Rodinsky O. G., Tkachenko S. S., Marazha I. O.

BIOELECTRIC ACTIVITY OF DORSAL SPINAL CORD FIBERS IN EXPERIMENTAL HYPOANDROGENEMIA


About the author:

Rodinsky O. G., Tkachenko S. S., Marazha I. O.

Heading:

CLINICAL AND EXPERIMENTAL MEDICINE

Type of article:

Scentific article

Annotation:

Aim. The purpose of these studies was to determine the excitability characteristics of the afferent fibers of the gluteal nerve, as well as to analyze the peculiarities of the responses of spinal ganglion neurons in the SC caused by stimulation of the gluteal nerve and registered in the proximal sections of the DC under experimental hypoandrogenemia at the onset of 4 months. Object and methods. The study was performed on 29 rats of 5-6-month-old Wistar males weighing 180-260 g, which were divided into experimental (n = 17) and control (n = 12) groups. The experimental model was created by surgical castration of adult male white rats. Both groups of animals were kept under standard vivarium conditions (t ° 22 ± 2 ° C, light / dark cycle – 12/12 h) on a standard diet for 120 days, after which the animals were involved in an acute experiment. Removal of the evoked activity was performed from the proximal portion of the dorsal root L5 with stimulation of the ipsilateral sciatic nerve with pulses of 0.3 ms duration and force from 1 to 5 thresholds, which provided activation of both low- and high-threshold nerve fibers. Threshold, chronoxia, latency, amplitude, and duration of evoked potentials were analyzed, and the phenomenon of refractivity was investigated by pairwise stimuli at intervals of 2 to 20 ms. Results. In animals of the control group, the mean threshold of the evoked response was 0.015 ± 0.001 mA, whereas in animals with experimental hypoandrogenemia, it was increased to 0.041 ± 0.003 mA, which was 281.63 ± 7.32% compared with the control group of animals (p < 0.001). Chronoxia in control rats was equal to 70.67 ± 1.49 µs, in animals with hypoandrogenemia decreased by 31.67 ± 4.04% (p <0.001), which in absolute terms equaled 48.29 ± 1.95 µs. The latent response period in castrated animals increased by 102.7 ± 4% (0.75 ± 0.03 ms) relative to that of control animals (0.37 ± 0.09 ms, p <0.001). The overall duration of the evoked response decreased and amounted to 84.53 ± 2.98% (2.35 ± 0.07 ms) relative to the control group index (2.78 ± 0.41 ms, p <0.01). The amplitude of the integral action potential of dorsal root fibers increased significantly by 97.28 ± 4.83% (2.90 ± 0.14 mV) compared to the control (1.47 ± 0.18 mV, p <0.001). Analysis of data obtained with the use of stimulation by paired pulses revealed almost complete restoration of the amplitude of the evoked response to the test stimulus in animals with orchiectomy already at the interstimulus interval of 1 ms (80,82 ± 3,29%, n = 14) with high reliability (p < 0.001) and 99.04 ± 2.85% (p <0.001) at the 2 ms interval, whereas in the animals of the control group the response to the test stimulus was first recorded at the 2 ms interval and its amplitude averaged only 17.95 ± 4.02% (n = 11) of the response amplitude of the conditioning stimulus. The full restoration of the amplitude of the second PD in the control group was at the interval of 10 ms (100.09 ± 1.84%). Conclusions. The influence of long-existing hypoandrogenemia has a different effect on the functioning of afferent leading pathways of the segmental somatic reflex arc, reducing the excitability of the nerve structures of the dorsal root, and increasing the amplitude of the evoked response. In addition, despite the increase in the duration of the latency period, afferent fibers under conditions of androgen deficiency showed a marked increase in lability

Tags:

androgen, castration, dorsal root, nerve, excitation.

