scholarly journals Identification of a resilient mouse facial motoneuron population following target disconnection by injury or disease

2018 ◽  
Vol 36 (3) ◽  
pp. 417-422
Author(s):  
Deborah O. Setter ◽  
Melissa M. Haulcomb ◽  
Taylor Beahrs ◽  
Rena M. Meadows ◽  
Nicole D. Schartz ◽  
...  
Keyword(s):  
Facial Motoneuron

scholarly journals Immune regulation of neuronal injury and repair by observing T cell activation

2018 ◽  
Vol 1 (1) ◽  
Author(s):  
Eric J. Regele ◽  
Elizabeth M. Runge ◽  
Felicia M. Kennedy ◽  
Virginia M. Sanders ◽  
Kathryn J. Jones
Keyword(s):  
T Cells ◽  
T Cell Activation ◽  
Cd4 T Cells ◽  
Cell Activation ◽  
Critical Role ◽  
Cd4 Cells ◽  
Knock Out ◽  
Facial Motoneuron ◽  
Injury And Repair ◽  
Antigen Presenting

Background and Hypothesis:  It is unknown how the immune system maintains the majority of facial motoneuron (FMN) survival after axotomy. IL-10 cytokine is necessary for FMN survival and CD4+ T cells are activated and play a critical role in survival, but do not produce IL-10. It was proposed that the source of IL-10 resides in the CNS; however, it is possible that antigen presenting cells (APC) produce IL-10 which activate CD4+ T cells to a neuroprotective phenotype. The regulation of IL-10 receptors (IL-10R) in immunodeficient compared to wild-type (WT) mice in the facial nucleus was studied in this experiment, as well as the possibility of the PNS producing IL-10.  Experimental Design or Project Methods:  To study APC’s role in motoneuron survival, we transferred WT whole splenocytes into global IL-10 knock out (KO) mice prior to axotomy. To study IL-10R gene expression, immunodeficient RAG-2 KO mice received WT or IL-10R-/- CD4+ T cells prior to axotomy.   Results:  qPCR revealed that WT mice upregulate IL-10R after axotomy, whereas RAG-2 KO mice had decreased expression comparatively. RAG-2 mice who received WT CD4+ T cells transfer restored IL-10R comparable to WT values.IL-10R was rescued in RAG-2 mice after the adoptive transfer of WT CD4+T cells. When IL-10R-/- CD4+ cells were transferred into RAG-2 mice, IL-10R values were restored; however, these T cells were unable to rescue FMN survival.   Conclusion and Potential Impact:  If WT whole splenocytes transferred into global IL-10 KO mice rescue FMN survival, it implies that APC play a role in producing IL-10. If they cannot mediate rescue, then peripheral IL-10 is unlikely sufficient for FMN survival. CD4+ T cells regulate central IL-10R response and must respond to IL-10 to mediate FMN survival. The transfer of whole splenocytes provides APCs capable of producing IL-10 and CD4+ T cells capable of responding to IL-10. 

CD4+CD25+ regulatory T cells and CD1-restricted NKT cells do not mediate facial motoneuron survival after axotomy

2006 ◽  
Vol 176 (1-2) ◽  
pp. 34-38 ◽  
Author(s):  
Cynthia A. DeBoy ◽  
Susanna C. Byram ◽  
Craig J. Serpe ◽  
Danielle Wisuri ◽  
Virginia M. Sanders ◽  
...  
Keyword(s):  
T Cells ◽  
Regulatory T Cells ◽  
Nkt Cells ◽  
Motoneuron Survival ◽  
Facial Motoneuron

scholarly journals Use of laser microdissection in the investigation of facial motoneuron and neuropil molecular phenotypes after peripheral axotomy

2010 ◽  
Vol 225 (1) ◽  
pp. 94-103 ◽  
Author(s):  
Nichole A. Mesnard ◽  
Thomas D. Alexander ◽  
Virginia M. Sanders ◽  
Kathryn J. Jones
Keyword(s):  
Laser Microdissection ◽  
Facial Motoneuron ◽  
Molecular Phenotypes

scholarly journals Exacerbation of Facial Motoneuron Loss after Facial Nerve Axotomy in CCR3-Deficient Mice

