Using a microelectrode technique, we studied the effects of alimentary vitamin В1 deficiency on synaptic transmission in isolated phrenico-hemidiaphragmatic murine preparations. Animals of group І (control) were on a standard thiamine-controlled diet (16 mg/kg thiamine) with no limitations. Animals of group II (control with alimentary limitation) were on the same diet, but daily consumption in these animals was limited and made similar to the amount of food consumed by the animals of group ІІІ within idential periods of cage housing (for differentiation of the effects of anorexia related to the thiamine-deficient state in group III and proper effects of В1 hypovitaminosis). Animals of group ІІІ (thiamine-deficient) were on a standard diet (with no limitations) mostly analogous to that in group І but containing no thiamine. In phrenicohemidiaphragmatic preparations obtained from animals of group ІІІ, the amplitude of end-plate potentials (EPPs) and miniature EPPs (mEPPs) on the 10th day of consumption of the thiamine-defficient diet and the quantum composition of EPPs on the 20th day became significantly (Р < 0.01) smaller than in preparations obtained from animals of both groups І and ІІ. The frequency of mEPPs and membrane potential of muscle fibers in group ІІІ remained unchanged. Two processes, a decrease in the dimension of the transmitter quantum (which is observed within rather early stages of the development of thiamine-defficient state) and a decrease in the quantum composition of evoked EPPs (at later stages) underlie a gradual decrease in the amplitude of EPPs related to the development of alimentary vitamin В1 deficiency.
This is a preview of subscription content, log in via an institution to check access.
Similar content being viewed by others
Explore related subjects
Discover the latest articles and news from researchers in related subjects, suggested using machine learning.References
C. Luxemburger, N. J. White, F. ter Kuile, et al., “Beri-beri: the major cause of infant mortality in Karen refugees,” Trans. Roy. Soc. Trop. Med. Hyg., 97, No. 2, 251–255 (2003).
A. D. Thomson and E. J. Marshall, “The treatment of patients at risk of developing Wernicke’s encephalopathy in the community,” Alcohol Alcoholism, 41, No. 2, 159–167 (2006).
B. M. Koffman, L. J. Greenfield, I. I. Ali, and N. A. Pirzada, “Neurologic complications after surgery for obesity,” Muscle Nerve, 33, No. 2, 166–176 (2006).
M. Gokce, E. Bulbuloglu, D. Tuncel, et al., “Nonalcoholic Wernicke’s encephalopathy with prominent astasia and optic neuropathy,” Med. Princ. Pract., 14, No. 6, 438–440 (2005).
S. C. Hung, S. H. Hung, D. C. Tarng, et al., “Thiamine deficiency and unexplained encephalopathy in hemodialysis and peritoneal dialysis patients,” Am. J. Kidney Dis., 38, No. 5, 941–947 (2001).
U. Undraccolo, G. Gentile, G. Pomili, et al., “Thiamine deficiency and beriberi features in a patient with hyperemesis gravidarum,” Nutrition, 21, No. 9, 967–968 (2005).
M. L. Alcaide, D. Jayaweera, L. Espinoza, and M. Kolber, “Wernicke’s encephalopathy in AIDS: a preventable cause of fatal neurological deficit,” Int. J. STD AIDS, 14, No. 10, 712–713 (2003).
H. Onishi, C. Kawanishi, M. Onose, et al., “Successful treatment of Wernicke encephalopathy in terminally ill cancer patients: report of 3 cases and review of the literature,” Support Care Cancer, 12, No. 8, 604–608 (2004).
A. Kesler, C. Stolovich, C. Hoffmann, et al., “Acute ophthalmoplegia and nystagmus in infants fed a thiamine-deficient formula: an epidemic of Wernicke encephalopathy,” J. Neuroophthalmol., 25, No. 3, 169–172 (2005).
