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Showing 2 results for Amygdala

Mohamadreza Palizvzn, Ehsan Elah Ghaznavi Rad,
Volume 8, Issue 2 (7-2005)
Abstract

Introduction: Epilepsy is one of the most common afflictions of human. The amygdala is one of the most sensitive epilepsy induction areas. This area has been the focus of interest, in large part due to its role in fear conditioning. It seems that any abnormality in the neuronal network in amygdala can increase the susceptibility of animal to seizure. The purpose of the present study was to evaluate the relationship between avoidance learning and kindeling susceptibility in rats.
Materials and Methods: In an experimental study, 20 Wistar male rats were trained for two way active avoidance learning in the shuttle box, and on the basis of escape response were divided into fast and slow learning animals. The rats were administered Pentylenetetrazole for induction of kindeling. Then seizure stages were noted. Data was analyzed using one way ANOVA and Tukey's test.
Results: Results of the present study demonstrated that slow learning animals comparing to fast learnings were more prone to kindeling and there was a significant difference in the seizure stage and stage 2 latency in the two groups.
Conclusion: On the basis of the present data it is possible to predict the predisposing of male rats to kindeling from the rate of fear conditioning that indicates the abnormality in amygdala neuronal circuits
Maryam Rahimi Tesiye, Farhad Valizadegan, Shahrbanoo Oryan,
Volume 22, Issue 1 (4-2019)
Abstract

Background and Aim: Working memory is a dynamic neural system for temporarily maintaining and processing of information. Prefrontal cortex (PFC) is the main processing center of Working memory by using different neurotransmitter systems communicate with other brain structures such as Basolateral Amygdala (BLA). In this study, we investigated the role of Opioidergic system in medial PFC and Dopaminergic system of BLA nucleus in working memory based on RAM test.
Materials and Methods: In this study, The male Wistar rats were used. Rats were cannulated with stereotaxic surgery in mPFC and BLA sites. After a recovery period, they were microinjected. Parameters such as working and reference memory errors were calculated with DSWS protocol.
Ethical Considerations: This study with research ethics code IR.UMZ.REC.1397.23 has been approved by Bioethics Committee at Mazandaran University, Iran.
Findings: High doses of Morphine (2 µg/rat) intra mPFC and Chloropromazine (2 µg/rat) intra BLA have improving effects on working and reference memory (p≤0.05). Low (0.005 µg/rat) and high dose (0.5 µg/rat) of Apomorphine had improving {(p≤0.05), (p≤0.01)} and the moderate dose (0.05 µg/rat) of it had decreasing effect on working and reference memory (p≤0.01). Microinjection of Morphine (0.5 µg/rat) with triple doses of Chloropromazine had no significant change on working and reference memory errors. Interaction of Morphine (0.5 µg/rat) with different doses of Apomorphine could change Apomorphine different effects. Coadministration of different doses of Apomorphine with effective dose of Chloropromazine (2 µg/rat) and Morphine (2 µg/rat) decreased the working and reference memory errors.
Conclusion: Our findings showed that in processing of working and reference memory, opioidergic system in mPFC and dopaminergic system in BLA, are interacting reciprocally.


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