Differential deletion of GDNF in the auditory system leads to altered sound responsiveness
Glial‐derived neurotrophic factor (GDNF) has been proposed as a potent neurotrophic factor with the potential to cure neurodegenerative diseases. In the cochlea, GDNF has been detected in auditory neurons and sensory receptor cells and its expression is upregulated upon trauma. Moreover, the applica...
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| Published in | Journal of neuroscience research Vol. 98; no. 9; pp. 1764 - 1779 |
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| Main Authors | , , , , , , , , , |
| Format | Journal Article |
| Language | English |
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Wiley Subscription Services, Inc
01.09.2020
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| Abstract | Glial‐derived neurotrophic factor (GDNF) has been proposed as a potent neurotrophic factor with the potential to cure neurodegenerative diseases. In the cochlea, GDNF has been detected in auditory neurons and sensory receptor cells and its expression is upregulated upon trauma. Moreover, the application of GDNF in different animal models of deafness has shown its capacity to prevent hearing loss and promoted its future use in therapeutic trials in humans. In the present study we have examined the endogenous requirement of GDNF during auditory development in mice. Using a lacZ knockin allele we have confirmed the expression of GDNF in the cochlea including its sensory regions during development. Global inactivation of GDNF throughout the hearing system using a Foxg1‐Cre line causes perinatal lethality but reveals no apparent defects during formation of the cochlea. Using TrkC‐Cre and Atoh1‐Cre lines, we were able to generate viable mutants lacking GDNF in auditory neurons or both auditory neurons and sensory hair cells. These mutants show normal frequency‐dependent auditory thresholds. However, mechanoelectrical response properties of outer hair cells (OHCs) in TrkC‐Cre GDNF mutants are altered at low thresholds. Furthermore, auditory brainstem wave analysis shows an abnormal increase of wave I. On the other hand, Atoh1‐Cre GDNF mutants show normal OHC function but their auditory brainstem wave pattern is reduced at the levels of wave I, III and IV. These results show that GDNF expression during the development is required to maintain functional hearing at different levels of the auditory system.
Deficiency of GDNF in cochlear hair cells (Atoh1‐Cre) reduces inner hair cell (IHC)/cochlear output, although outer hair cell (OHC) function is normal. Deficiency of GDNF in cochlear neurons (TrkC‐Cre) leads to increased OHC and IHC/auditory nerve responses. Tissue‐specific GDNF expression during development is thus required to maintain normal hearing. |
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| AbstractList | Glial‐derived neurotrophic factor (GDNF) has been proposed as a potent neurotrophic factor with the potential to cure neurodegenerative diseases. In the cochlea, GDNF has been detected in auditory neurons and sensory receptor cells and its expression is upregulated upon trauma. Moreover, the application of GDNF in different animal models of deafness has shown its capacity to prevent hearing loss and promoted its future use in therapeutic trials in humans. In the present study we have examined the endogenous requirement of GDNF during auditory development in mice. Using a
lacZ
knockin allele we have confirmed the expression of GDNF in the cochlea including its sensory regions during development. Global inactivation of GDNF throughout the hearing system using a
Foxg1‐
Cre line causes perinatal lethality but reveals no apparent defects during formation of the cochlea. Using
TrkC‐
Cre and
Atoh1‐
Cre lines, we were able to generate viable mutants lacking GDNF in auditory neurons or both auditory neurons and sensory hair cells. These mutants show normal frequency‐dependent auditory thresholds. However, mechanoelectrical response properties of outer hair cells (OHCs) in
TrkC‐
Cre
GDNF
mutants are altered at low thresholds. Furthermore, auditory brainstem wave analysis shows an abnormal increase of wave I. On the other hand,
Atoh1‐
Cre
GDNF