S. Sekiyama, S. Takagi, and Y. Kondo, “Peripheral neuropathy due to thiamine deficiency after inappropriate diet and total gastrectomy,” Tokai J. Exp. Clin. Med., 30, No. 3, 137–140 (2005).
A. P. Betrosian, E. Thireos, K. Toutouzas, et al., “Occidental beriberi and sudden death,” Am. J. Med. Sci., 327, No. 5, 250–252 (2004).
H. Koike, K. Misu, N. Hattori, et al., “Postgastrectomy polyneuropathy with thiamine deficiency,” J. Neurol., Neurosurg., Psychiat., 71, No. 3, 357–362 (2001).
G. E. Gibson, H. Ksiezak-Reding, K. F. R. Sheu, et al., “Correlation of enzymatic, metabolic and behavioral deficits in thiamine deficits and its reversal,” Neurochem. Res., 9, 803–814 (1984).
A. V. Romanenko and S. E. Shepelev, “Effect of В1 hypovitaminosis on the efficacy of neuromuscular transmission in the murine diaphragm,” Neurophysiology, 39, Nos. 4/5, 366–368 (2007).
A. V. Romanenko and S. E. Shepelev, “Thiamineinduced modification of neuromuscular transmission at В1 hypovitaminosis,” Klin. Eksp. Patol., 7, No. 1, 92–97 (2008).
О. Nakagawasai, T. Tadano, S. Hozumi, et al., “Characteristics of depressive behavior induced by feeding thiamine-deficient diet in mice,” Life Sci., 69, No. 10, 1181–1191 (2001).
P. G. Kostyuk, Microelectrode Technique [in Russian], Publishing House of Acad. Sci. of Ukrainian SSR, Kyiv (1966).
O. P. Balesina and A. N. Bukiya, “Spontaneous activity of murine neuromuscular junctions in the presence of dantrolene,” Neurophysіology, 33, No. 2, 79–85 (2001).
D. P. Matyushkin, T. M. Drabkina, and I. A. Shabunova, “Quantitative estimate of the function of presynaptic apparatus in single and multiple synapses,” Usp. Fiziol. Nauk, 11, No. 2, 49–70 (1980).
R. F. Rokitskii, Biological Statistics [in Russian], Vyssh. Shkola, Minsk (1973).
S. S. Kelly, “Dietary restriction and miniature end-plate potentials,” J. Physiol., 277, 72P (1978).
L. G. Ermilov, C. B. Mantilla, K. L. Rowley, and G. C. Sieck, “Safety factor for neuromuscular transmission at type-identified diaphragm fibers,” Muscle Nerve, 35, No. 6, 800–803 (2007).
A. Szutowicz, M. Tomaszewicz, and H. Bielarczyk, “Disturbances of acetyl-CoA, energy and acetylcholine metabolism in some encephalopathies,” Acta Neurobiol. Exp., 56, No. 1, 323–339 (1996).
R. H. Edwards, “The neurotransmitter cycle and quantal size,” Neuron, 55, 835–858 (2007).
D. Elmqvist and D. M. J. Quastel, “Presynaptic action of hemicholinium at the neuromuscular junction,” J. Physiol., 177, 463–482 (1965).
H. Aikawa, I. S. Watanabe, T. Furuse, et al., “Low energy levels in thiamine-deficient encephalopathy,” J. Neuropathol. Exp. Neurol., 43, 276–287 (1984).
W. D. Parker, R. Haas, D. A. Stumpf, et al., “Brain mitochondrial metabolism in experimental thiamine deficiency,” Neurology, 34, 477–481 (1984).
R. B. Kelly, “Storage and release of neurotransmitters,” Cell, 72, 43–53 (1993).
A. L. Zefirov, “Vesicular cycle in the presynaptic nerve terminal,” Ross. Fiziol. Zh., 93, No. 5, 544–562 (2007).
D. Sulzer and E. N. Pothos, “Regulation of quantal size by presynaptic mechanisms,” Rev. Neurosci., 11, 159–212 (2000).
J. Czerniecki, G. Chanas, M. Verlaet, et al., “Neuronal localization of the 5-kDa specific thiamine triphosphatase in rodent brain,” Neuroscience, 125, No. 4, 833–840 (2004).
