We studied the interactions between short- and long-term plastic changes taking place during the acquisition of a classical eyeblink conditioning and following high-frequency stimulation (HFS) of the reuniens nucleus in behaving mice. Synaptic changes in strength were studied at the reuniens-medial prefrontal cortex (mPFC) and the reuniens-CA1 synapses. Input/output curves and a paired-pulse study enabled determining the functional capabilities of the two synapses and the optimal intensities to be applied at the reuniens nucleus during classical eyeblink conditioning and for HFS applied to the reuniens nucleus. Animals were conditioned using a trace paradigm, with a tone as conditioned stimulus (CS) and an electric shock to the trigeminal nerve as unconditioned stimulus (US). A single pulse was presented to the reuniens nucleus to evoke field EPSPs (fEPSPs) in mPFC and CA1 areas during the CS-US interval. No significant changes in synaptic strength were observed at the reuniens-mPFC and reuniens-CA1 synapses during the acquisition of eyelid conditioned responses (CRs). Two successive HFS sessions carried out during the first two conditioning days decreased the percentage of CRs, without evoking any long-term potentiation (LTP) at the recording sites. HFS of the reuniens nucleus also prevented the proper acquisition of an object discrimination task. A subsequent study revealed that HFS of the reuniens nucleus evoked a significant decrease of paired-pulse facilitation. In conclusion, reuniens nucleus projections to prefrontal and hippocampal circuits seem to participate in the acquisition of associative learning through a mechanism that does not required the development of LTP.

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We investigated whether the expression of glycinergic receptor (GLYR) subunits of gephyrin and of their mRNAs in the medial vestibular nuclei are affected following unilateral labyrinthectomy. Specific radioactive oligonucleotide probes recognizing the sequences encoding alpha1-3 and ss subunits of GLYR and the anchoring protein gephyrin were used to probe sections of vestibular nuclei. Signals in these in situ hybridization experiments were detected with film or by emulsion photography. Animals were killed at various times following the lesion: 5 h, 1, 3, 8, 30 and 60 days. Specific monoclonal GLYR and gephyrin antibodies were also used to determine GLYR and gephyrin immunoreactivity in control and operated rats (5 h, 1, 3 and 8 days post-lesion). In normal animals, several brainstem regions including the lateral, medial, superior and inferior vestibular nuclei contained mRNAs for gephyrin and the alpha1 and beta subunits of GLYR, and expressed the GLYR and gephyrin polypeptides. In unilaterally labyrinthectomized rats, no asymmetry was detected on autoradiographs between the two medial vestibular nuclei with any of the oligonucleotide probes used, or at any time following the lesion. No difference in the immunofluorescence staining was observed between the intact and deafferented medial vestibular nuclei of lesioned animals or between the vestibular nuclei of lesioned and controls rats. Thus, deafferentation of the vestibular nuclei did not affect the expression of gephyrin, of the various GLYR subunits, or of their mRNAs in the deafferented and intact medial vestibular nuclei. It is therefore unlikely that GLYR and gephyrin modulation contribute significantly to the recovery of the resting discharge of the deafferented medial vestibular neurons and consequently to the restoration of a normal posture and eye position.