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A Contusion Model of Severe Spinal Cord Injury in Rats
Published on: August 17, 2013
Brainstem structures are primarily affected in an experimental model of severe scorpion envenomation
Patrícia Alves Maia Guidine1, Diana Cash, Luciana Estefani Drumond
1* Núcleo de Neurociências (NNC), Departamento de Fisiologia e Biofísica, Instituto de Ciências Biológicas and.
Insights
Severe scorpion envenoming in children primarily affects the brainstem, leading to neurovegetative dysfunction. This study reveals how scorpion toxins target brainstem areas, triggering life-threatening symptoms in severe envenoming cases.
Area of Science:
- Neuroscience
- Toxicology
- Pediatrics
Background:
- Severe scorpion envenoming (SSE) disproportionately affects children, carrying a significant mortality risk.
- The central nervous system (CNS) is increasingly recognized as critical in SSE pathogenesis.
- Hypotheses suggest age-dependent CNS vulnerability, particularly concerning neurovegetative control.
Purpose of the Study:
- To investigate the role of the central nervous system (CNS) in severe scorpion envenoming (SSE).
- To elucidate the specific brain regions targeted by Tityus serrulatus scorpion toxin (TsTX).
- To understand the neurophysiological mechanisms underlying SSE-induced systemic dysfunction.
Main Methods:
- Pharmacological magnetic resonance imaging (phMRI) was employed to assess changes in relative cerebral blood volume (rCBV).
- Laser Doppler measurements were used to confirm cortical cerebral blood flow alterations.
- 14C-2-deoxyglucose autoradiography evaluated metabolic activity, and Alexa Fluor 568-labeled TsTX assessed toxin affinity to neurons.
Main Results:
- TsTX administration caused a rapid reduction in rCBV in the brainstem within 1 minute.
- Rostral brain areas exhibited a delayed increase in rCBV.
- Metabolic activity and toxin-labeling studies indicated a primary targeting of brainstem neurons involved in neurovegetative control.
Conclusions:
- The brainstem, particularly areas regulating neurovegetative functions, is a primary target of Tityus serrulatus scorpion toxin (TsTX).
- TsTX-induced dysfunction in these brainstem areas likely initiates the cascade of systemic symptoms observed in severe scorpion envenoming.
- These findings highlight the critical role of the CNS, specifically the brainstem, in the pathophysiology and lethality of SSE in children.
Abstract:
Severe scorpion envenoming (SSE) is more frequent in children and is characterized by systemic dysfunctions with a mortality rate of up to 9%. Recent evidence shows that the central nervous system (CNS) plays a key role in triggering the cascade of symptoms present in SSE. The age-dependent role of the CNS in SSE lethality may be summarized in 3 hypotheses: (1) the shown increased blood brain barrier permeability of infants to the toxins would especially and primarily compromise neurovegetative control areas, (2) the neurons within these areas have high affinity to the toxins, and (3) the neurovascular interaction is such that SSE metabolically compromises proper function of toxin-targeted areas. A pharmacological magnetic resonance imaging paradigm was used to evaluate localized hemodynamic changes in relative cerebral blood volume (rCBV) for 30 min after the injection of TsTX, the most lethal toxin from the venom of the Tityus serrulatus scorpion. The brainstem showed significant rCBV reduction 1 min after TsTX administration, whereas rostral brain areas had delayed increase in rCBV (confirmed by laser Doppler measurements of cortical cerebral blood flow). Moreover, metabolic activity by 14C-2-deoxyglucose autoradiography showed the highest relative increase at the brainstem. To test whether TsTX has high affinity to brainstem neurons, the lateral ventricle was injected with Alexa Fluor 568 TsTX. Although some neurons showed intense fluorescence, the labeling pattern suggests that specific neurons were targeted. Altogether, these results suggest that brainstem areas involved in neurovegetative control are most likely within the primary structures triggering the cascade of symptoms present in SSE.
