Neuroprotective gap-junction-mediated bystander transformations in the adult zebraﬁsh spinal cord after injury

Nature Communications, 2024 · DOI: 10.1038/s41467-024-48729-9 · Published: May 7, 2024

Spinal Cord Injury Regenerative Medicine Neurology

Simple Explanation

The adult zebraﬁsh spinal cord can regenerate after injury. This study shows zebraﬁsh motoneurons are resilient and remain functional after injury. After spinal cord injury, motoneurons experience changes in glutamatergic input, excitability and calcium signaling. Calretinin (CR) is critical in buffering intracellular calcium. The study demonstrates neuron-to-neuron neuroprotection via gap junction channels. Glutamate signaling, calcium buffering, and intercellular cooperation promote cell survival and regeneration.

Study Duration

7 days

Participants

Adult (8–12 weeks old) wild-type zebraﬁsh

Evidence Level

Not specified

Key Findings

1
Large-size fast spinal zebraﬁsh motoneurons are remarkably resilient by remaining viable and functional after spinal cord injury.
2
Dynamic changes occur in motoneuron glutamatergic input, excitability, and calcium signaling following injury, with calretinin playing a critical role in calcium buffering.
3
Neuron-to-neuron bystander neuroprotection is mediated through gap junction channels, highlighting intercellular cooperation in cell survival and regeneration initiation.

Research Summary

The study investigates adaptive cellular mechanisms in adult zebraﬁsh spinal cord regeneration after traumatic injury, revealing that zebraﬁsh motoneurons are remarkably resilient and remain functional. Key findings include dynamic changes in motoneuron glutamate signaling, excitability, and calcium signaling, along with the crucial role of calretinin in intracellular calcium buffering. The research highlights a neuron-to-neuron bystander neuroprotective mechanism mediated by gap junction channels, emphasizing the importance of intercellular cooperation for cell survival and regeneration.

Practical Implications

Therapeutic strategies for spinal cord injury

The study suggests potential therapeutic strategies by targeting glutamate signaling, calcium buffering, and gap junction-mediated intercellular communication.

Understanding neuroprotective mechanisms

The findings provide insights into neuroprotective mechanisms in the context of spinal cord regeneration.

Comparative vertebrate biology

The research contributes to the comparative biology of spinal cord injury and regeneration across vertebrates.

Study Limitations

1
The study is limited to zebraﬁsh models.
2
The research focuses primarily on primary motoneurons (pMNs).
3
Further investigation is needed to reveal all potential biochemical signaling molecules engaged in the exchange process between neurons.

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