Kainic acid-induced early genes activation and neuronal death in the medial extended amygdala of rats

Pereno, Germán Leandro; Balaszczuk, Verónica; Beltramino, C.

doi:10.1016/j.etp.2010.02.001

Cited by 11 publications

(7 citation statements)

References 52 publications

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“…We did not find C8A in any area and any age neither in controls nor in alcohol-treated animals. Because it is known that caspase-8 is implicated in neuronal cell death following seizures (Li et al, 2006), we used as a positive control of C8A brain samples of animals treated with kainic acid which parameters were described by Pereno et al (2011), and we found positive immunolabeling in those samples (data not shown) demonstrating that the lack in the immunoreactions in the alcohol-treated animals is not due to a defective antibody. The data found in our study suggest than the extrinsic pathway is not involved in alcohol-induced neuroapoptosis (results not shown).…”

Section: Caspase 8-activated Stained (C8a) Sectionsmentioning

confidence: 94%

Alcohol‐induced neuronal death in central extended amygdala and pyriform cortex during the postnatal period of the rat

Balaszczuk

Bender

Pereno

et al. 2011

Intl J of Devlp Neuroscience

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Mothers who consume alcohol during pregnancy may cause a neurotoxic syndrome defined as fetal alcohol spectrum disorder (FASD) in their offspring. This disorder is characterized by reduction in brain size, cognitive deficits and emotional/social disturbances. These alterations are thought to be caused by an alcohol-induced increase in apoptosis during neurodevelopment. Little is known about neuroapoptosis in the central extended amygdala and the pyriform cortex, which are key structures in emotional/social behaviors. The goal of this study was to determine the vulnerability of neuroapoptotic alcohol effects in those areas. Rats were administered alcohol (2.5g/kg s.c. at 0 and 2h) or saline on postnatal day (PND) 7, 15 and 20. The Amino-cupric-silver technique was used to evaluate neurodegeneration and immunohistochemistry to detect activated caspases 3-8 and 9 at 2h, 4, 6, 8, 12 and 24h after drug administration. We measured blood alcohol levels each hour, from 2 to 8h post second administration of alcohol in each of the ages studied. Results showed alcohol induced apoptotic neurodegeneration in the central extended amygdala on PND 7 and 15, and pyriform cortex on PND 7, 15 and 20. These structures showed activation of caspase 3 and 9 but not of caspase 8 suggesting that alcohol-induced apoptosis could occur by the intrinsic pathway. The pharmacokinetic differences between ages did not associate with the neurodegeneration age dependence. In conclusion, these limbic areas are damaged by alcohol, and each one has their own window of vulnerability during the postnatal period. The possible implications in emotional/social features in FASD are discussed.

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Section: Caspase 8-activated Stained (C8a) Sectionsmentioning

confidence: 94%

Alcohol‐induced neuronal death in central extended amygdala and pyriform cortex during the postnatal period of the rat

Balaszczuk

Bender

Pereno

et al. 2011

Intl J of Devlp Neuroscience

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“…δFos-B modulates immature spines of the nucleus accumbens in a model of drug addiction (Grueter et al, 2013). Certain chemical stimulators such as kainic acid lead to neurodegeneration via upregulated expression of immediate early genes, including that of Fos-B (Pereno et al, 2011). The hyperexcitability hypothesis is a major theme in proposing the pathomechanism of ALS (Wainger et al, 2014).…”

Section: Development Of a Microfluidic Device For Larger-scale Omics mentioning

confidence: 99%

Omics Approach to Axonal Dysfunction of Motor Neurons in Amyotrophic Lateral Sclerosis (ALS)

et al. 2020

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Amyotrophic lateral sclerosis (ALS) is an intractable adult-onset neurodegenerative disease that leads to the loss of upper and lower motor neurons (MNs). The long axons of MNs become damaged during the early stages of ALS. Genetic and pathological analyses of ALS patients have revealed dysfunction in the MN axon homeostasis. However, the molecular pathomechanism for the degeneration of axons in ALS has not been fully elucidated. This review provides an overview of the proposed axonal pathomechanisms in ALS, including those involving the neuronal cytoskeleton, cargo transport within axons, axonal energy supply, clearance of junk protein, neuromuscular junctions (NMJs), and aberrant axonal branching. To improve understanding of the global changes in axons, the review summarizes omics analyses of the axonal compartments of neurons in vitro and in vivo, including a motor nerve organoid approach that utilizes microfluidic devices developed by this research group. The review also discusses the relevance of intra-axonal transcription factors frequently identified in these omics analyses. Local axonal translation and the relationship among these pathomechanisms should be pursued further. The development of novel strategies to analyze axon fractions provides a new approach to establishing a detailed understanding of resilience of long MN and MN pathology in ALS.

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“…It acts on neuronal receptors inducing an excitotoxic effect, causing neuronal death in different regions of the CNS (Bayrakdar et al, 2013;Ben-Ari and Kainate, 2000;Kuzhandaivel et al, 2010;Pereno et al, 2011). Taccola et al (2008) showed that 24 h after a time-constrained (1 h) kainate application, KA causes extensive neuronal network damage and early irreversible loss of neuronal activity.…”

Section: Introductionmentioning

confidence: 98%

Functional and histopathological changes induced by intraparenchymal injection of kainic acid in the rat cervical spinal cord

et al. 2015

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Kainic acid (KA) is an analog of the neurotransmitter glutamate and is widely used as an excitotoxic agent to lesion spinal cord networks, thus, providing an interesting model to learn basic mechanisms of spinal cord injury. The present work was aimed to evaluate motor and sensory performance of rats and analyze morphometric parameters of spinal cord neurons after KA injection. Animals were injected either with 0.75, 1 or 1.25 mM of KA at the C5 segment of the cervical spinal cord. Motor and sensory performance of the rats were evaluate at day 0 (before injection) and at days 1, 2, 3 and 7 post-injection (pi) and compared with those of saline-treated and non-operated animals. Animals were sacrificed at each time point for morphometric and histopathological analysis and compared among groups. All KA-treated animals showed a significant impairment at the motor and sensory tests for the ipsilateral forelimb in a concentration-dependent manner in comparison to saline-treated and non-operated animals. Neuronal cell count showed a significant loss of neurons at C4, C5 and C6 cervical segments when compared with those of saline-treated and non-operated animals. The contralateral side of the cervical segments in KA-treated rats remained unchanged. Some improvement at the motor and sensory tests was observed in animals injected with 0.75 and 1mM KA. Moreover, a mild increase in the neuronal count of the damaged segments was also recorded. The improvement recorded in the motor and sensory tests by day 7 pi may be a consequence of a neuron repairing mechanism triggered soon after the KA excitotoxic effect.

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Kainic acid-induced early genes activation and neuronal death in the medial extended amygdala of rats

Cited by 11 publications

References 52 publications

Alcohol‐induced neuronal death in central extended amygdala and pyriform cortex during the postnatal period of the rat

Alcohol‐induced neuronal death in central extended amygdala and pyriform cortex during the postnatal period of the rat

Omics Approach to Axonal Dysfunction of Motor Neurons in Amyotrophic Lateral Sclerosis (ALS)

Functional and histopathological changes induced by intraparenchymal injection of kainic acid in the rat cervical spinal cord

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