Post-training intrahippocampal infusion of nicotine–bucladesine combination causes a synergistic enhancement effect on spatial memory retention in rats

Sharifzadeh, Mohammad; Zamanian, Ali-Reza; Gholizadeh, Saber; Tabrizian, Kaveh; Etminani, Maryam; Khalaj, Siavash; Zarrindast, Mohammad‐Reza; Roghani, Ali

doi:10.1016/j.ejphar.2007.01.065

Cited by 28 publications

(29 citation statements)

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“…In addition, a large number of studies indicate the important roles of protein kinases in memory processing [6,12,[20][21][22]33]. For instance, our previous findings show that the inhibition of PKA can affect spatial memory retention [12,15,21]. Thus, we assume that the spatial memory retention enhancement observed in this study is caused in part by the interaction of Boswellia papyrifera extract and BAs fraction with protein kinase pathways in the brain.…”

Section: Discussionsupporting

confidence: 51%

“…Memory formation is a complex process that requires distinct neuronal networks and multiple pre-and postsynaptic events [12][13][14][15][16]. Several studies have been conducted to investigate the molecular mechanisms underlying activity-dependent synaptic changes during memory formation.…”

Section: Introductionmentioning

confidence: 99%

“…As a result, a subset of molecules has been identified that play important roles in different aspects of memory processes [17][18][19]. These molecules include neurotransmitters, hormones, signaling substances, and transcription factors [12][13][14][15]. There is additional evidence that various protein kinase signaling pathways are involved in associative memory storage [12,15,20,21].…”

Section: Introductionmentioning

confidence: 99%

“…These molecules include neurotransmitters, hormones, signaling substances, and transcription factors [12][13][14][15]. There is additional evidence that various protein kinase signaling pathways are involved in associative memory storage [12,15,20,21]. Our previous studies showed that intra-hippocampal inhibition of protein kinase A (PKA) impaired spatial memory retention in rats [12,21].…”

Section: Introductionmentioning

confidence: 99%

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Evaluation of systemic administration of Boswellia papyrifera extracts on spatial memory retention in male rats

et al. 2011

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Time-dependent effects of ethanolic extract of Boswellia papyrifera, administered systemically, on spatial memory retention in the Morris water maze were investigated in male rats. A total extract of Boswellia papyrifera (300 mg/kg) was administered every eight hours to three groups of rats by gavage for 1, 2 and 4 weeks. In a separate set of experiments, three doses of a fraction of the extract, called the boswellic acids (100, 200 and 300 mg/kg) were administered by gavage to three groups of rats three times a day for 2 weeks. Following these applications, animals were trained for 4 days. Behavioral testing for evaluation of spatial memory retention was performed 48 h after completion of training. Boswellia papyrifera extracts and boswellic acids caused a significant reduction in escape latency and distance traveled but had no influence on swimming speed. These findings provide evidence that Boswellia papyrifera extracts affect spatial memory retention irrespective of the treatment period. In addition our data show that systemic administration of the boswellic acids fraction enhanced spatial memory retention in a dose-dependent manner. These improving effects may be due to some extent to the interactions of these products with inflammatory mediators, neurotransmitter signaling cascades or protein kinase pathways in the brain.

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Section: Discussionsupporting

confidence: 51%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Evaluation of systemic administration of Boswellia papyrifera extracts on spatial memory retention in male rats

et al. 2011

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“…Various behavioral and molecular approaches have focused on the involvement of neuronal nicotinic acetylcholine receptor in memory and cognition processes [15,16]. Protective role of nicotine on memory impairments induced by different brain lesions has been shown in numerous experimental studies [15,17].…”

Section: Introductionmentioning

confidence: 99%

Zinc Chloride and Lead Acetate-Induced Passive Avoidance Memory Retention Deficits Reversed by Nicotine and Bucladesine in Mice

