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The Journal of Neuroscience, October 26, 2005, 25(43):9902-9906; doi:10.1523/JNEUROSCI.2061-05.2005

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BRIEF COMMUNICATION
Cooperative Glutamatergic and Cholinergic Mechanisms Generate Short-Term Modifications of Synaptic Effectiveness in Prepositus Hypoglossi Neurons

Juan de Dios Navarro-López,¹ José M. Delgado-García,² and Javier Yajeya³

¹Centro Regional de Investigaciones Biomédicas, Universidad de Castilla-La Mancha, 02071 Albacete, Spain, ²División de Neurociencias, Universidad Pablo de Olavide, 41013 Sevilla, Spain, and ³Instituto de Neurociencias de Castilla y León, Universidad de Salamanca, 37007 Salamanca, Spain

To maintain horizontal eye position on a visual target after a saccade, extraocular motoneurons need a persistent (tonic) neural activity, called "eye-position signal," generated by prepositus hypoglossi (PH) neurons. We have shown previously in vitro and in vivo that this neural activity depends, among others mechanisms, on the interplay of glutamatergic transmission and cholinergic synaptically triggered depolarization. Here, we used rat sagittal brainstem slices, including PH nucleus and paramedian pontine reticular formation (PPRF). We made intracellular recordings of PH neurons and studied their synaptic activation from PPRF neurons. Train stimulation of the PPRF area evoked a cholinergic-sustained depolarization of PH neurons that outlasted the stimulus. EPSPs evoked in PH neurons by single pulses applied to the PPRF presented a short-term potentiation (STP) after train stimulation. APV (an NMDA-receptor blocker) or chelerythrine (a protein kinase-C inhibitor) had no effect on the sustained depolarization, but they did block the evoked STP, whereas pirenzepine (an M₁ muscarinic antagonist) blocked both the sustained depolarization and the STP of PH neurons. Thus, electrical stimulation of the PPRF area activates both glutamatergic and cholinergic axons terminating in the PH nucleus, the latter producing a sustained depolarization probably involved in the genesis of the persistent neural activity required for eye fixation. M₁-receptor activation seems to evoke a STP of PH neurons via NMDA receptors. Such STP could be needed for the stabilization of the neural network involved in the generation of position signals necessary for eye fixation after a saccade.

Key words: acetylcholine; glutamate; short-term potentiation; prepositus hypoglossi; oculomotor system; rats

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Received May 22, 2005; revised September 11, 2005; accepted September 12, 2005.

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