Chronic cerebrolysin administration attenuates neuronal abnormalities in the basolateral amygdala induced by neonatal ventral hippocampus lesion in the rat

Authors

  • Rubén Antonio Vázquez-Roque,

    1. Laboratorio de Neuropsiquiatría, Instituto de Fisiología, Universidad Autónoma de Puebla, Puebla, México
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  • Kiren Ubhi,

    1. Department of Neurosciences, University of California, San Diego, La Jolla, California
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  • Eliezer Masliah,

    Corresponding author
    1. Laboratorio de Neuropsiquiatría, Instituto de Fisiología, Universidad Autónoma de Puebla, Puebla, México
    • Correspondence to: Eliezer Masliah, Department of Neurosciences, University of California, San Diego, La Jolla, California 92093-0624, USA. E-mail: emasliah@ucsd.edu or Gonzalo Flores, Laboratorio de Neuropsiquiatría, Instituto de Fisiología, Universidad Autónoma de Puebla, 14 Sur 6301, CP. 72570, Puebla, Mexico. E-mail: gonzaloflores52@gmail.com

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  • Gonzalo Flores

    Corresponding author
    1. Laboratorio de Neuropsiquiatría, Instituto de Fisiología, Universidad Autónoma de Puebla, Puebla, México
    • Correspondence to: Eliezer Masliah, Department of Neurosciences, University of California, San Diego, La Jolla, California 92093-0624, USA. E-mail: emasliah@ucsd.edu or Gonzalo Flores, Laboratorio de Neuropsiquiatría, Instituto de Fisiología, Universidad Autónoma de Puebla, 14 Sur 6301, CP. 72570, Puebla, Mexico. E-mail: gonzaloflores52@gmail.com

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ABSTRACT

The neonatal ventral hippocampal lesion (nVHL) has emerged as a model of schizophrenia-related behavior in the rat. Our previous report demonstrated that cerebrolysin (Cbl), a neuropeptide preparation which mimics the action of endogenous neurotrophic factors on brain protection and repair, promoted recovery of dendritic and neuronal damage of the prefrontal cortex and nucleus accumbens and behavioral improvements in postpubertal nVHL rats. We recently demonstrated that nVHL animals exhibit dendritic atrophy and spine loss in the basolateral amygdala (BLA). This study aimed to determine whether Cbl treatment was capable of reducing BLA neuronal alterations observed in nVHL rats. The morphological evaluation included examination of dendrites using the Golgi-Cox procedure and stereology to quantify the total cell number in BLA. Golgi-Cox staining revealed that nVHL induced dendritic retraction and spine loss in BLA pyramidal neurons. Stereological analysis demonstrated nVHL also produced a reduction in cells in BLA. Interestingly, repeated Cbl treatment ameliorated dendritic pathology and neuronal loss in the BLA of the nVHL rats. Our data show that Cbl may foster recovery of BLA damage in postpubertal nVHL rats and suggests that the use of neurotrophic agents for the management of some schizophrenia-related symptoms may present an alternative therapeutic pathway in these disorders. Synapse, 68:31–38, 2014. © 2013 Wiley Periodicals, Inc.

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