Bibliography:

  1. Armagan A, Hatsushi K, Toselli P. The effects of testosterone deficiency on the structural integrity of the penile dorsal nerve in the rat. International Journal of Impotence Research. 2008;20:73-8.
  2. Sarkey S, Azcoitia I, Garcia-Segura LM. Classical androgen receptors in non-classical sites in the brain. Horm Behav. 2008 May;53(5):753- 64.
  3. Biatek M, Zaremba P, Borowicz KK. Neuroprotective role of testosterone in the nervous system. Polish journal of pharmacology. 2004;56:509-18.
  4. Beitel LK, Alvarado C, Mokhtar S. Mechanisms mediating spinal and bulbar muscular atrophy: investigations into polyglutamine-expanded androgen receptor function and dysfunction. Frontiers in Neurology. 2013;53(4):1-16.
  5. Hussain R, Ghoumari AM, Bielecki B. The neural androgen receptor: a therapeutic target for myelin repair in chronic demyelination. Brain a journal of neurology. 2013;136:132-46.
  6. Verhovshek T, Rudolph LM, Sengelaub DR. BDNF and androgen interactions in spinal neuromuscular systems. Neuroscience. 2013 June 3;239:103-14.
  7. Pesaresi M, Soon-Shiong R, French L. Axon diameter and axonal transport: In vivo and in vitro effects of androgens. Neuroimage. 2015 July 15;115:191-201.
  8. Rodynskyy OH, Tkachenko SS, Huz LV. Vyklykana bioelektrychna aktyvnist eferentnykh volokon sidnychnoho nerva bilykh shchuriv za umov eksperymental`noyi menopauzy. Medychni perspektyvy. 2016;106(1):167-71. [in Ukrainian].
  9. Rodynskyy OH, Tkachenko SS, Zynov’yeva OH. Zmina zbudlyvosti rukhovykh volokon sidnychnoho nerva bilykh shchuriv za umov tryvaloyi hipoestrohenemiyi. Ukrayinskyy zhurnal medytsyny, biolohiyi ta sportu. 2015;2:169-71. [in Ukrainian].
  10. Keast JR, Gleeson RJ. Androgen receptor immunoreactivity is present in primary sensory neurons of male rats. Neuroreport. 1998 Dec 21;9(18):4137-40. DOI: 10.1097/00001756-199812210-00025
  11. Hammond J, Le Q, Goodyer C. Testosterone-mediated neuroprotection through the androgen receptor in human primary neurons. Journal of Neurochemistry. 2001;77:1319-26.
  12. Pike CJ, Carroll JC, Rosario ER. Protective actions of sex steroid hormones in Alzheimer’s disease. Frontiers in Neuroendocrinology. 2009 July;30(2):239-58.
  13. Dmitriyeva OA, Sherstyuk BV. Vliyaniye stress-indutsirovannogo snizheniya urovnya testosterona na gistokhimicheskiye izmeneniya polovykh organov krys. Pacific Medical Journal. 2007;3:55-7. [in Russiаn].
  14. Foradori CD, Weiser MJ, Handa RJ. Non-genomic Actions of Androgens. Frontiers in Neuroendocrinology. 2008 May;29(2):169-81.
  15. Asuthkar S, Demirkhanyan L, Sun X, Elustondo PA, Krishnan V, Baskaran P, et al. The TRPM8 Protein Is a Testosterone Receptor. Journal of Biological Chemistry. 2015 Jan 30;290(5):2670-88. DOI: 10.1074/jbc.M114.610873
  16. Narayanan R, Mohler ML, Bohl CE. Selective androgen receptor modulators in preclinical and clinical development. The Open Access Journal of the Nuclear Receptor Signaling Atlas. 2008;6:1-26.
  17. Estrada M, Varshney A, Ehrlich BE. Elevated testosterone induces apoptosis in neuronal cells. J. Biological chemistry. 2006;281(35):25492- 501.
  18. Makiy YeA, Rodynskyy OH, Mozhunov OV. Efaptychne zbudzhennya v nervoviy systemi ta umovy yoho vynyknennya pry patolohichnykh stanakh. Medychni perspektyvy. 2003;8(1):37-42. [in Ukrainian].
  19. Makiy YeA, Nerush PA, Rodinskiy AG. Kharakteristika vyzvannykh otvetov afferentnykh i efferentnykh volokon sedalishchnogo nerva u krys v usloviyakh eksperimental’nogo gipertireoza. Neyrofiziologiya. 2002;34(1):51-9. [in Russiаn].

Publication of the article:

«Bulletin of problems biology and medicine» Issue 2 (156), 2020 year, 154-158 pages, index UDK 612.83:612.662.9:618.173-073.7/-076-085:615.2.1-092.9

DOI: