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Plasticity of Scarpa's Ganglion Neurons as a Possible Basis for Functional Restoration within Vestibular Endorgans.

Travo C, Gaboyard-Niay S, Chabbert C - Front Neurol (2012)

Bottom Line: When co-cultured with vestibular epithelia, primary vestibular neurons were able to establish de novo contacts with hair cells.Under the present paradigm, these contacts displayed morphological features of immature synaptic contacts.Preliminary observations using co-cultures of adult rodents suggest that this reparative capacity remained in older mice although to a lesser extent.

View Article: PubMed Central - PubMed

Affiliation: INSERM U1051, Institute for Neurosciences Montpellier, France.

ABSTRACT
In a previous study, we observed spontaneous restoration of vestibular function in young adult rodents following excitotoxic injury of the neuronal connections within vestibular endorgans. The functional restoration was supported by a repair of synaptic contacts between hair cells and primary vestibular neurons. This process was observed in 2/3 of the animals studied and occurred within 5 days following the synaptic damage. To assess whether repair capacity is a fundamental trait of vestibular endorgans and to decipher the cellular mechanisms supporting such a repair process, we studied the neuronal regeneration and synaptogenesis in co-cultures of vestibular epithelia and Scarpa's ganglion from young and adult rodents. We demonstrate that, under specific culture conditions, primary vestibular neurons from young mice or rats exhibit robust ability to regenerate nervous processes. When co-cultured with vestibular epithelia, primary vestibular neurons were able to establish de novo contacts with hair cells. Under the present paradigm, these contacts displayed morphological features of immature synaptic contacts. Preliminary observations using co-cultures of adult rodents suggest that this reparative capacity remained in older mice although to a lesser extent. Identifying the basic mechanisms underlying the repair process may provide a basis for novel therapeutic strategies to restore mature and functional vestibular synaptic contacts following damage or loss.

No MeSH data available.


Related in: MedlinePlus

PMA potentiates vestibular synapse formation in vitro. Eighteen DIV co-cultures of P6 rat ganglion (G), utricle (U), and crista (C) in presence of PMA (A–E) illustrates the potentiation of neurite outgrowth and synapse formation in vitro. Insets show higher magnification of utricles (B,C) and cristae (D,E). Multiple neurites were observed inside the utricles and detailed observation [inset, (B)] on nerve endings reconstructed in 3D (C) showed the additional formation of calyceal innervations in utricles. In cristae, PMA increased the number of neurites entering the sensory epithelia (D), and the number of calyces as shown in the 3D reconstruction (E). Neurofilaments stained in green and nuclei in red. Scale bar 100 μm (A).
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Figure 3: PMA potentiates vestibular synapse formation in vitro. Eighteen DIV co-cultures of P6 rat ganglion (G), utricle (U), and crista (C) in presence of PMA (A–E) illustrates the potentiation of neurite outgrowth and synapse formation in vitro. Insets show higher magnification of utricles (B,C) and cristae (D,E). Multiple neurites were observed inside the utricles and detailed observation [inset, (B)] on nerve endings reconstructed in 3D (C) showed the additional formation of calyceal innervations in utricles. In cristae, PMA increased the number of neurites entering the sensory epithelia (D), and the number of calyces as shown in the 3D reconstruction (E). Neurofilaments stained in green and nuclei in red. Scale bar 100 μm (A).

Mentions: Phorbol 12-myristate 13-acetate (PMA), an activator of PKC, has been implicated in the regulation of diverse cellular functions (Giorgi et al., 2010), among them, potentiation of dendritic spine development and plasticity (Goldin and Segal, 2003; Ethell and Pasquale, 2005). We tested for potential modulatory effects of PMA on the re-innervation process in vestibular co-cultures of young rodents by examining neurite outgrowth in presence of PMA (0.1 μM; rats n = 5) in the bathing medium. Confocal imaging was used to track de novo neurite outgrowth from vestibular ganglion neurons up to the contacted hair cells in the sensory epithelia (Figures 3A,B,D). In our model, addition of PMA potentiated the neurite outgrowth process. Gross observation indicated that the presence of PMA increased the number of neural processes growing toward and entering the sensory epithelia (Figures 3A–D). Moreover, under these conditions calyx-type contacts could be observed using 3D reconstruction in both the utricles (Figure 3C) and cristae (Figure 3E). Table 1 summarizes the results concerning the density, type of innervation, and cell-to-cell contacts in the different culture conditions. Evaluation is ranged as a mean observation obtained from the indicated number of repeated cultures. Although the mechanism underlying PMA potentiation of hair cell re-innervation by primary vestibular neurons remains unknown, it demonstrates the potential for modulating the re-innervation of peripheral vestibular targets.