Tabrizian

Yazdani

Baheri

et al. 2015

Biol Trace Elem Res

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It is very important to investigate the neurotoxic effects of metals on learning and memory processes. In this study, we tried to investigate the effects and time course properties of oral administration of zinc chloride (25, 50, and 75 mg/kg, for 2 weeks), lead acetate (250, 750, 1,500, and 2,500 ppm for 4, 6 and 8 weeks), and their possible mechanisms on a model of memory function. For this matter, we examined the intra-peritoneal injections of nicotine (0.25, 0.5, 1, and 1.5 mg/kg) and bucladesine (50, 100, 300, and 600 nM/mouse) for 4 days alone and in combination with mentioned metals in the step-through passive avoidance task. Control animals received saline, drinking water, saline, and DMSO (dimethyl sulfoxide)/deionized water (1:9), respectively. At the end of each part of studies, animals were trained for 1 day in step-through task. The avoidance memory retention alterations were evaluated 24 and 48 h later in singular and combinational studies. Zinc chloride (75 mg/kg) oral gavage for 2 weeks decreased latency times compared to control animals. Also, lead acetate (750 ppm oral administrations for 8 weeks) caused significant lead blood levels and induced avoidance memory retention impairments. Four-days intra-peritoneal injection of nicotine (1 mg/kg) increased latency time compared to control animals. Finally, findings of this research showed that treatment with intra-peritoneal injections of nicotine (1 mg/kg) and/or bucladesine (600 nM/mouse) reversed zinc chloride- and lead acetate-induced avoidance memory retention impairments. Taken together, these results showed the probable role of cholinergic system and protein kinase A pathways in zinc chloride- and lead acetate-induced avoidance memory alterations.

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Reduction of autophagy markers mediated protective effects of JNK inhibitor and bucladesine on memory deficit induced by Aβ in rats

Mohammadi

Guan

Khodagholi

et al. 2016

Naunyn-Schmiedeberg's Arch Pharmacol

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Autophagy, the process of self-degradation of cellular components, has an important role in neurodegenerative diseases, such as Alzheimer's disease. In this study, we investigated the effects of SP600125 as c-Jun N-terminal kinase (JNK) inhibitor and bucladesine as a cyclic adenosine 3',5'-monophosphate (cAMP) analog on spatial memory and expression of autophagic factors in Aβ-injected rats. Male Wistar rats were used. Rats were randomly allocated into five groups as following: amyloid beta (Aβ)-only group, Aβ + SP600125 (30 μg/1 μ/side, n = 7) and/or bucladesine (100 μM/1 μl/side, n = 7), and the normal control (vehicle only) group. The treatments were administered bilaterally to the CA1 sub-region of the hippocampus stereotaxically. Spatial reference memory was performed using Morris Water Maze 21 days later. The expression of authophagy markers (beclin1, Atg7, Atg12, and LC3 II/LC3 I) in the hippocampus was evaluated using western blotting. Compared to the vehicle group, Aβ administration reduced spatial reference learning (P < 0.001) and memory (P < 0.01) and upregulated the expression of beclin1, Atg7, Atg12, and LC3 II/I (P < 0.0001). Compare to Aβ-only group, the administration of SP600125 and/or bucladesine improved spatial reference learning (P < 0.001) and memory (P < 0.01). Compared to the Aβ-only group, the treatment with SP600125 and/or bucladesine also reduced beclin1, Atg7, Atg12, and LC3 II/I (P < 0.0001) which was similar to amount of normal rats. In summary, it seems that the improvement of spatial memory by SP600125 and/or bucladesine in Aβ-injected rats is in relation with normalizing of autophagy to the physiologic level, possibly through neuroprotection and/or neuroplasticity.

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Post-training intrahippocampal infusion of nicotine–bucladesine combination causes a synergistic enhancement effect on spatial memory retention in rats

Cited by 28 publications

References 80 publications

Evaluation of systemic administration of Boswellia papyrifera extracts on spatial memory retention in male rats

Evaluation of systemic administration of Boswellia papyrifera extracts on spatial memory retention in male rats

Zinc Chloride and Lead Acetate-Induced Passive Avoidance Memory Retention Deficits Reversed by Nicotine and Bucladesine in Mice

Reduction of autophagy markers mediated protective effects of JNK inhibitor and bucladesine on memory deficit induced by Aβ in rats

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