Comparison of the subsequent LTP in hippocampal synapses primed by low frequency stimulations ranging from 0.5 to 5 Hz: An in vivo study

TAN B., DURSUN N., Stier C.

NEUROSCIENCE LETTERS, cilt.767, 2022 (SCI-Expanded) identifier identifier identifier

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 767
  • Basım Tarihi: 2022
  • Doi Numarası: 10.1016/j.neulet.2021.136311
  • Dergi Adı: NEUROSCIENCE LETTERS
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus, Academic Search Premier, Animal Behavior Abstracts, BIOSIS, CAB Abstracts, Chemical Abstracts Core, EMBASE, MEDLINE, Veterinary Science Database
  • Anahtar Kelimeler: Hippocampus, Synaptic plasticity, BCM theory, Long-term potentiation
  • Erciyes Üniversitesi Adresli: Evet

Özet

According to the Bienenstock, Cooper, and Munro's (BCM) model, the level of afferent activity regulates the point of crossover from long-term depression (LTD) to long-term potentiation (LTP) of the active synapses. Although experimental results from the hippocampus and visual cortex have supported the BCM theory, it remains unclear whether previous activity of synapses regulates the output of neuron populations in vivo, as expected from the theory. In the present study, we studied the effects of priming stimulations at different frequencies (LFS, 0.5, 1, 2 and 5 Hz) on the magnitude of LTP at synaptic and somatic levels in the dentate gyrus of hippocampal formation. LTP in the dentate gyrus (DG) of LFS-primed or unprimed hippocampal formation was induced by delivering of tetanic stimulation to the perforant pathway (PP) in anesthetized rats. The field excitatory postsynaptic potential (fEPSP) slope and the population spike (PS) amplitude were evaluated to measure the magnitude of LTP. 1 Hz-and 5 Hz-(not 0.5 Hz and 2 Hz) stimulation of the PP led to an early LTD of fEPSP. The LTP of fEPSP was completely inhibited by previously delivering 0.5 Hz and 2 Hz LFS, but instead converted to LTD by 1 Hz LFS. However, none of the frequencies used was able to inhibit the LTP of PS. These results suggest that temporal dynamics which are critical to determine the direction of synaptic plasticity has no impact on the plasticity of neuronal output. We concluded that it is needed to explain why neuronal output does not behave within the framework of the BCM theory.