Many theories, but no one knows exactly why we are sleeping. We know one thing for sure: Sleepless nights won't help you get through th...
Many theories, but no one knows exactly why we are sleeping. We know one thing for sure: Sleepless nights won't help you get through the day. Many studies have examined how sleep in the brain and its goals work. However, the synapse, the basic component of the brain that contributes to the formation of neural circuits, works in relation to sleep. A research team led by Director KIM Eunjoon from the Center for Synaptic Brain Dysfunction at the Institute for Basic Sciences (IBS, South Korea) reported in vivo the results of a presynaptic cell adhesion molecule called PTPδ is critical for the development of synapses in the developing brain. Therefore, the genetic elimination of PTPδ leads to disturbances in the structural, functional and biochemical composition in the brain of affected mice, which leads to changes in innate behavior such as hyperlocomotor activity, increased anxiety and reduced dream. .
The human brain contains billions of neurons that communicate with each other via synapses. The signals that one neuron sends to another through the release of neurotransmitters at presynaptic sites are captured by neurotransmitter receptors located at postsynaptic sites in other neurons. Neural networks in turn determine the expression of all behavior and body functions controlled by the brain. At the heart of all of these complete networks for brain functions are the synaptic cell adhesion molecules (CAM). CAMs are important for regulating the development of synapses by connecting the pre- and post-synaptic side. To ensure normal development of neuronal circuits and brain functions, it is important to correctly pair pre- and post-synaptic CAMs between many different types during the development of young neurons.
The research team focused on finding specific roles for PTPδ, since it was only suspected to play a key role in synaptic training. They developed a version of PTPδ that was labeled with a fluorescent molecule and whose expression in the brain enabled a precise and clear visualization of the natural location of PTPδ by the brain and at the position in the synapse with precision at nanoscale. They also accepted conditional deletions of PTPδ to identify the key component of the joint in synaptic training. Basically, the team showed that disorders in the presynaptic interaction of PTPδ with its postsynaptic link partner IL1RAPL1 cause all important changes in innate behavior, as shown in Figures 2 and 3.
It has previously been shown that the transsynaptic interaction (the interaction that extends across the synapse from one neuron to the next) depends on a short peptide sequence that is six amino acids long (known as meA) within the PTPδ protein. The research team used this knowledge to specifically block the PTPδ-IL1RAPL1 interaction. If the meA key sequence is deleted and the rest of PTPδ remains functional and intact, IL1RAPL1 cannot bind to PTPδ and therefore cannot remain on the postsynaptic side of a synapse. This leads to a significant reduction in the number of synapses in the brain, disrupting the complex neural circuits that form and determine the outcome of behavior such as sleep. They also selectively eliminated PTPδ in excitatory neurons and confirmed the hypothesis that synaptic behavioral disorders were localized in excitatory neurons.
The research team also showed that the chemical composition of IL1RAPL1 changes if IL1RAPL1 is unable to bind to PTPδ via the synapse, almost completely blocking a process called tyrosine phosphorylation in its amino acid sequence. This change in the innate nature of IL1RAPL1 is accompanied by the exclusion of IL1RAPL1 from the synapse. Since IL1RAPL1 is crucial for the maturation of synapses, this exclusion leads to structural and functional declines in the synapse. Brain dysfunction at such a basic level leads to increased anxiety and reduced sleep, which are observed in mutant PTPδ mice.
Several studies have linked synaptic CAMs to abnormal mouse behavior. In particular, this study provides the first comprehensive description of how CAMs are linked to sleep, a basic brain function. In addition, no previous studies have associated a specific pair of pre- and post-synaptic CAMs with sleep or sleep, or with sleep-related behaviors such as hyperactivity and anxiety. Because mutations in the PTPδ-encoding gene are associated with many psychiatric disorders, including schizophrenia, attention deficit hyperactivity disorder (ADHD), and restless legs syndrome (a type of sleep disorder), each of these disorders affects 1% to 5% of the world's population. This study shows how changes in PTPδ can lead to symptoms reminiscent of the above disorders.
The development of the brain in the embryonic and early postnatal stage is crucial for the correct expression of the behavior and functions of the brain. This study shows that even the singular disruption of the PTPδ-IL1RAPL1 interaction between many possible pairs of pre- and post-synaptic CAMs has lifelong ramifications, such as: B. a permanent reduction in sleep. Because sleep is essential for survival, the disruption of a single pair of connections to the synapse can have far-reaching consequences that demonstrate the importance of this discovery and enable us to better understand the elements. Components of the brain affect complex behaviors such as sleeping
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Material from the Institute for Basic Sciences . Note: The content can be changed in terms of style and length.
