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hy do mice lacking GAD67 die immediately after birth
Before understanding the cause of death of GAD67-deficient mice, let us first briefly introduce what GAD67 is. Glutamate decarboxylase (GAD) is an enzyme that catalyzes the conversion of glutamate into γ-aminobutyric acid (GABA) and carbon dioxide, of which GAD67 is one of the isozymes. The activity of GAD67 directly affects the production of GABA in the nervous system, and GABA is an important inhibitory neurotransmitter in the central nervous system.
In mammals, the expression of these two isozymes, GAD67 and GAD65, in the brain is critical because they are responsible for regulating neuronal activity and neural plasticity. However, according to research, the loss of GAD67 can lead to serious consequences, especially during embryonic development. Today's focus is: Why do mice lacking GAD67 die immediately after birth?
The loss of GAD67 causes a sharp drop in the production of GABA in the nervous system, which directly leads to the inability of neurons to develop normally.
In mice lacking GAD67, scientists found that these mice died on the first day of life. This phenomenon is closely related to the role of GAD67 in nerve cells: GAD67 is the main enzyme for synthesizing GABA, which is essential for inhibiting nerve signals, regulating nerve excitability, and maintaining the overall balance of the nervous system.
GABA deficiency can lead to a series of conditions in which neurons become overexcited, which in turn can cause developmental abnormalities. Specifically, the study found that mice lacking GAD67 had craniofacial malformations, including cleft lip and palate, which may be related to the role of GABA in neuronal proliferation and differentiation during embryonic development.
This deficiency not only leads to structural changes, but also severely disrupts signal transmission within the brain.
In addition to its effects on anatomical structures, GAD67 deficiency has also been shown to threaten life-sustaining functions. In the experiment, mice lacking GAD67 were unable to effectively perform normal physiological functions such as breathing and autonomous movement. This suggests that during early development, the presence of GABA is not only required for interneuronal communication, but is also a critical physiological requirement.
According to research, GABA not only plays a low-excitability role in the brain, but also affects the development of the heart and respiratory system. When GAD67 is deficient, these functional roles are disrupted, causing the physiological system to not function properly and ultimately leading to the death of mice on the first day of life.
GAD67 activity is critical for the stability of the nervous system and the maintenance of physiological functions during embryonic development.
GAD67 deficiency has been shown to have similar effects in other animal models. In contrast, although the loss of GAD65 does not immediately affect survival, it can cause epileptic seizures and other neurotransmission abnormalities, demonstrating the diverse roles of different isozymes in organisms.
Ultimately, these studies lead us to rethink the function of GAD67, which is not just an enzyme, but a cornerstone of the nervous system. For the real world we live in, is the regulation of GABA synthesis and transmission more complex and important than we expected?
