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Somatostatin (SRIF) prevents natural motoneuron cell death in embryonic chick spinal cord
1Department of Neurology, Louisiana State University Medical Center, New Orleans.
Abstract:
Natural motoneuron cell death is a developmental process that effects the loss of about 50% of the cells in the lateral motor column of the spinal cord. The present study demonstrates that the systemic treatment of developing chick embryos with somatostatin (somatotropin release-inhibiting factor, SRIF) during the period of natural motoneuron cell death resulted in a 13-22% increase in the number of surviving motoneurons, suggesting that SRIF may be an endogenous contributor to motoneuron survival during normal development. It is hypothesized that SRIF may act, through its ability to reduce intraneuronal calcium, as an endogenous antagonist of neuronal death both during development and in the course of adult neurodegenerative diseases.
Insights
Somatostatin (SRIF) treatment increased motoneuron survival by 13-22% in developing chick embryos. This suggests SRIF may protect neurons from death during development and in adult neurodegenerative diseases.
Area of Science:
- Neuroscience
- Developmental Biology
- Cell Biology
Background:
- Natural motoneuron cell death is a critical developmental process.
- Approximately 50% of spinal cord lateral motor column neurons undergo programmed cell death during development.
Purpose of the Study:
- To investigate the role of somatostatin (SRIF) in regulating motoneuron survival during development.
- To determine if SRIF can mitigate natural motoneuron cell death.
Main Methods:
- Developing chick embryos were systemically treated with somatostatin (SRIF).
- Treatment was administered during the natural period of motoneuron cell death.
- The number of surviving motoneurons in the lateral motor column was quantified.
Main Results:
- Systemic SRIF treatment resulted in a significant increase in surviving motoneurons (13-22%).
- This indicates SRIF promotes motoneuron survival during embryonic development.
Conclusions:
- SRIF may function as an endogenous factor promoting motoneuron survival during normal development.
- SRIF's ability to reduce intraneuronal calcium suggests a potential therapeutic role in neurodegenerative diseases.