diabetes also resulted in a depolarizing shift of steady-state inactivation of fast T-current in the hyperalgesic group and slow T-current in the hypo- and normalgesic groups. We suggest that the observed changes may contribute to expression of different types of peripheral diabetic neuropathy occurring during the development of diabetes mellitus.