Abstract
The effect of chronic administration of the sigma agonist: 1,3-di-o-tolyl-guanidine (DTG), in neonatal ventral hippocampal lesioned (nVHL) rats, on the immobility by clamping and dorsal immobility, were investigated. The nVHL increases the duration of immobility by clamping, but does not affect the duration of the dorsal immobility. We found that DTG augments the duration of the dorsal immobility in the unlesioned rats, but does not modify the duration of immobility induced by clamping the neck. DTG also counteracts the increase in the duration of the immobility by clamping produced by nVHL. However, the increase in the duration of the dorsal immobility produced by DTG is counteracted by nVHL. These results are discussed with respect to the differential effect on the two immobility responses tested, suggesting that they are different forms of immobility mediated by different mechanisms although they behaviorally share common characteristics.
Highlights
Immobility response is expressed in a wide variety of circumstances, which share some neural mechanisms and may occur in response to natural stimuli, by the action of some drugs or in certain diseases of the nervous system
We evaluated the effect of sub chronic administration of sigma receptor agonist 1,3-di-o-tolyl-guanidine (DTG) on two immobility responses in neonatal ventral hippocampal lesion rats as a neurodevelopmental model of schizophrenia
Cresyl violet-stained sections obtained from adult neonatal ventral hippocampal lesioned (nVHL)-lesioned animals revealed significant bilateral damage of the ventral hippocampus with neuronal loss, atrophy and apparent retraction of the hippocampal formation (Figure 1) as reported in earlier studies [9] [15] [51] [52]
Summary
Immobility response is expressed in a wide variety of circumstances, which share some neural mechanisms and may occur in response to natural stimuli, by the action of some drugs or in certain diseases of the nervous system. It is a state of complete absence of movements and relative unresponsiveness, which can be triggered in a variety of species by several different kinds of stimuli. Some features include temporary immobility response [1]-[3], defecation, muscle rigidity and tremors of the extremities, abnormal EEG patterns, changes in heart rate, breathing and core temperature [4] This behavior can be induced by pharmacological means. Other forms of immobility appear in certain diseases of the central nervous system that cause people to disconnect from the world
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