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Article

Ceftriaxone Treatment Weakens Long-Term Synaptic Potentiation in the Hippocampus of Young Rats

by
Tatyana Y. Postnikova
,
Sergey L. Malkin
,
Maria V. Zakharova
,
Ilya V. Smolensky
,
Olga E. Zubareva
and
Aleksey V. Zaitsev
*
Sechenov Institute of Evolutionary Physiology and Biochemistry of RAS, 44, Toreza Prospekt, 194223 Saint Petersburg, Russia
*
Author to whom correspondence should be addressed.
Int. J. Mol. Sci. 2021, 22(16), 8417; https://doi.org/10.3390/ijms22168417
Submission received: 19 July 2021 / Revised: 28 July 2021 / Accepted: 2 August 2021 / Published: 5 August 2021

Abstract

Disrupted glutamate clearance in the synaptic cleft leads to synaptic dysfunction and neurological diseases. Decreased glutamate removal from the synaptic cleft is known to cause excitotoxicity. Data on the physiological effects of increased glutamate clearance are contradictory. This study investigated the consequences of ceftriaxone (CTX), an enhancer of glutamate transporter 1 expression, treatment on long-term synaptic potentiation (LTP) in the hippocampus of young rats. In this study, 5-day administration of CTX (200 mg/kg) significantly weakened LTP in CA3-CA1 synapses. As shown by electrophysiological recordings, LTP attenuation was associated with weakening of N-Methyl-D-aspartate receptor (NMDAR)-dependent signaling in synapses. However, PCR analysis did not show downregulation of NMDAR subunits or changes in the expression of α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor (AMPAR) subunits. We assume that extracellular burst stimulation activates fewer synapses in CTX-treated animals because increased glutamate reuptake results in reduced spillover, and neighboring synapses do not participate in neurotransmission. Attenuation of LTP was not accompanied by noticeable behavioral changes in the CTX group, with no behavioral abnormalities observed in the open field test or Morris water maze test. Thus, our experiments show that increased glutamate clearance can impair long-term synaptic plasticity and that this phenomenon can be considered a potential side effect of CTX treatment.
Keywords: long-term potentiation; NMDA receptor; hippocampus; EAAT2; memory long-term potentiation; NMDA receptor; hippocampus; EAAT2; memory

Share and Cite

MDPI and ACS Style

Postnikova, T.Y.; Malkin, S.L.; Zakharova, M.V.; Smolensky, I.V.; Zubareva, O.E.; Zaitsev, A.V. Ceftriaxone Treatment Weakens Long-Term Synaptic Potentiation in the Hippocampus of Young Rats. Int. J. Mol. Sci. 2021, 22, 8417. https://doi.org/10.3390/ijms22168417

AMA Style

Postnikova TY, Malkin SL, Zakharova MV, Smolensky IV, Zubareva OE, Zaitsev AV. Ceftriaxone Treatment Weakens Long-Term Synaptic Potentiation in the Hippocampus of Young Rats. International Journal of Molecular Sciences. 2021; 22(16):8417. https://doi.org/10.3390/ijms22168417

Chicago/Turabian Style

Postnikova, Tatyana Y., Sergey L. Malkin, Maria V. Zakharova, Ilya V. Smolensky, Olga E. Zubareva, and Aleksey V. Zaitsev. 2021. "Ceftriaxone Treatment Weakens Long-Term Synaptic Potentiation in the Hippocampus of Young Rats" International Journal of Molecular Sciences 22, no. 16: 8417. https://doi.org/10.3390/ijms22168417

APA Style

Postnikova, T. Y., Malkin, S. L., Zakharova, M. V., Smolensky, I. V., Zubareva, O. E., & Zaitsev, A. V. (2021). Ceftriaxone Treatment Weakens Long-Term Synaptic Potentiation in the Hippocampus of Young Rats. International Journal of Molecular Sciences, 22(16), 8417. https://doi.org/10.3390/ijms22168417

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