Plasticity of Scarpa's Ganglion Neurons as a Possible Basis for Functional Restoration within Vestibular Endorgans.

Travo C, Gaboyard-Niay S, Chabbert C - Front Neurol (2012)

PMA potentiates vestibular synapse formation in vitro. Eighteen DIV co-cultures of P6 rat ganglion (G), utricle (U), and crista (C) in presence of PMA (A–E) illustrates the potentiation of neurite outgrowth and synapse formation in vitro. Insets show higher magnification of utricles (B,C) and cristae (D,E). Multiple neurites were observed inside the utricles and detailed observation [inset, (B)] on nerve endings reconstructed in 3D (C) showed the additional formation of calyceal innervations in utricles. In cristae, PMA increased the number of neurites entering the sensory epithelia (D), and the number of calyces as shown in the 3D reconstruction (E). Neurofilaments stained in green and nuclei in red. Scale bar 100 μm (A).
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC3368229&req=5

Figure 3: PMA potentiates vestibular synapse formation in vitro. Eighteen DIV co-cultures of P6 rat ganglion (G), utricle (U), and crista (C) in presence of PMA (A–E) illustrates the potentiation of neurite outgrowth and synapse formation in vitro. Insets show higher magnification of utricles (B,C) and cristae (D,E). Multiple neurites were observed inside the utricles and detailed observation [inset, (B)] on nerve endings reconstructed in 3D (C) showed the additional formation of calyceal innervations in utricles. In cristae, PMA increased the number of neurites entering the sensory epithelia (D), and the number of calyces as shown in the 3D reconstruction (E). Neurofilaments stained in green and nuclei in red. Scale bar 100 μm (A).
Mentions: Phorbol 12-myristate 13-acetate (PMA), an activator of PKC, has been implicated in the regulation of diverse cellular functions (Giorgi et al., 2010), among them, potentiation of dendritic spine development and plasticity (Goldin and Segal, 2003; Ethell and Pasquale, 2005). We tested for potential modulatory effects of PMA on the re-innervation process in vestibular co-cultures of young rodents by examining neurite outgrowth in presence of PMA (0.1 μM; rats n = 5) in the bathing medium. Confocal imaging was used to track de novo neurite outgrowth from vestibular ganglion neurons up to the contacted hair cells in the sensory epithelia (Figures 3A,B,D). In our model, addition of PMA potentiated the neurite outgrowth process. Gross observation indicated that the presence of PMA increased the number of neural processes growing toward and entering the sensory epithelia (Figures 3A–D). Moreover, under these conditions calyx-type contacts could be observed using 3D reconstruction in both the utricles (Figure 3C) and cristae (Figure 3E). Table 1 summarizes the results concerning the density, type of innervation, and cell-to-cell contacts in the different culture conditions. Evaluation is ranged as a mean observation obtained from the indicated number of repeated cultures. Although the mechanism underlying PMA potentiation of hair cell re-innervation by primary vestibular neurons remains unknown, it demonstrates the potential for modulating the re-innervation of peripheral vestibular targets.

Bottom Line: When co-cultured with vestibular epithelia, primary vestibular neurons were able to establish de novo contacts with hair cells.Under the present paradigm, these contacts displayed morphological features of immature synaptic contacts.Preliminary observations using co-cultures of adult rodents suggest that this reparative capacity remained in older mice although to a lesser extent.

View Article: PubMed Central - PubMed

Affiliation: INSERM U1051, Institute for Neurosciences Montpellier, France.

ABSTRACT
In a previous study, we observed spontaneous restoration of vestibular function in young adult rodents following excitotoxic injury of the neuronal connections within vestibular endorgans. The functional restoration was supported by a repair of synaptic contacts between hair cells and primary vestibular neurons. This process was observed in 2/3 of the animals studied and occurred within 5 days following the synaptic damage. To assess whether repair capacity is a fundamental trait of vestibular endorgans and to decipher the cellular mechanisms supporting such a repair process, we studied the neuronal regeneration and synaptogenesis in co-cultures of vestibular epithelia and Scarpa's ganglion from young and adult rodents. We demonstrate that, under specific culture conditions, primary vestibular neurons from young mice or rats exhibit robust ability to regenerate nervous processes. When co-cultured with vestibular epithelia, primary vestibular neurons were able to establish de novo contacts with hair cells. Under the present paradigm, these contacts displayed morphological features of immature synaptic contacts. Preliminary observations using co-cultures of adult rodents suggest that this reparative capacity remained in older mice although to a lesser extent. Identifying the basic mechanisms underlying the repair process may provide a basis for novel therapeutic strategies to restore mature and functional vestibular synaptic contacts following damage or loss.

No MeSH data available.


Related in: MedlinePlus