What causes spine shrinkage?
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Causes of Spine Shrinkage: An Overview
Mechanical Loading and Physical Activity
Repetitive Torsional Motions
Spine shrinkage can be significantly influenced by repetitive physical activities, particularly those involving torsional motions. A study involving 20 subjects performing controlled torsional, lateral bend, and flexion motions found that torsional motions led to notable spinal shrinkage, with measurements showing a reduction in stature by 1.81 to 3.2 mm after 20 minutes of repetitive twisting. This suggests that torsional motions impose a larger cumulative load on the spine compared to lateral or flexion motions.
Type of Work and Physical Load
The type of work and the physical load it imposes also play a crucial role in spinal shrinkage. Research indicates that heavy workloads result in more significant spinal shrinkage compared to light workloads, highlighting the impact of physical exertion on spinal health. Additionally, activities such as fast bowling in cricket have been shown to cause a decrease in stature by approximately 2.30 mm over a 30-minute period, further emphasizing the effect of high-impact sports on spinal shrinkage.
Molecular and Cellular Mechanisms
Actin-Depolymerizing Factor/Cofilin
At the cellular level, the actin-depolymerizing factor cofilin is a key player in spine shrinkage. Cofilin's activity, regulated by its phosphorylation state, influences the structural plasticity of dendritic spines. During spine shrinkage, dephosphorylated cofilin diffuses into neighboring spines, leading to a reduction in spine size and synaptic strength. This diffusion mechanism underlies the spread of spine shrinkage and long-term depression (LTD) in neural circuits.
Non-Ionotropic NMDA Receptor Signaling
Non-ionotropic signaling through NMDA receptors (NMDARs) also contributes to spine shrinkage. This process is independent of calcium ion influx and involves signaling pathways such as p38 MAPK. Studies using two-photon imaging have demonstrated that low-frequency glutamatergic stimulation can induce spine shrinkage through non-ionotropic NMDAR signaling, which is crucial for synaptic plasticity and the refinement of neural circuits .
Synaptic Plasticity and Spine Shrinkage
Long-Term Depression (LTD)
Spine shrinkage is closely associated with LTD, a process that weakens synaptic connections. Activation of NMDARs and subsequent calcium influx are essential for LTD and spine shrinkage. However, different molecular pathways are involved in these processes. For instance, while LTD requires protein phosphatase 1 (PP1), spine shrinkage is mediated by cofilin, indicating distinct regulatory mechanisms.
Dissociation of Functional and Structural Plasticity
Interestingly, there is a dissociation between functional and structural plasticity in dendritic spines. For example, AMPA receptor subunit GluR1 (GluA1) serine-845 is involved in synaptic depression but not in spine shrinkage, suggesting that these two forms of plasticity can be regulated independently. This dissociation is further supported by findings in fragile X model mice, where mGluR activation causes LTD without spine shrinkage, whereas NMDAR activation induces both LTD and spine shrinkage.
Conclusion
Spine shrinkage is a multifaceted phenomenon influenced by mechanical loading, physical activity, and molecular mechanisms. Repetitive torsional motions and heavy physical workloads are significant contributors to spinal shrinkage. At the cellular level, proteins like cofilin and non-ionotropic NMDAR signaling play crucial roles in regulating spine shrinkage and synaptic plasticity. Understanding these mechanisms provides valuable insights into the factors affecting spinal health and the potential for developing interventions to mitigate spine shrinkage.
Sources and full results
Most relevant research papers on this topic
Spinal shrinkage during repetitive controlled torsional, flexion and lateral bend motion exertions
State-dependent diffusion of actin-depolymerizing factor/cofilin underlies the enlargement and shrinkage of dendritic spines
Non-Ionotropic NMDA Receptor Signaling Drives Activity-Induced Dendritic Spine Shrinkage
Molecular Mechanisms of Non-ionotropic NMDA Receptor Signaling in Dendritic Spine Shrinkage
Shrinkage of Dendritic Spines Associated with Long-Term Depression of Hippocampal Synapses
AMPA receptor subunit GluR1 (GluA1) serine-845 site is involved in synaptic depression but not in spine shrinkage associated with chemical long-term depression.
Dissociation of functional and structural plasticity of dendritic spines during NMDAR and mGluR-dependent long-term synaptic depression in wild-type and fragile X model mice
Effects of Type of Work and Age on Spinal Shrinkage
Spinal shrinkage in fast bowling.
Spinal shrinkage as a parameter of functional load.
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