mutants show normal OHC function but their auditory brainstem wave pattern is reduced at the levels of wave I, III and IV. These results show that GDNF expression during the development is required to maintain functional hearing at different levels of the auditory system. Glial‐derived neurotrophic factor (GDNF) has been proposed as a potent neurotrophic factor with the potential to cure neurodegenerative diseases. In the cochlea, GDNF has been detected in auditory neurons and sensory receptor cells and its expression is upregulated upon trauma. Moreover, the application of GDNF in different animal models of deafness has shown its capacity to prevent hearing loss and promoted its future use in therapeutic trials in humans. In the present study we have examined the endogenous requirement of GDNF during auditory development in mice. Using a lacZ knockin allele we have confirmed the expression of GDNF in the cochlea including its sensory regions during development. Global inactivation of GDNF throughout the hearing system using a Foxg1‐Cre line causes perinatal lethality but reveals no apparent defects during formation of the cochlea. Using TrkC‐Cre and Atoh1‐Cre lines, we were able to generate viable mutants lacking GDNF in auditory neurons or both auditory neurons and sensory hair cells. These mutants show normal frequency‐dependent auditory thresholds. However, mechanoelectrical response properties of outer hair cells (OHCs) in TrkC‐Cre GDNF mutants are altered at low thresholds. Furthermore, auditory brainstem wave analysis shows an abnormal increase of wave I. On the other hand, Atoh1‐Cre GDNF mutants show normal OHC function but their auditory brainstem wave pattern is reduced at the levels of wave I, III and IV. These results show that GDNF expression during the development is required to maintain functional hearing at different levels of the auditory system. Glial-derived neurotrophic factor (GDNF) has been proposed as a potent neurotrophic factor with the potential to cure neurodegenerative diseases. In the cochlea, GDNF has been detected in auditory neurons and sensory receptor cells and its expression is upregulated upon trauma. Moreover, the application of GDNF in different animal models of deafness has shown its capacity to prevent hearing loss and promoted its future use in therapeutic trials in humans. In the present study we have examined the endogenous requirement of GDNF during auditory development in mice. Using a lacZ knockin allele we have confirmed the expression of GDNF in the cochlea including its sensory regions during development. Global inactivation of GDNF throughout the hearing system using a Foxg1-Cre line causes perinatal lethality but reveals no apparent defects during formation of the cochlea. Using TrkC-Cre and Atoh1-Cre lines, we were able to generate viable mutants lacking GDNF in auditory neurons or both auditory neurons and sensory hair cells. These mutants show normal frequency-dependent auditory thresholds. However, mechanoelectrical response properties of outer hair cells (OHCs) in TrkC-Cre GDNF mutants are altered at low thresholds. Furthermore, auditory brainstem wave analysis shows an abnormal increase of wave I. On the other hand, Atoh1-Cre GDNF mutants show normal OHC function but their auditory brainstem wave pattern is reduced at the levels of wave I, III and IV. These results show that GDNF expression during the development is required to maintain functional hearing at different levels of the auditory system.Glial-derived neurotrophic factor (GDNF) has been proposed as a potent neurotrophic factor with the potential to cure neurodegenerative diseases. In the cochlea, GDNF has been detected in auditory neurons and sensory receptor cells and its expression is upregulated upon trauma. Moreover, the application of GDNF in different animal models of deafness has shown its capacity to prevent hearing loss and promoted its future use in therapeutic trials in humans. In the present study we have examined the endogenous requirement of GDNF during auditory development in mice. Using a lacZ knockin allele we have confirmed the expression of GDNF in the cochlea including its sensory regions during development. Global inactivation of GDNF throughout the hearing system using a Foxg1-Cre line causes perinatal lethality but reveals no apparent defects during formation of the cochlea. Using TrkC-Cre and Atoh1-Cre lines, we were able to generate viable mutants lacking GDNF in auditory neurons or both auditory neurons and sensory hair cells. These mutants show normal frequency-dependent auditory thresholds. However, mechanoelectrical response properties of outer hair cells (OHCs) in TrkC-Cre GDNF mutants are altered at low thresholds. Furthermore, auditory brainstem wave analysis shows an abnormal increase of wave I. On the other hand, Atoh1-Cre GDNF mutants show normal OHC function but their auditory brainstem wave pattern is reduced at the levels of wave I, III and IV. These results show that GDNF expression during the development is required to maintain functional hearing at different levels of the auditory system. Glial‐derived neurotrophic factor (GDNF) has been proposed as a potent neurotrophic factor with the potential to cure neurodegenerative diseases. In the cochlea, GDNF has been detected in auditory neurons and sensory receptor cells and its expression is upregulated upon trauma. Moreover, the application of GDNF in different animal models of