H. O. Nghiêm, L. Bettendorff, and J. P. Changeux, “Specific phosphorylation of Torpedo 43 K rapsyn by endogenous kinase(s) with thiamine triphosphate as the phosphate donor,” FASEB J., 14, No. 3, 543–554 (2000).
V. J. Armet and J. R. Cooper, “The role of thiamine in nervous tissue: effect of antimetabolites of vitamin on conduction in mammalian non-myelinated nerve fibers,” J. Pharmacol. Exp. Ther., 148, No. 2, 137–146 (1965).
J. M. Eichenbaum and J. R. Cooper, “Restoration by thiamine of the action potential in ultraviolet irradiated nerve,” Brain Res., 32, 258–260 (1971).
J. M. Fox and W. Duppel, “The action of thiamine and its di- and triphosphates on the slow exponential decline of the ionic currents in the node of Ranvier,” Brain Res., 89, 287–302 (1974).
A. L. Zefirov and G. F. Sitdikova, “Ion channels of the nerve terminal,” Usp. Fiziol. Nauk, 33, No. 4, 3–33 (2002).
J. I. Brigant and A. Mallart, “Presynaptic currents in mouse motor endings,” J. Physiol., 333, 619–639 (1984).
A. Mallart, “А calcium-activated potassium current in motor nerve terminals of the mouse,” J. Physiol., 368, 577–591 (1985).
B. Sh. Gafurov, A. L. Zefirov, and D. M. Shakir’yanova, “Ion currents in a motor nerve terminal of the mouse (electrophysiology and computer simulation),” Neurophysiology, 29, No. 1, 57–64 (1997).
A. V. Romanneko, “The effect of thiamine on neuromuscular transmission in frog,” Neirofiziologiya, 17, No. 6, 794–800 (1985).
S. K. Sharma and J. H. Quastel, “Transport and metabolism of thiamine in rat brain cortex in vitro,” Biochem. J., 94, No. 3, 790–800 (1965).
R. Spector, “Thiamine transport in the central nervous system,” Am. J. Physiol., 230, No. 4, 1101–1107 (1976).
J. Greenwood, R. E. Love, and O. E. Pratt, “Kinetics of thiamine transport across blood-brain barrier in the rat,” J. Physiol., 327, 95–103 (1982).
Y. M. Ostrovskii, Active Centers and Grouping in the Thiamine Molecule [in Russian], Nauka Technika, Minsk (1975).
A. Muralt, “The role of thiamine in neurophysiology,” Ann. N. Y. Acad. Sci., 98, No. 2, 499–507 (1962).
L. Waldenlind, “Release of thiamine and formation of metylthiamine-like substance in the phrenic nervediaphragm preparation of the rat,” Acta Physiol. Scand., 101, No. 1, 22–27 (1977).
V. A. Dyatlov, “Effect of thiamine on the processes responsible for acetylcholine secretion in the frog neuromuscular synapses,” Neurophysiology, 26, No. 4, 243–249 (1994).
Author information
Authors and Affiliations
Corresponding author
Additional information
Neirofiziologiya/Neurophysiology, Vol. 40, No. 4, pp. 322–331, July–August, 2008.
Rights and permissions
About this article
Cite this article
Romanenko, A.V., Shepelev, S.E. Effect of Vitamin В1 Alimentary Deficiency on Spontaneous and Evoked Transmitter Release in Murine Neuromuscular Synapses. Neurophysiology 40, 270–278 (2008). https://doi.org/10.1007/s11062-009-9043-x
Received:
Published:
Issue Date:
DOI: https://doi.org/10.1007/s11062-009-9043-x