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Mohammad-reza Zarrindast - One of the best experts on this subject based on the ideXlab platform.

  • activation and inactivation of nicotinic receptnors in the dorsal hippocampal region restored negative effects of total tsd and rem sleep deprivation rsd on Memory Acquisition locomotor activity and pain perception
    Neuroscience, 2020
    Co-Authors: Bibi Zahra Javadmoosavi, Mohammad Nasehi, Salar Vaseghi, Seyed Hamid Jamaldini, Mohammad-reza Zarrindast
    Abstract:

    Abstract Sleep deprivation (SD) is a common issue in today’s society. Sleep is essential for proper cognitive functions, including learning and Memory. Furthermore, sleep disorders can alter pain information processing. Meanwhile, hippocampal nicotinic receptors have a role in modulating pain and Memory. The goal of this study is to investigate the effect of dorsal hippocampal (CA1) nicotinic receptors on behavioral changes induced by Total (TSD) and REM Sleep Deprivation (RSD). A modified water box and multi-platform apparatus were used to induce TSD and RSD, respectively. To investigate the interaction between nicotinic receptors and hippocampus-dependent Memory, nicotinic receptor agonist (nicotine) or antagonist (mecamylamine) was injected into the CA1 region. The results showed, nicotine at the doses of 0.001 and 0.1 µg/rat and mecamylamine at the doses of 0.01 and 0.1 µg/rat decreased Memory Acquisition, while both at the doses of 0.01 and 0.1 µg/rat enhanced locomotor activity. Additionally, all doses used for both drugs did not alter pain perception. Also, 24 h TSD or RSD attenuated Memory Acquisition with no effect on locomotor activity and only TSD induced an analgesic effect. Intra-CA1 administration of subthreshold dose of nicotine (0.0001 µg/rat) and mecamylamine (0.001 µg/rat) did not alter Memory Acquisition, pain perception and locomotor activity in sham of TSD/RSD rats. Both drugs reversed all behavioral changes induced by TSD. Furthermore, both drugs reversed the effect of RSD on Memory Acquisition, while only mecamylamine reversed the effect of RSD on locomotor activity. In conclusion, CA1 nicotinic receptors play a significant role in TSD/RSD-induced behavioral changes.

  • the role of 5 ht4 serotonin receptors in the ca1 hippocampal region on Memory Acquisition impairment induced by total tsd and rem sleep deprivation rsd
    Physiology & Behavior, 2020
    Co-Authors: Zainab Eydipour, Mohammad Nasehi, Salar Vaseghi, Seyed Hamid Jamaldini, Mohammad-reza Zarrindast
    Abstract:

    Sleep is a circadian rhythm that is modulated by endogenous circadian clock located in the suprachiasmatic nucleus (SCN). Sleep modulates Memory Acquisition and promotes Memory consolidation. Studies have shown that sleep deprivation (SD) impairs different types of Memory including passive avoidance. Furthermore, the hippocampus plays a significant role in modulating passive avoidance Memory. On the other hand, 5-HT4 receptors are expressed in the hippocampus and involved in learning and Memory processes. In this study, we aimed to investigate the role of CA1 hippocampal 5-HT4 receptors in Memory Acquisition impairment induced by total sleep deprivation (TSD: 24 h) and REM sleep deprivation (RSD: 24 h). The water box apparatus was used to induce TSD, while multi-platform apparatus was applied to induce RSD. Passive avoidance Memory test was also used to evaluate Memory Acquisition. The results showed that, intra-CA1 pre-training injection of RS67333 (5-HT4 agonist) and RS23597 (5-HT4 antagonist) at the doses of 0.01 and 0.1 µg/rat decreased Memory Acquisition, but did not alter pain perception and locomotor activity. Furthermore, TSD and RSD decreased Memory Acquisition; however, only TSD decreased locomotor activity and induced analgesic effect. The sub-threshold doses of RS67333 and RS23597, 0.001 and 0.0001 µg/rat, respectively, reversed the effect of TSD on Memory Acquisition and locomotor activity. In addition, only RS23597 reversed TSD-induced analgesia. In RSD condition, the subthreshold dose of RS23597 improved RSD-induced Memory Acquisition deficit. In conclusion, CA1 hippocampal 5-HT4 receptors play an important role in TSD/RSD-induced cognitive alterations.

