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Layer-specific NO dependence of long-term potentiation and biased NO release in layer V in the rat auditory cortex

Hidemitsu Wakatsuki *¹, Hiroshi Gomi *, Masaharu Kudoh *, Shinji Kimura *, Kota Takahashi ¹, Masayuki Takeda ¹ and Katsuei Shibuki *

We investigated the role of nitric oxide (NO) in the induction of long-term potentiation (LTP) in slices prepared from the rat auditory cortex.

Tetanic stimulation of layer IV elicited LTP of field potentials in layer II-III (LTP_II-III) and in layer V (LTP_V). The magnitude of LTP_II-III measured at 30 min after tetanic stimulation was 171 ± 9 % (n = 15, mean ± s.e.m.) of the control measured before tetanic stimulation, while that of LTP_V was 138 ± 3 % (n = 17).

NO synthase (NOS) inhibitors had no apparent effect on LTP_II-III, but LTP_V was significantly suppressed (P < 0·001). This suppression of LTP_V was significantly antagonized by a NO donor (P < 0·001) or a cGMP analogue (P < 0·001).

Small non-pyramidal neurones in the auditory cortex were stained with an anti-neuronal NOS antibody. More neurones were stained with the antibody in the deeper cortical layers.

We measured neocortical NO release with electrochemical NO probes. Layer IV stimulation elicited significantly more NO release in layer V than in layer II-III (P < 0·001). The amplitude of the increase in NO concentration elicited by stimulation at 20 Hz for 5 s was 380 ± 14 pM (n = 55) in layer V and 55 ± 8 pM (n = 5) in layer II-III.

NO release in layer V was partially but significantly suppressed by non-NMDA (P < 0·002) or NMDA (P < 0·002) receptor antagonists. Simultaneous application of the antagonists of the two types blocked NO release almost completely.

These results clearly indicate the NO dependence of the induction of LTP_V, and the greater NO release in the deeper layer of the rat auditory cortex.

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