Some Observations of Anxiety-related Behavior in Young Adult Rats Following Late Adolescent Exposure to Methamphetamine with and without Environmental Enrichment

2018 ◽  
Vol 6 (2) ◽  
Author(s):  
Emma K. Peterson ◽  
Robert N. Hughes
2019 ◽  
Vol 12 (5) ◽  
pp. 86
Author(s):  
K. M. H. Cavalcante

Environmental enrichment (EE) has been shown to produce beneficial effects in animal models of a wide variety of neurological and psychiatric disorders. EE exhibits antidepressant function; reduces anxiety, improves spatial learning and memory impairment. EE can reduce sensitivity to loss of reward by reducing frustration-like emotional states and facilitates the extinction of conditioned fear. However, some studies related to the emotional effects of EE present controversial results such as reduction or increase in anxiety. The time of exposure to an enriched environment seems to be an important factor in the behavioral responses presented by animals subjected to aversive stimuli. The present study compared the effects of two and four week exposure to EE with young adult Wistar rats under the same conditions and protocol on fear behavioral parameters in the face of footshock (unconditioned fear) and on re-exposure to an environment after electrical shock pairing (conditioned fear). We showed that the EE with a duration of two weeks reduced the freezing response of the animals in an unconditioned fear situation, that is, with the aversive stimulus present in the environment, however, did not influence the same behavior in a conditioned fear situation. In addition, the short-term EE developed the locomotor and exploratory activity, identified by the high rearing behavior, which may also suggest a low level of anxiety in these animals. We can conclude that EE changes the unconditioned fear responses of young adult rats. In addition, the duration of EE interferes differently, being two weeks of treatment with EE sufficient to cause improvement in coping with unconditioned aversive situations. We suggest that the emotional benefits resulting from the welfare provided by EE can be abolished by the longer duration of this treatment, due to the already known effect of tolerance to lasting or abundant rewards.


2014 ◽  
Author(s):  
Dalnim Cho ◽  
Crystal L. Park ◽  
Alexis Berglund ◽  
Jack Olexovitch ◽  
Alexandra Snavely ◽  
...  

Molecules ◽  
2021 ◽  
Vol 26 (12) ◽  
pp. 3568
Author(s):  
Bernardita Cayupe ◽  
Carlos Morgan ◽  
Gustavo Puentes ◽  
Luis Valladares ◽  
Héctor Burgos ◽  
...  

Prenatally malnourished rats develop hypertension in adulthood, in part through increased α1-adrenoceptor-mediated outflow from the paraventricular nucleus (PVN) to the sympathetic system. We studied whether both α1-adrenoceptor-mediated noradrenergic excitatory pathways from the locus coeruleus (LC) to the PVN and their reciprocal excitatory CRFergic connections contribute to prenatal undernutrition-induced hypertension. For that purpose, we microinjected either α1-adrenoceptor or CRH receptor agonists and/or antagonists in the PVN or the LC, respectively. We also determined the α1-adrenoceptor density in whole hypothalamus and the expression levels of α1A-adrenoceptor mRNA in the PVN. The results showed that: (i) agonists microinjection increased systolic blood pressure and heart rate in normotensive eutrophic rats, but not in prenatally malnourished subjects; (ii) antagonists microinjection reduced hypertension and tachycardia in undernourished rats, but not in eutrophic controls; (iii) in undernourished animals, antagonist administration to one nuclei allowed the agonists recover full efficacy in the complementary nucleus, inducing hypertension and tachycardia; (iv) early undernutrition did not modify the number of α1-adrenoceptor binding sites in hypothalamus, but reduced the number of cells expressing α1A-adrenoceptor mRNA in the PVN. These results support the hypothesis that systolic pressure and heart rate are increased by tonic reciprocal paraventricular–coerulear excitatory interactions in prenatally undernourished young-adult rats.


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