**Neuroplasticity Mechanisms in Spiny Mice Following Stroke Without Tissue Regeneration**
Stroke is a leading cause of disability worldwide, often resulting in long-term neurological deficits due to the brain’s limited capacity for tissue regeneration. However, recent research has highlighted the remarkable ability of the brain to adapt and reorganize itself through neuroplasticity, even in the absence of tissue regeneration. Among the emerging models for studying neuroplasticity, the spiny mouse (*Acomys spp.*) has garnered significant attention due to its unique physiological traits and regenerative capabilities in other tissues. This article explores the neuroplasticity mechanisms observed in spiny mice following stroke, focusing on their ability to recover function without direct tissue regeneration in the brain.
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### **The Spiny Mouse as a Model Organism**
Spiny mice are small rodents native to arid regions of Africa and the Middle East. They are renowned for their extraordinary regenerative abilities, such as the capacity to heal skin wounds without scarring, regenerate ear tissue, and repair cardiac damage. These traits make them a valuable model for studying tissue repair and recovery mechanisms. However, unlike their regenerative prowess in peripheral tissues, spiny mice do not exhibit significant brain tissue regeneration following stroke. Instead, their recovery relies heavily on neuroplasticity, offering a unique opportunity to study how the brain compensates for damage through rewiring and functional reorganization.
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### **Neuroplasticity in the Absence of Tissue Regeneration**
Neuroplasticity refers to the brain’s ability to reorganize its structure, function, and connections in response to injury or environmental changes. In spiny mice, neuroplasticity mechanisms following stroke include synaptic remodeling, axonal sprouting, and functional reorganization of neural circuits. These processes enable the brain to compensate for lost functions and restore some degree of normalcy, even when damaged tissue is not replaced.
#### **1. Synaptic Remodeling**
One of the primary mechanisms of neuroplasticity in spiny mice is synaptic remodeling. After a stroke, the brain undergoes a period of heightened plasticity, during which surviving neurons form new synaptic connections to bypass damaged areas. Studies in spiny mice have shown an upregulation of synaptic proteins, such as synaptophysin and PSD-95, in peri-infarct regions (areas surrounding the stroke site). This suggests that surviving neurons actively reorganize their synaptic networks to restore communication between brain regions.
#### **2. Axonal Sprouting**
Axonal sprouting is another critical mechanism observed in spiny mice following stroke. Surviving neurons extend new axons to form connections with distant, undamaged regions of the brain. This process is facilitated by the upregulation of growth-associated proteins, such as GAP-43, and the release of neurotrophic factors like brain-derived neurotrophic factor (BDNF) and nerve growth factor (NGF). Axonal sprouting allows the brain to establish alternative pathways for signal transmission, compensating