  • critical role of ca1 nicotinic receptors on Memory Acquisition deficit under induction of total sleep deprivation and rem sleep deprivation
    International Clinical Neuroscience Journal, 2018
    Co-Authors: Bibi Zahra Javadmoosavi, Mohammad Nasehi, Gholamhassan Vaezi, Seyed Ali Haeri Rouhani, Mohammad-reza Zarrindast
    Abstract:

    Objective : Sleep disorder or sleep deprivation (SD) is a common issue in today’s society. Numerous evidences show that sleep is essential for proper brain performance and cognitive processes; on the other hand, cognitive functions have a broad range with learning and long-term Memory as the most important ones related to attention. Since many studies show that cholinergic system has a significant role in sleep, learning, and Memory, this study aims to investigate the impacts of CA1 Cholinergic Nicotinic Receptors on Memory Acquisition deficit which is stimulated by total sleep deprivation (TSD) and REM sleep deprivation (RSD). Methodology : In this study a water box or a multi-platform apparatus was used in order to induce total sleep deprivation (TSD) or REM sleep deprivation (RSD). In order to investigate interactions of cholinergic system and hippocampus-dependent Memory, nicotinic receptor agonist (nicotine) or nicotinic receptor antagonist (mecamylamine) was injected in hippocampal CA1. Results : According to the results of this study, 24 hours TSD or RSD decreased Memory Acquisition and injection of nicotine (0.0001  or mecamylamine (0.001  in TSD and RSD sham groups didn’t change Memory Acquisition. However, injection of sub-threshold dose of nicotine (0.0001  and mecamylamine (0.001  could reduce negative effects of SD in both TSD and RSD. Discussion ; According to the present study, cholinergic nicotinic receptors are effective in learning and Memory improvement.

  • Role of CA1 GABAA and GABAB receptors on learning deficit induced by D-AP5 in passive avoidance step-through task.
    Brain research, 2017
    Co-Authors: Mohaddeseh Ebrahimi-ghiri, Mohammad Nasehi, Masoumeh Rostampour, Mehdi Jamshidi-mehr, Mohammad-reza Zarrindast
    Abstract:

    Abstract To investigate the interaction between hippocampal γ-aminobutyric acid GABA A receptor (GABA A R) or GABA B receptor (GABA B R) and N-methyl-D-aspartate receptor (NMDAR) in the Acquisition of passive avoidance Memory in rats, we used GABA A or GABA B agents, D-AP5 (as a NMDAR antagonist), and a combination of the mentioned drugs in a step-through task. All agents were microinjected into the intra-CA1 regions at a volume of 1 µl/rat, prior to training. GABA A R agonist muscimol (0.2 µg/rat), selective GABA B R agonist baclofen (0.5 µg/rat) or NMDAR antagonist D-AP5 (0.25 µg/rat) decreased step-through latency, indicating a Memory retention impairment. Neither GABA A R antagonist bicuculline (0.0625–0.25 µg/rat) nor GABA B R antagonist phaclofen (0.1–0.5 µg/rat) altered Memory retrieval by itself. Moreover, the lower dose of muscimol (0.05 µg/rat) decreased D-AP5 (0.125 µg/rat) response on Memory Acquisition, but bicuculline did not alter the D-AP5 response. Furthermore, baclofen and phaclofen at the dose of 0.1 µg/rat potentiated D-AP5 response at the doses of 0.0625 and 0.125 µg/rat, but abolished Memory impairment induced by D-AP5 at the higher dose (0.25 µg/rat). The results suggest that the microinjection of GABA A and GABA B agents into the CA1 region differently affects Memory Acquisition deficit induced by D-AP5. The activation of GABA A Rs increased the impairment effect of D-AP5 on passive avoidance Memory, but their blockade did not have an effect. Also, the activation or blockade of GABA B Rs induced a similar and dual effect.