deafness has shown its capacity to prevent hearing loss and promoted its future use in therapeutic trials in humans. In the present study we have examined the endogenous requirement of GDNF during auditory development in mice. Using a lacZ knockin allele we have confirmed the expression of GDNF in the cochlea including its sensory regions during development. Global inactivation of GDNF throughout the hearing system using a Foxg1‐Cre line causes perinatal lethality but reveals no apparent defects during formation of the cochlea. Using TrkC‐Cre and Atoh1‐Cre lines, we were able to generate viable mutants lacking GDNF in auditory neurons or both auditory neurons and sensory hair cells. These mutants show normal frequency‐dependent auditory thresholds. However, mechanoelectrical response properties of outer hair cells (OHCs) in TrkC‐Cre GDNF mutants are altered at low thresholds. Furthermore, auditory brainstem wave analysis shows an abnormal increase of wave I. On the other hand, Atoh1‐Cre GDNF mutants show normal OHC function but their auditory brainstem wave pattern is reduced at the levels of wave I, III and IV. These results show that GDNF expression during the development is required to maintain functional hearing at different levels of the auditory system. Deficiency of GDNF in cochlear hair cells (Atoh1‐Cre) reduces inner hair cell (IHC)/cochlear output, although outer hair cell (OHC) function is normal. Deficiency of GDNF in cochlear neurons (TrkC‐Cre) leads to increased OHC and IHC/auditory nerve responses. Tissue‐specific GDNF expression during development is thus required to maintain normal hearing. |
| Author | Rüttiger, Lukas López‐Barneo, José Wolter, Steffen Schimmang, Thomas Harasztosi, Csaba Gutsche, Katja Durán‐Alonso, María Beatriz Pascual, Alberto López‐Hernández, Iris Knipper, Marlies |
| Author_xml | – sequence: 1 givenname: Csaba surname: Harasztosi fullname: Harasztosi, Csaba organization: University of Tübingen – sequence: 2 givenname: Steffen surname: Wolter fullname: Wolter, Steffen organization: University of Tübingen – sequence: 3 givenname: Katja surname: Gutsche fullname: Gutsche, Katja organization: Universidad de Valladolid y Consejo Superior de Investigaciones Científicas – sequence: 4 givenname: María Beatriz surname: Durán‐Alonso fullname: Durán‐Alonso, María Beatriz organization: Universidad de Valladolid y Consejo Superior de Investigaciones Científicas – sequence: 5 givenname: Iris surname: López‐Hernández fullname: López‐Hernández, Iris organization: Universidad de Valladolid y Consejo Superior de Investigaciones Científicas – sequence: 6 givenname: Alberto surname: Pascual fullname: Pascual, Alberto organization: Universidad de Sevilla – sequence: 7 givenname: José surname: López‐Barneo fullname: López‐Barneo, José organization: Universidad de Sevilla – sequence: 8 givenname: Marlies surname: Knipper fullname: Knipper, Marlies organization: University of Tübingen – sequence: 9 givenname: Lukas surname: Rüttiger fullname: Rüttiger, Lukas organization: University of Tübingen – sequence: 10 givenname: Thomas orcidid: 0000-0002-3801-1640 surname: Schimmang fullname: Schimmang, Thomas email: schimman@ibgm.uva.es organization: Universidad de Valladolid y Consejo Superior de Investigaciones Científicas |
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| CitedBy_id | crossref_primary_10_3389_fcell_2020_614954 crossref_primary_10_3389_fauot_2024_1423853 |
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| Keywords | cochlea RRID:AB_2314839 glial-derived neurotrophic factor RRID:AB_90760 RRID:AB_2195374 RRID:AB_477329 RRID:AB_477272 mouse RRID:AB_291611 RRID:AB_2286684 RRID:AB_10000321 inner ear organ of Corti |
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| Snippet | Glial‐derived neurotrophic factor (GDNF) has been proposed as a potent neurotrophic factor with the potential to cure neurodegenerative diseases. In the... Glial-derived neurotrophic factor (GDNF) has been proposed as a potent neurotrophic factor with the potential to cure neurodegenerative diseases. In the... |
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| SubjectTerms | Animal models Auditory defects Auditory system Brain stem Cochlea Deactivation Deafness Foxg1 protein Glial cell line-derived neurotrophic factor glial‐derived neurotrophic factor Hair Hair cells Hearing loss Inactivation inner ear Lethality Math1 protein mouse Mutants Neurodegenerative diseases Neuronal-glial interactions Neurons organ of Corti Outer hair cells RRID:AB_10000321 RRID:AB_2195374 RRID:AB_2286684 RRID:AB_2314839 RRID:AB_291611 RRID:AB_477272 RRID:AB_477329 RRID:AB_90760 Sensory neurons Thresholds Trauma Wave analysis |
| Title | Differential deletion of GDNF in the auditory system leads to altered sound responsiveness |
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