Background and Objectives: Learning is essential for understanding mental disorders, normal behavior, and forgetfulness. In this regard, the hippocampus plays an important role in the learning process. It has been reported that gammaaminobutyric acid (GABA) receptors in the hippocampus are involved in learning and MEMORY mechanisms and some diseases, such as epilepsy and Alzheimer's. This study aimed to investigate the effect of coumarin on RETENTION, tissue index, and GABA type A receptor gene expression in the hippocampus of male gonadectomy rats. Methods: The population of this study consisted of 40 Wistar rats, which were randomized into 5 groups (n=8 each). These groups included healthy without treatment, gonadectomized without treatment, gonadectomized receiving solvent or Dimethyl sulfoxide, and gonadectomized receiving coumarin at a dose of 3. 5 mg/kg. The treatment was administered intraperitoneally once daily in 2 weeks. A shuttle box was used to test the MEMORY RETENTION of the rats. At the end of the research process, the rats were exterminated in accordance with research ethics. After removing the brains of rats, in each group, in four brains histology test was implemented with Niels staining, and in four other brains, the hippocampus was removed quickly. The hippocampi were placed inside the micro type and frozen with liquid nitrogen. Finally, a gene expression test was taken from the hippocampus using a real-time polymerase chain reaction. Results: Based on the findings, in the MEMORY RETENTION test of initial latency to enter the dark room (step through latency), the gonadectomy group showed a reduction, compared to the healthy group. Moreover, a significant decrease was observed in the number of healthy hippocampal pyramidal neurons; however, GABAA gene expression showed no significant difference. In the gonadectomy groups receiving treatments with different doses of coumarin, the amount of STL (Step Through Latency) and number of healthy pyramidal neurons in the MEMORY RETENTION test showed a significant decrease, compared to the gonadectomy group receiving solvent; nonetheless, a significant increase was revealed in the GABAA-α 2 gene expression. Conclusion: It can be concluded that Gonadectomy caused MEMORY impairment and coumarin affects MEMORY impairment by increasing the GABAA-α 2 gene expression and decreasing the number of healthy hippocampal neurons.

There are two approaches for simulating MEMORY as well as learning in artificial intelligence; the functionalistic approach and the cognitive approach. The necessary condition to put the second approach into account is to provide a model of brain activity that contains a quite good congruence with observational facts such as mistakes and forgotten experiences. Given that human MEMORY has a solid core that includes the components of our identity, our family and our hometown, the major and determinative events of our lives, and the countless repeated and accepted facts of our culture, the more we go to the peripheral spots the data becomes flimsier and more easily exposed to oblivion. It was essential to propose a model in which the topographical differences are quite distinguishable. In our proposed model, we have translated this topographical situation into quantities, which are attributed to the nodes. The result is an edge-weighted graph with mass-based values on the nodes which demonstrates the importance of each atomic proposition, as a truth, for an intelligent being. Furthermore, it dynamically develops and modifies, and in successive phases, it changes the mass of the nodes and weight of the edges depending on gathered inputs from the environment.

In the present study, the effects of the histamine and cholinergic systems on MEMORY RETENTION in adult male rats were investigated. Post-training intracerebroventricular injections were carried out in all the experiments. Cholinoceptor agonists, acetylcholine (1-10 mg/rat) or nicotine (1-10 mg/rat) increased, while a cholinoceptor antagonist, scopolamine (5-20 mg/rat), decreased MEMORY RETENTION. The response to acetylcholine was attenuated by scopolamine. Administration of histamine (5-20 mg/rat) reduced, but the histamine H1 receptor antagonist, pyrilamine (10-50 mg/rat), and the histamine H2 receptor antagonist, cimetidine (1-50 mg/rat) increased MEMORY RETENTION in rats. The histamine receptor antagonists attenuated the response to histamine. Histamine reduced the acetylcholine- or nicotine-induced enhancement. The histamine receptor antagonists enhanced the nicotine- or acetylcholine-induced response. Histamine potentiated the inhibitory effect induced by scopolamine. It is concluded that histaminergic and cholinergic systems have opposing effects on MEMORY RETENTION. Also, the histaminergic system elicits an interaction with the cholinergic system in MEMORY RETENTION.

Learning new cues in all branches of biological organisms, ranging from unicellular organisms to mammals, occurs in different ways. In spite of their small size and short life span, insects have an extraordinary ability to learn, memorize and use environmental cues associated with the hosts and their food sources. Having the ability to learn and recalling the cues associated with the presence of prey / host is a key factor that increases the performance and foraging capacity of biocontrol agents including the ichneumonid parasitoid wasp Venturia canescens which is one of the most important parasitoids of the family Pyralidae in the world. In this research the learning ability of V. canescens in presence of peppermint and lemon odors was investigated by Y- Olfactometer. Results showed that the wasp had no significant preference towards peppermint or lemon, but after conditioning the female wasp, a meaningful difference was observed between her response to the conditioned odor (peppermint) and unconditioned odors (lemon). Her MEMORY's lasting period continued for 27 hours after conditioning in the absence of the learned cues. Recognizing the learning ability and MEMORY RETENTION of the biocontrol agent V. canescens helps improve the efficiency of its application in biological control programs.

