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Neonatal Tactile Stimulation Downregulates Dendritic Spines in Layer V Pyramidal Neurons of the WAG/Rij Rat Somatosensory Cortex

Summary

Researchers found that gently brushing young rats with epilepsy-prone genetics helps prevent abnormal brain development. Specifically, this tactile stimulation reduces the excessive spiny connections on brain cells in the sensory cortex that are associated with seizures. The study shows that simple, early physical stimulation can have lasting protective effects on brain structure in epilepsy-prone individuals.

Background

WAG/Rij rats are a genetic model of absence epilepsy with dendritic abnormalities in the somatosensory cortex. Early life manipulations like tactile stimulation and maternal separation have been shown to affect seizure activity in adulthood. Environmental experiences during early development can induce permanent changes in brain structure and synaptic organization.

Objective

To examine the effects of neonatal tactile stimulation on dendritic spine morphology and density in layer V pyramidal neurons of the somatosensory cortex in WAG/Rij rats with genetic absence epilepsy compared to healthy Wistar rats and maternally separated controls.

Results

WAG/Rij control rats displayed significantly higher dendritic spine density compared to Wistar rats. Neonatal tactile stimulation reduced spine density in WAG/Rij rats to levels comparable to healthy Wistar controls. Maternal separation produced the lowest spine density. Mushroom-type spines were predominant in control WAG/Rij rats and were selectively reduced by tactile stimulation.

Conclusion

Neonatal tactile stimulation downregulates dendritic spines and alters spine morphology in the somatosensory cortex of genetically epileptic rats, potentially regulating the epileptic focus through neuronal plasticity mechanisms. These findings demonstrate that early sensory experiences can produce long-term structural changes in epileptic brains.
  • Published in:Neural Plasticity,
  • Study Type:Experimental Animal Study,
  • Source: PMID: 35465396, DOI: 10.1155/2022/7251460
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