Behavioral Impairments In Rats Research Articles

Succinyl phosphonate, a protector of the 2-oxoglutarate dehydrogenase complex, corrects behavioral impairments in rats exposed to hypoxia or ethanol

Succinyl phosphonate, a protector of the 2-oxoglutarate dehydrogenase complex, corrects behavioral impairments in rats exposed to hypoxia or ethanol

Role of NOS‐NO signaling in clonidine‐ethanol evoked synergistic behavioral impairment

Clonidine‐ethanol combination induces synergistic behavioral impairment in rats as measured by rotorod performance and loss of righting reflex (LORR) duration. We tested the hypothesis that NOS‐NO signaling in the locus ceruleus (LC) is implicated in this interaction. Pretreatment (i.c.) with non‐selective NOS inhibitor (L‐NAME) or nNOS‐selective inhibitor (NPLA) enhanced the impairment of rotorod performance caused by clonidine‐ethanol combination. Prolongation of behavioral impairment was caused by L‐NAME enhancement of the effect of ethanol, not clonidine. LORR caused by clonidine‐ethanol combination was abolished by eNOS‐selective inhibition (L‐NIO), but not nNOS inhibition. Western blot analyses complemented the pharmacological evidence by demonstrating that clonidine‐ethanol combination inhibits phosphorylation (activation) of nNOS (p‐nNOS) and increases levels of phosphorylated eNOS (p‐eNOS) in the LC; the change in p‐nNOS, but not p‐eNOS, was paralleled by similar change in LC p‐ERK1/2. Therefore, NOS‐derived NO in the LC is differentially involved in underlying mechanisms for clonidine‐ethanol induced behavioral impairment. A decrease in nNOS‐derived NO contributes to impaired rotorod performance, while an increase in eNOS‐derived NO contributes to LORR duration elicited by clonidine‐ethanol combination. [Supported by NIH grants 5F31AA015472 (TSB) and 2R01AA07839 (ARA)]

Developmental disruptions and behavioral impairments in rats following in utero RNAi of Dyx1c1

Developmental malformations of cortex have been shown to co-occur with language, learning, and other cognitive deficits in humans. Rodent models have repeatedly shown that animals with such developmental malformations have deficits related to auditory processing and learning. More specifically, freeze-lesion induced microgyria as well as molecular layer ectopias have been found to impair rapid auditory processing ability in rats and mice. In humans, deficits in rapid auditory processing appear to relate to later impairments of language. Recently, genetic variants of four different genes involved in early brain development have been proposed to associate with an elevated incidence of developmental dyslexia in humans. Three of these, DYX1C1, DCDC2, and KIAA0319, have been shown by in utero RNAi to play a role in neuronal migration in developing neocortex. The present study assessed the effects of in utero RNAi of Dyx1c1 on auditory processing and spatial learning in rats. Results indicate that RNAi of Dyx1c1 is associated with cortical heterotopia and is suggestive of an overall processing deficit of complex auditory stimuli in both juvenile and adult periods ( p = .051, one-tail). In contrast, adult data alone reveal a significant processing impairment among RNAi treated subjects compared to shams, indicating an inability for RNAi treated subjects to improve detection of complex auditory stimuli over time ( p = .022, one-tail). Further, a subset of RNAi treated rats exhibited hippocampal heterotopia centered in CA1 (in addition to cortical malformations). Malformations of hippocampus were associated with robust spatial learning impairment in this sub-group ( p < .01, two-tail). In conclusion, in utero RNAi of Dyx1c1 results in heterogeneous malformations that correspond to distinct behavioral impairments in auditory processing, and spatial learning.

The significance of individual resistance to hypoxia for correction of the consequences of craniocerebral trauma

Experiments on rats showed that the individual resistance of the body to acute hypoxia is of decisive importance in the early recovery period after mechanical craniocerebral trauma. I.p. administration of ethomersol (25 mg/kg) during the three days following trauma decreased behavioral impairments in rats with different levels of resistance to acute hypoxia, restored the structure of individual behavior, and prevented metabolic disturbances in the brain. The results led to the conclusion that the antioxidant ethomersol is effective in hypoxia due to craniocerebral trauma.

Effects of hypothermia and gender on survival and behavior after perinatal asphyxia in rats

Previous studies in rats have demonstrated that perinatal asphyxia (PA) produces long-term morphological alterations, particularly affecting hippocampus, neostriatum, and cerebral cortex. These changes were prevented by applying hypothermia during the asphyctic insult. Because these cerebral areas are involved in cognitive and motor functions, the aim of the present study was to determine whether periods of PA during normothermia or hypothermia produces long-term behavioral impairments in rats of both sexes. The cognitive and motor functions were studied using the spatial Morris water maze (MWM) task at 1.5 months, and the open field at 5 months, respectively. The present study revealed that female rats had a higher survival rate than males after PA in normothermic conditions ( p < 0.014), and that hypothermia drastically prolonged the time of survival in both sexes ( p < 0.001). There were no differences in learning and memory functions between groups or male and female rats when tested with MWM. Rats subjected to hypothermia treatment did not show differences in the MWM compared to controls. A lower locomotor activity in the open field test was only observed in male rats that suffered 15 and 20 min of PA in normothermia ( p < 0.05). Hypothermia treatment prevented this hypoactivity. PA in females, even if severe, did not affect the motor activity. The data of both behavioral tests showed differences between sexes, i.e., the female rats learned the MWM task slower, and were more active in the open field. This work lends further support for the hypothesis that hypothermia can prevent mortality as well as long-term sequelae induced by PA.

Poststress glucose mitigates behavioral impairment in rats in the “learned helplessness” model of psychopathology

Three experiments examined the effects of poststress glucose treatment in the learned helplessness model of psychopathology in rats. In experiment 1, rats were given access to water or 40% aqueous glucose immediately following exposure to inescapable tailshocks or simple restraint in a 2 x 2 factorial design. Inescapably shocked rats failed to drink the glucose solution during the poststress interval and failed to show any improvement 24 hours after stress induction in shuttle-escape performance. Consequently, all rats received preexposure to a sweetened glucose cocktail in an attempt to increase poststress ingestion following inescapable shock treatment in experiment 2. Under these conditions, poststress intake of the glucose cocktail eliminated behavioral impairment in inescapably shocked rats relative to water-treated shocked rats and water- and glucose-treated restrained controls. Experiment 3 demonstrated that glucose prophylaxis occurs in the absence of sucrose when rats are preexposed to a 40% glucose solution prior to stress induction.

P3-189 - Effects of TAK-147, a novel acetylcholinesterase inhibitor, on behavioral impairments in rats with basal forebrain lesions

P3-189 - Effects of TAK-147, a novel acetylcholinesterase inhibitor, on behavioral impairments in rats with basal forebrain lesions

Behavioral measurements in nutritional studies.

Studies on the effects of dietary deficiencies have shown marked behavioral impairments in rats deprived of adequate quantities of specific vitamins. In at least one study, such impairment was evident even when body weight did not differ from vitamin-supplemented but pair-fed controls. Recently, experiments have demonstrated that restriction of maternal dietary intake during gestation and lactation results in a variety of physiological and behavioral abnormalities in the progeny. These offspring are stunted, retarded in neuromotor development, impaired in ability to learn a maze, slow in extinction of the conditional reflex and show a low level of exploratory activity, a high degree of emotional behavior and marked anti-social interaction. Furthermore, patterns of change with increasing age in some of these measurements also distinguish these experimental animals from controls born of adequately-fed dams.