Objective(s): Auraptene (7-geranyloxycoumarin) (AUR), from Citrus species has shown antiinflammatory, neuroprotective, and acetylcholinesterase (AChE) and beta-secretase inhibitory effects.Scopolamine is a nonselective muscarinic receptor antagonist which causes short‐term MEMORY impairments and is used for inducing animal model of Alzheimer’s disease (AD). This research aimed to investigate the effect of AUR on scopolamine-induced avoidance MEMORY RETENTION deficits in stepthrough task in mice.Materials and Methods: The effect of four‐day pre-training injections of AUR (50, 75, and 100 mg/kg, subcutaneous (SC)) and scopolamine (1 mg/kg, IP), and their co-administration on avoidance MEMORY RETENTION in step‐through passive avoidance task, was investigated by measuring the latency to enter to the dark chamber.Results: Pre-training administration of AUR caused significant increase in step‐through latency in comparison with control group, 48, 96, and 168 hr after training trial. The findings of this study showed that scopolamine (1 mg/kg, IP, for four consecutive days) impaired passive avoidance MEMORY RETENTION compared to saline-treated animals. Step-through passive avoidance task results showed that AUR markedly reversed scopolamine-induced avoidance MEMORY RETENTION impairments, 24 and 168 hr after training trial in step-through task.Conclusion: Results from co-administration of AUR and scopolamine showed that AUR reversed scopolamine-induced passive avoidance MEMORY RETENTION impairments.

Background: Glucose increases MEMORY in rats, and inhibit MEMORY impairments produced by morphine. One mechanism by which glucose might act on MEMORY via regulating the ATP-sensitive potassium channel.Objective: The aim of present study was to investigate the effects of glibenclamide on MEMORY RETENTION of passive avoidance learning in rats.Methods: This experimental study has been conducted in Qazvin University of Medical Sciences (2016). Forty male Wistar rats were divided into: Control, DMSO and glibenclamide groups (n=8). All rats were trained in a passive avoidance task (50 Hz, 1 mA, 3 s). DMSO (0.2 ml) or glibenclamide (1, 2, 5mg/kg, i.p.) were injected for 10 days before training. RETENTION test was done 48 h later. MEMORY RETENTION of each animal was measured as latency takes to enter the dark chamber.Findings: The time spent in the light chamber area before entering to the dark area and total time spent in the light chamber in the glibenclamide groups were less than control group. These times in the glibenclamide (5 mg/kg) group was significantly lower than control group (P<0.05), conversely total time spent in the dark chamber in the glibenclamide groups were higher than control group.Conclusion: Glibenclamide, as an ATP-sensitive potassium channel blocker, may reduce MEMORY RETENTION by increasing insulin levels and, consequently, reducing blood glucose levels.

BACKGROUND AND OBJECTIVE: Phenytoin (DPH) is widely used as prophylactic in partial and generalized epilepsy and also in the treatment of status epilepticus. Since long-term use of phenytoin may affect nervous system function, this study was done to determine the effect of phenytoin on RETENTION and retrieval of MEMORY in mice.METHODS: In this study, using the passive avoidance apparatus, the effect of acute and chronic DPH (IP) on MEMORY of male and female mice were randomly investigated. The effect of acute and chronic doses of DPH on MEMORY was determined by comparison between complete stepped down time of animals receiving DPH and blank group (receiving 30% propylenglycol) and control group (Untreated).FINDINGS: The results of this study showed impairment in MEMORY RETENTION by 125 mg/kg acute dosage of DPH, although it did not change MEMORY retrieval. Also, 50 and 75mg/kg acute dosage of DPH (for 21 consecutive days) impair MEMORY. CONCLUSION: Results obtained from recent study showed acute and chronic administration of phenytoin impair MEMORY in mice.

Background: It is well known that morphine influence learning and MEMORY processes. The Nucleus accumbens (N.ac) which has an important role in reward participates in morphine-induced impairment of MEMORY RETENTION. Considering the cholinergic system is involved in the effects of morphine on learning and MEMORY, in the present study, the effects of intra-N.ac injections of acetylcholine receptor antagonists alone or with morphine on MEMORY RETENTION and morphine-induced MEMORY has been investigated in rats.Materials and Methods: In this original research animals were bilaterally cannulated in the N.ac and a step-through passive avoidance task was used for the assessment of MEMORY RETENTION.Results: Post-training subcutaneous administration of morphine dose dependently decreased the learning and induced amnesia. The administration of the same dose of morphine as pre-test treatment induced state-dependent learning. Pre-test intra- N.ac administration of atropine, scopolamine and mecamylamine in different doses alone cannot affect on MEMORY RETENTION. While, pretest intra- N.ac injection of these drugs before the administration of morphine dose dependently inhibited morphine state-dependent learning. The level of statistical significance was set at p<0.05.Conclusion: The processes of learning in animals can be affected by morphine and the opioids produce state-dependent learning. Moreover, it can be concluded that inactivation of the muscarinic and nicotinic acethylcoline receptors in the N.ac are involved in mediating morphine state-dependent learning.

TRH has an important role in the maintenance of consciousness and emotional or intellectual functions in the brain. The functional relation between TRH and cholinergic system and efficiency of TRH in treatment of amnesia are suggested. The binding sites of TRH found in limbic structures especially in septum and hippocampus GABA as an inhibitory neurotransmitter has an important effect on learning and MEMORY. The presence of GABA receptor in amygdala, medial septum and hippocampus is revealed.In this study, interaction between TRH and baclofen (GABAB agonist) on MEMORY process through intra hippocampal microinjection and passive avoidance task in adult male rat are evaluated. Bilateral microinjections into the dorsal hippocampus were carried out in all the experiments. After training of animal, TRH (1, 2.5, 5, 10 mg/ml), baclofen (0.2, 0.3, 0.5, 1 mg/ml) and co-injection of TRH and baclofen are injected. After a 48hr. period of time, the level of RETENTION of MEMORY was measured. The results showed that TRH could be increase; baclofen could be decrease and co-injection of TRH and baclofen increase level of RETENTION and consolidation of MEMORY.