Nitric oxide synthase inhibitors block long-term potentiation induced by weak but not strong tetanic stimulation at physiological brain temperatures in rat hippocampal slices

Haley, Jane E.; Malen, Peter; Chapman, Paul F.

doi:10.1016/0304-3940(93)90919-c

Cited by 100 publications

(59 citation statements)

References 11 publications

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“…One possible explanation for this apparent discrepancy is that, like the ability of NO synthase inhibitors to block LTP (Haley et al 1993;Williams et al 1993b), the ability of cGMP to cause LTP depends critically on the experimental conditions. Because of the potential significance of these observations in elucidating the site and mechanisms of LTP expression, we have reexamined the effects on synaptic strength of pairing tetanic stimulation (in the presence of an NMDA receptor antagonist) with application of 8-bromocGMP using a variety of experimental conditions in several different laboratories.…”

Section: Cgmp and Ltpmentioning

confidence: 99%

Examination of the role of cGMP in long-term potentiation in the CA1 region of the hippocampus.

et al. 1996

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The mechanisms underlying the generation of NMDA receptor-dependent LTP in the CA1 region of the hippocampus continue to receive a great deal of attention because of the postulated importance of LTP as a synaptic mechanism for learning and memory. It is well accepted that the initial induction of LTP occurs in the postsynaptic cell, but the site of expression remains controversial. One prominent hypothesis is that LTP involves the release of one or more retrograde messengers that act on the presynaptic terminal to enhance transmitter release. Recently, evidence has been presented that retrograde messengers function to activate presynaptic guanylyl cyclase and that the resulting rise in presynaptic cGMP levels, when accompanied by presynaptic activity, is responsible for generating an early component of LTP. We have tested this hypothesis by examining whether synaptic strength is increased by coupling tetanic stimulation with application of a membrane-permeable analog of cGMP. The experiments were done in the presence of an NMDA receptor antagonist to block postsynaptic induction mechanisms. Under a variety of 6Corresponding author. experimental conditions, this manipulation failed to generate LTP, suggesting that an increase in cGMP levels accompanied by presynaptic activity is not sufficient to generate LTP in the CA1 region of the hippocampus.

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Section: Cgmp and Ltpmentioning

confidence: 99%

Examination of the role of cGMP in long-term potentiation in the CA1 region of the hippocampus.

et al. 1996

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“…arachidonic acid, carbon monoxide, and nitric oxide) may interact ultimately orchestrate the observed increases in synaptic strength. In addition, the possibility that given biochemical pathways may be selectively invoked based on the stimulation parameters used to induce LTP (Gribkoff et al 1992, Haley et al 1993 or the preexisting history of the synapse (Izumi et al 1992, Larkman et al 1992 needs to be explored further.…”

Section: Long-term Potentiationmentioning

confidence: 99%

Nitric Oxide and Synaptic Function

Schuman

Madison²

1994

Annu. Rev. Neurosci.

752

273

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“…However, the contribution of NO to the induction of hippocampal LTP is dependent on various experimental conditions such as temperature and animal age (Williams et al 1993), or stimulus patterns (Lum-Ragan & Gribkoff, 1993). In addition, there are discrepant reports regarding the stimulus intensity for induction of LTP (Lum-Ragan & Gribkoff, 1993;Haley et al 1993). Cerebellar long-term depression (LTD) in parallel fibre (PF)-Purkinje cell synapses is also dependent on NO signalling.…”

mentioning

confidence: 99%

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

Wakatsuki

Gomi²,

Kudoh³

et al. 1998

The Journal of Physiology

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1. We investigated the role of nitric oxide (NO) in the induction of long-term potentiation (LTP) in slices prepared from the rat auditory cortex. 2. Tetanic stimulation of layer IV elicited LTP of field potentials in layer II-III (LTPII-III) and in layer V (LTPV). The magnitude of LTPII-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 LTPV was 138 ± 3% (n = 17). 3. NO synthase (NOS) inhibitors had no apparent effect on LTPII-III, but LTPV was significantly suppressed (P < 0·001). This suppression of LTPV was significantly antagonized by a NO donor (P < 0·001) or a cGMP analogue (P < 0·001). 4. 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. 5. 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 pÒ (n = 55) in layer V and 55 ± 8 pÒ (n = 5) in layer II-III. 6. 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. 7. These results clearly indicate the NO dependence of the induction of LTPV, and the greater NO release in the deeper layer of the rat auditory cortex.8152

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Nitric oxide synthase inhibitors block long-term potentiation induced by weak but not strong tetanic stimulation at physiological brain temperatures in rat hippocampal slices

Cited by 100 publications

References 11 publications

Examination of the role of cGMP in long-term potentiation in the CA1 region of the hippocampus.

Examination of the role of cGMP in long-term potentiation in the CA1 region of the hippocampus.

Nitric Oxide and Synaptic Function

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

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