Synaptic influences of pontine nuclei on cochlear nucleus cells

Abstract

Using the in vitro isolated whole brain preparation of the guinea pig, we tested the synaptic effects induced by the stimulation of pontine nuclei (PN) in intracellularly recorded and stained principal cells of the cochlear nucleus (CN). Twenty percent of the recorded cells in all CN subdivisions responded to stimulation of either ipsilateral or contralateral PN, and 12% of the cells exhibited convergence of inputs from both sides. The responses were recorded only in stellate cells of the ventral CN and in the pyramidal cells of the dorsal CN, whereas no responses were observed in bushy, octopus, and giant cells. PN stimulation produced excitatory and inhibitory postsynaptic potentials as well as mixed responses. The heterogeneous nature and the wide latency range (3.2-18 ms) of observed responses suggest significant variability in the underlying synaptic mechanisms and the implicated pathways. We propose that PN projections to the CN, terminating mainly in the granule cell domain (GCD), together with other non-auditory and auditory inputs contribute to multimodal convergence in the GCD leading ultimately to modulatory actions on the output activity of CN principal cells.

Cochlear Damage Changes the Distribution of Vesicular Glutamate Transporters Associated with Auditory and Nonauditory Inputs to the Cochlear Nucleus

“…The possibility that axonal sprouting may occur following cochlear damage has been suggested by reports of the re-emergence of GAP-43 and synaptophysin following acoustic trauma (Bilak et al, 1997; Fuentes-Santamaria et al, 2007; Illing and Horvath, 1995). The present study provides evidence that some of these new axons are glutamatergic and originate in somatosensory nuclei, reticular formation, pontine nucleus and other non-auditory areas (Babalian, 2005; Haenggeli et al, 2005; Shore et al, 2000; Zhan and Ryugo, 2007; Zhou et al, 2007; Zhou and Shore, 2004) to compensate for the loss of excitatory input from the cochlea. The signaling pathways needed to initiate these changes would likely be the parallel fibers, the axons of granule cells that carry the non-auditory information to the principal cells of the dorsal cochlear nucleus (Manis, 1989; Mugnaini et al, 1980).…”

Serotonergic Modulation of Sensory Representation in a Central Multisensory Circuit Is Pathway Specific

“…The layout of input pathways is clear and can be readily accessed using in vitro preparations ( Figure 1A ). Fusiform principal cells receive two distinct glutamatergic inputs: auditory input from auditory nerve fibers (ANFs) terminating on their basal dendrites ( Brown and Ledwith, 1990 ; Ryugo and May, 1993 ; Smith and Rhode, 1985 ) and diverse multisensory input from parallel fibers (PFs) that terminate on their apical dendrites ( Babalian, 2005 ; Davis et al, 1996 ; Itoh et al, 1987 ; Mugnaini et al, 1980 ; Shore et al, 2000 ; Weinberg and Rustioni, 1987 ; Zhou and Shore, 2004 ). The inhibitory microcircuits of the DCN are well characterized.…”

Acoustic Overexposure Increases the Expression of VGLUT-2 Mediated Projections from the Lateral Vestibular Nucleus to the Dorsal Cochlear Nucleus

“…The DCN also plays an important role in the integration of non auditory inputs from sensory locations [9]. DCN granule cells and their parallel fiber axons are a site of integration of multimodal sensory inputs such as those from the trigeminal ganglion [10], the spinal trigeminal nucleus [11]–[13], the pontine nucleus [14], the cuneate nucleus and gracile nuclei [13], [15]–[18] and the raphe nucleus [19] possibly encoding proprioceptive information on the position of the ears relative to the sound source [20] or suppressing body-generated sounds or vocal feedback [9], [21], [22]. Although multisensory integration also includes projections from primary and secondary vestibular afferent fibers to the DCN [23], [24], the nature of synaptic projections from vestibular nuclei to the DCN remains unidentified.…”