Reduced axon sprouting after treatment that diminishes microglia accumulation at lesions in the leech CNS.
Research article published in The Journal of comparative neurology (2007)
Abstract
The role of mammalian microglia in central nervous system (CNS) repair is controversial. Microglia accumulate at lesions where they act as immune cells and phagocytize debris, and they may secrete neurotrophins, but they also produce molecules that can be cytotoxic, like nitric oxide (NO). To determine the importance of microglial accumulation at lesions on growth of severed CNS axons in the leech (Hirudo medicinalis), in which axon and synapse regeneration are notably successful even when isolated in tissue culture medium, microglial migration to lesions was reduced. Pressure (P) sensory neurons were injected with biocytin to reveal the extent of their sprouting 24 hours after lesioning. To reduce microglia accumulation at lesions, cords were treated for 3.5 hours with 3 mM ATP or 2 mM N(omega)-nitro-L-arginine methyl ester (L-NAME) or 50 microM Reactive blue-2 (RB2) beginning 30 minutes before injury. Lesioned controls were either not treated with drug or treated 3 hours later with one of the drugs, after the migration and subsequent accumulation of most microglia had occurred, but before the onset of axon sprouting, for a total of seven separate conditions. There was a significant reduction in total sprout lengths compared with controls when microglial accumulation was reduced. The results suggest that microglial cells are necessary for the usual sprouting of injured axons.
Abstract sourced from PubMed (NCBI) for the cited record. See the original publication for the authoritative version.
Resumen
The role of mammalian microglia in central nervous system (CNS) repair is controversial. Microglia accumulate at lesions where they act as immune cells and phagocytize debris, and they may secrete neurotrophins, but they also produce molecules that can be cytotoxic, like nitric oxide (NO).
Por qué esto importa para la hirudoterapia
Este estudio (Ngu et al., 2007, J. Comp. Neurol.) utilizó el sistema nervioso central (CNS) de la sangradora medicinal (Hirudo medicinalis) como modelo para probar si los microglia son necesarios para el crecimiento de axones lesionados: después de la lesión, reducir farmacológicamente la acumulación de microglia (con ATP, L-NAME o Reactive blue-2) produjo una reducción significativa en las longitudes totales de brotes de neuronas sensoriales seccionadas en comparación con los controles, lo que sugiere que los microglia son necesarios para el brote habitual de axones lesionados. Su relevancia para ASH es indirecta pero real — se basa en la misma especie de Hirudo medicinalis que es central a la hirudoterapia y refleja el valor de la sangradora como modelo de regeneración en neurociencia, parte del interés científico más amplio en el organismo, en lugar de evidencia sobre la terapia de sangradora en pacientes. Cautela honesta: esto es neurobiología invertebrada preclínica sobre la regeneración del axón; no dice nada sobre el secretoma salival de la sangradora medicinal, la anticoagulación o cualquier resultado de hirudoterapia clínica, y no debe citarse como evidencia terapéutica.
Citación
Reduced axon sprouting after treatment that diminishes microglia accumulation at lesions in the leech CNS.
Ngu et al. · The Journal of comparative neurology, 2007
Contexto clínico relacionado
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Añadido a la biblioteca ASH: May 28, 2026 · Última actualización del sitio: June 18, 2026