ASN NEURO ◽  
2009 ◽  
Vol 1 (5) ◽  
pp. AN20090017 ◽  
Author(s):  
Derek A Wainwright ◽  
Junping Xin ◽  
Nichole A Mesnard ◽  
Taylor R Beahrs ◽  
Christine M Politis ◽  
...  
Keyword(s):  
Facial Nerve ◽  
Facial Motoneuron ◽  
Facial Nerve Axotomy ◽  
Deficient Mice

Role of the immune system in the maintenance of mouse facial motoneuron viability after nerve injury

2005 ◽  
Vol 19 (1) ◽  
pp. 12-19 ◽  
Author(s):  
Kathryn J. Jones ◽  
Craig J. Serpe ◽  
Susanna C. Byram ◽  
Cynthia A. DeBoy ◽  
Virginia M. Sanders
Keyword(s):  
Immune System ◽  
Nerve Injury ◽  
Facial Motoneuron

Hypoglossal, trigeminal, and facial motoneuron involvement in amyotrophic lateral sclerosis

Neurology ◽  
1988 ◽  
Vol 38 (2) ◽  
pp. 281-281 ◽  
Author(s):  
R. DePaul ◽  
J. H. Abbs ◽  
M. Caligiuri ◽  
V. L. Gracco ◽  
B. R. Brooks
Keyword(s):  
Amyotrophic Lateral Sclerosis ◽  
Facial Motoneuron ◽  
Lateral Sclerosis

Pulmonary C-fiber receptor activation abolishes uncoupled facial nerve activity from phrenic bursting during positive end-expired pressure in the rat

2008 ◽  
Vol 104 (1) ◽  
pp. 119-129 ◽  
Author(s):  
Kun-Ze Lee ◽  
David D. Fuller ◽  
I-Jung Lu ◽  
Li-Chi Ku ◽  
Ji-Chuu Hwang
Keyword(s):  
Facial Nerve ◽  
Phrenic Nerve ◽  
Wistar Rats ◽  
Receptor Activation ◽  
Respiratory Cycle ◽  
Inhibitory Effects ◽  
Nerve Activity ◽  
Facial Motoneuron ◽  
C Fiber ◽  
Rhythmic Discharge

Phasic respiratory bursting in the facial nerve (FN) can be uncoupled from phrenic bursting by application of 9 cmH2O positive end-expired pressure (PEEP). This response reflects excitation of expiratory-inspiratory (EI) and preinspiratory (Pre-I) facial neurons during the Pre-I period and inhibition of EI neurons during inspiration (I). Because activation of pulmonary C-fiber (PCF) receptors can inhibit the discharge of EI and Pre-I neurons, we hypothesized that PCF receptor activation via capsaicin would attenuate or abolish uncoupled FN bursting with an increase from 3 cmH2O (baseline) to 9 cmH2O PEEP. Neurograms were recorded in the FN and phrenic nerve in anesthetized, ventilated, vagally intact adult Wistar rats. Increasing PEEP to 9 cmH2O resulted in a persistent rhythmic discharge in the FN during phrenic quiescence (i.e., uncoupled bursting). Combination of PEEP with intrajugular capsaicin injection severely attenuated or eliminated uncoupled bursting in the FN ( P < 0.05). Additional experiments examined the pattern of facial motoneuron (vs. neurogram) bursting during PEEP application and capsaicin treatment. These single-fiber recordings confirmed that Pre-I and EI (but not I) neurons continued to burst during PEEP-induced phrenic apnea. Capsaicin treatment during PEEP substantially inhibited Pre-I and EI neuron discharge. Finally, analyses of FN and motoneuron bursting across the respiratory cycle indicated that the inhibitory effects of capsaicin were more pronounced during the Pre-I period. We conclude that activation of PCF receptors can inhibit FN bursting during PEEP-induced phrenic apnea by inhibiting EI and I facial motoneuron discharge.

Sign in / Sign up

Export Citation Format

Share Document