TY - JOUR
T1 - The sigma agonist 1,3-Di-o-tolyl-guanidine reduces the morphological and behavioral changes induced by neonatal ventral hippocampus lesion in rats
AU - Jaramillo-Loranca, Blanca Estela
AU - Garcés-Ramírez, Linda
AU - Munguía Rosales, Alicia Angélica
AU - Luna Ramírez, Carolina
AU - Vargas Hernández, Genaro
AU - Morales-Dionisio, Oscar
AU - González-Elizalde, Kateri
AU - Flores, Gonzalo
AU - Zamudio, Sergio
AU - De La Cruz-López, Fidel
N1 - Publisher Copyright:
© 2015 Wiley Periodicals, Inc.
PY - 2015/4/1
Y1 - 2015/4/1
N2 - Sigma (σ) receptors have generated a great deal of interest due to their possible role in psychosis, neuroprotection, and various other behaviors including addictive processes. Sigma receptors have been located in brain areas involved in motor functions, including the dopaminergic projections from the substantia nigra to the striatum. Evidence suggests that one of their major roles might be to regulate the activity of the glutamatergic system via the N-methyl-d-aspartate receptor. The sigma receptor agonist 1,3-di-o-tolyl-guanidine (DTG) was found to increase dopamine release in the striatum, nucleus accumbens, and prefrontal cortex, in a dose-dependent manner, after central as well as peripheral administration, suggesting a modulatory role of these receptors on the dopaminergic system. The present study examines whether chronic administration of the DTG sigma agonist induces neuromorphological and behavioral changes in neonatal ventral hippocampal lesioned (nVHL) rats as a neurodevelopmental model of schizophrenia. The results show that the DTG administration reduces the hyperlocomotor activity in nVHL rats and reverses the neuronal hypotrophy generated in nVHL rats in the prefrontal cortex, amygdala, and nucleus accumbens. Our results demonstrate that DTG, a sigma-1 receptor agonist, reverses some of the behavioral and neuromorphological effects of nVHL on the rat and supports the possibility that DTG may have beneficial effects in the management of symptoms of schizophrenia.
AB - Sigma (σ) receptors have generated a great deal of interest due to their possible role in psychosis, neuroprotection, and various other behaviors including addictive processes. Sigma receptors have been located in brain areas involved in motor functions, including the dopaminergic projections from the substantia nigra to the striatum. Evidence suggests that one of their major roles might be to regulate the activity of the glutamatergic system via the N-methyl-d-aspartate receptor. The sigma receptor agonist 1,3-di-o-tolyl-guanidine (DTG) was found to increase dopamine release in the striatum, nucleus accumbens, and prefrontal cortex, in a dose-dependent manner, after central as well as peripheral administration, suggesting a modulatory role of these receptors on the dopaminergic system. The present study examines whether chronic administration of the DTG sigma agonist induces neuromorphological and behavioral changes in neonatal ventral hippocampal lesioned (nVHL) rats as a neurodevelopmental model of schizophrenia. The results show that the DTG administration reduces the hyperlocomotor activity in nVHL rats and reverses the neuronal hypotrophy generated in nVHL rats in the prefrontal cortex, amygdala, and nucleus accumbens. Our results demonstrate that DTG, a sigma-1 receptor agonist, reverses some of the behavioral and neuromorphological effects of nVHL on the rat and supports the possibility that DTG may have beneficial effects in the management of symptoms of schizophrenia.
KW - DTG
KW - Golgi-Cox
KW - Neonatal ventral hippocampal lesion
KW - Schizophrenia
KW - Sigma receptor
UR - http://www.scopus.com/inward/record.url?scp=84925363363&partnerID=8YFLogxK
U2 - 10.1002/syn.21811
DO - 10.1002/syn.21811
M3 - Artículo
SN - 0887-4476
VL - 69
SP - 213
EP - 225
JO - Synapse
JF - Synapse
IS - 4
ER -