PubMed · 9381142
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D Johnston. 1997-10-17. A missing link? LTP and learning.. https://doi.org/10.1126/science.278.5337.401
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The effects of high frequency stimulation (HFS) of the primary vestibular afferents on synaptic transmission in the ventral part of the medial vestibular nuclei (vMVN) were studied during postnatal development and compared with the changes in the expression of the group I metabotropic glutamate receptor (mGluR) subtypes, mGluR1 and mGluR5. During the first stages of development, HFS always induced a mGluR5- and GABAA-dependent long-term depression (LTD) which did not require NMDA receptor and mGluR1 activation. The probability of inducing LTD decreased progressively throughout the development and it was zero at about the end of the second postnatal week. Conversely, long-term potentiation (LTP) appeared at the beginning of the second week and its occurrence increased to reach the adult value at the end of the third week. Of interest, the sudden change in the LTP frequency occurred at the time of eye opening, about the end of the second postnatal week. LTP depended on NMDA receptor and mGluR1 activation. In parallel with the modifications in synaptic plasticity, we observed that the expression patterns and localizations of mGluR5 and mGluR1 in the medial vestibular nuclei (MVN) changed during postnatal development. At the earlier stages the mGluR1 expression was minimal, then increased progressively. In contrast, mGluR5 expression was initially high, then decreased. While mGluR1 was exclusively localized in neuronal compartments and concentrated at the postsynaptic sites at all stages observed, mGluR5 was found mainly in neuronal compartments at immature stages, then preferentially in glial compartments at mature stages. These results provide the first evidence for a progressive change from LTD to LTP accompanied by a distinct maturation expression of mGluR1 and mGluR5 during the development of the MVN.
In a rat corticostriatal slice, brief, suprathreshold, repetitive cortical stimulation evoked long-lasting plateau potentials in neostriatal neurons. Plateau potentials were often followed by spontaneous voltage transitions between two preferred membrane potentials. While the induction of plateau potentials was disrupted by non-NMDA and NMDA glutamate receptor antagonists, the maintenance of spontaneous voltage transitions was only blocked by NMDA receptor and L-type Ca2+ channel antagonists. The frequency and duration of depolarized events, resembling up-states described in vivo, were increased by NMDA and L-type Ca2+ channel agonists as well as by GABAA receptor and K+ channel antagonists. NMDA created a region of negative slope conductance and a positive slope crossing indicative of membrane bistability in the current-voltage relationship. NMDA-induced bistability was partially blocked by L-type Ca2+ channel antagonists. Although evoked by synaptic stimulation, plateau potentials and voltage oscillations could not be evoked by somatic current injection--suggesting a dendritic origin. These data show that NMDA and L-type Ca2+ conductances of spiny neurons are capable of rendering them bistable. This may help to support prolonged depolarizations and voltage oscillations under certain conditions.
RATIONALE: Nitric oxide (NO) is a gas neurotransmitter that may facilitate glutamate release in the central nervous system. NO donors or glutamate agonists injected into the dorsolateral periaqueductal grey (dlPAG) induce flight behaviour. OBJECTIVES: To test the hypothesis that the defensive reactions induced by an NO donor in the dlPAG would be attenuated by pretreatment with AMPA/kainate or NMDA glutamate receptor antagonists. METHODS: Male Wistar rats with cannulae aimed at the dlPAG received vehicle, AP7 (a NMDA receptor antagonist, 2 nmol) or NBQX (an AMPA/kainite receptor antagonist, 100 nmol) injection 10 min before the administration of SIN-1 (an NO donor, 300 nmol). Immediately after the last injection, their behavior was observed in an open arena during 10 min. RESULTS: SIN-1 induced flight reactions characterized by running and jumps. Pretreatment with AP7 or NBQX completely prevented the effects of SIN-1. CONCLUSION: The results suggest that the aversive reactions induced by an NO donor in the dlPAG depend on ionotropic glutamate receptor activation.