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Strontium‐induced asynchronous transmitter release during central sensitization in the mouse spinal cord dorsal horn
Author(s) -
Iwata Hideaki,
Fukushima Teruyuki,
Takasusuki Toshifumi,
Furukawa Naoki,
Watanabe Masashi,
Yamaguchi Shigeki,
Kitajima Toshimitsu,
Hori Yuuichi
Publication year - 2006
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.20.5.a1415-d
Long‐term potentiation (LTP) and long‐term depression (LTD) in synaptic strength have been observed in the spinal dorsal horn. It is suggested that spinal LTP and LTD underlie central sensitization leading to hyperalgesia and allodynia. At present, however, the mechanisms modulating neuronal plastic changes in the spinal cord has not been elucidated in detail. Clarification of cellular mechanisms underlying neuronal plasticity in the spinal dorsal horn was attempted in the present study. We made patch‐clamp recordings of excitatory postsynaptic currents (EPSCs) from superficial dorsal horn neurons in the spinal cord slices and analyzed strontium‐induced asynchronous neurotransmitter release from stimulated synapses. The amplitude distribution of strontium‐induced asynchronous EPSCs was quite similar to that of miniature EPSCs recorded in the presence of tetrodotoxin. The frequency of strontium‐induced asynchronous EPSCs at stimulated synapses increased after LTP induction and decreased after LTD induction. The mean amplitude of asynchronous EPSCs in the presence of strontium did not change in many cases of both LTP and LTD. However, the mean amplitude of EPSCs significantly increased and decreased in some instances of LTP and LTD, respectively. These findings may suggest both pre‐ and postsynaptic mechanisms of central sensitization in the mouse spinal cord dorsal horn.