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Gustafsson B, Asztely F, Hanse E, et al. Onset Characteristics of Long-Term Potentiation in the Guinea-Pig Hippocampal CA1 Region in Vitro. Eur J Neurosci. 1989;1(4):382-394doi: 10.1111/j.1460-9568.1989.tb00803.x.
Gustafsson, B., Asztely, F., Hanse, E., & Wigström, H. (1989). Onset Characteristics of Long-Term Potentiation in the Guinea-Pig Hippocampal CA1 Region in Vitro. The European journal of neuroscience, 1(4), 382-394. https://doi.org/10.1111/j.1460-9568.1989.tb00803.x
Gustafsson, B., et al. "Onset Characteristics of Long-Term Potentiation in the Guinea-Pig Hippocampal CA1 Region in Vitro." The European journal of neuroscience vol. 1,4 (1989): 382-394. doi: https://doi.org/10.1111/j.1460-9568.1989.tb00803.x
Gustafsson B, Asztely F, Hanse E, Wigström H. Onset Characteristics of Long-Term Potentiation in the Guinea-Pig Hippocampal CA1 Region in Vitro. Eur J Neurosci. 1989 Jul;1(4):382-394. doi: 10.1111/j.1460-9568.1989.tb00803.x. PMID: 12106147.
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Eur J Neurosci. 1989 Jul;1(4):382-394. doi: 10.1111/j.1460-9568.1989.tb00803.x.

Onset Characteristics of Long-Term Potentiation in the Guinea-Pig Hippocampal CA1 Region in Vitro.

The European journal of neuroscience

B. Gustafsson, F. Asztely, E. Hanse, H. Wigström

Affiliations

  1. Department of Physiology and.

PMID: 12106147 DOI: 10.1111/j.1460-9568.1989.tb00803.x

Abstract

The temporal development of long-term potentiation (LTP) was examined in the CA1 region of the hippocampal slice preparation (bath temperature 30 degrees C). LTP was evoked by a single brief afferent tetanus (3 - 40 impulses at 50 Hz) given in the presence of picrotoxin (to facilitate LTP induction). Short-lasting potentiation processes unrelated to LTP were excluded by comparing the potentiation obtained in picrotoxin solution with that obtained in normal solution or in the presence of the N-methyl-D-aspartate receptor antagonist 2-amino-5-phosphonovalerate. LTP was also evoked by pairing single test volleys with brief (2 - 3 impulses) heterosynaptic tetani in picrotoxin solution. Both methods showed no significant rise of LTP until about 3 s after the induction event. LTP thereafter developed almost linearly towards a peak within 20 - 25 s after the tetanus, the time course being practially independent of the induction method and of the relative amount of LTP evoked. The latency and rise time of LTP depended on bath temperature, being about twice as long at 25 degrees C as at 30 degrees C. Following the peak, LTP rapidly decayed to less than half its peak value in 8 min, the decay tending to be less with longer trains. The LTP component reaching its peak 20 - 25 s after a tetanus was practically occluded after a saturating homosynaptic tetanization, and was only partially recovered 1 h afterwards. The latency to the onset of LTP suggests an indirect coupling between the calcium influx, presumed to trigger the potentiation, and the expression of LTP. The independence of the early time course with respect to the induction strength indicates that the intervening system(s) operates in a linear manner.

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