  • critical role of ca1 muscarinic receptors on Memory Acquisition deficit induced by total tsd and rem sleep deprivation rsd
    Progress in Neuro-psychopharmacology & Biological Psychiatry, 2017
    Co-Authors: Bibi Zahra Javadmoosavi, Mohammad Nasehi, Gholamhassan Vaezi, Seyedali Haerirouhani, Mohammad-reza Zarrindast
    Abstract:

    Abstract Aim Despite different theories regarding sleep physiological function, an overall census indicates that sleep is useful for neural plasticity which eventually strengthens cognition and brain performance. Different studies show that sleep deprivation (SD) leads to impaired learning and hippocampus dependent Memory. According to some studies, cholinergic system plays an important role in sleep (particularly REM sleep), learning, Memory, and its retrieval. So this study has been designed to investigate the effect of CA1 Cholinergic Muscarinic Receptors on Memory Acquisition deficit induced by total sleep deprivation (TSD) and REM sleep deprivation (RSD). Method A modified water box (locomotor activity may be provide a limiting factor in this method of SD) or multiple platforms were used for induction of TSD or RSD, respectively. Inhibitory passive avoidance apparatus has been used to determine the effects of SD and its changes by physostigmine (as cholinesterase inhibitor) or scopolamine (muscarinic receptor antagonist) on Memory formation. Because locomotor activity and pain perception induce critical roles in passive avoidance Memory formation, we also measured these factors by open field and hot-plate instruments, respectively. Results The results showed that TSD and RSD for 24 hours impaired Memory formation but they did not alter locomotor activity. TSD also induced analgesia effect, but RSD did not alter it. Intra-CA1 injection of physostigmine (0.0001 μg/rat) and scopolamine (0.01 μg/rat) did not alter Memory Acquisition in the sham-TSD or sham-RSD, by themselves. Moreover, intra-CA1 injection of sub-threshold dose of physostigmine (0.0001 μg/rat) and scopolamine (0.01 μg/rat) could restore the Memory Acquisition deficit induced by RSD, while scopolamine could restore TSD-induced amnesia. Both drugs reversed analgesia induced by TSD. None of previous interventions altered locomotor activity. Conclusion According to this study, CA1 cholinergic muscarinic receptors play an important role in amnesia induced by both TSD and RSD. However further studies are needed for showing cellular and molecular mechanisms of surprising result of similar pharmacological effects using compounds with opposite profiles.

Mohammad Nasehi - One of the best experts on this subject based on the ideXlab platform.

  • activation and inactivation of nicotinic receptnors in the dorsal hippocampal region restored negative effects of total tsd and rem sleep deprivation rsd on Memory Acquisition locomotor activity and pain perception
    Neuroscience, 2020
    Co-Authors: Bibi Zahra Javadmoosavi, Mohammad Nasehi, Salar Vaseghi, Seyed Hamid Jamaldini, Mohammad-reza Zarrindast
    Abstract:

    Abstract Sleep deprivation (SD) is a common issue in today’s society. Sleep is essential for proper cognitive functions, including learning and Memory. Furthermore, sleep disorders can alter pain information processing. Meanwhile, hippocampal nicotinic receptors have a role in modulating pain and Memory. The goal of this study is to investigate the effect of dorsal hippocampal (CA1) nicotinic receptors on behavioral changes induced by Total (TSD) and REM Sleep Deprivation (RSD). A modified water box and multi-platform apparatus were used to induce TSD and RSD, respectively. To investigate the interaction between nicotinic receptors and hippocampus-dependent Memory, nicotinic receptor agonist (nicotine) or antagonist (mecamylamine) was injected into the CA1 region. The results showed, nicotine at the doses of 0.001 and 0.1 µg/rat and mecamylamine at the doses of 0.01 and 0.1 µg/rat decreased Memory Acquisition, while both at the doses of 0.01 and 0.1 µg/rat enhanced locomotor activity. Additionally, all doses used for both drugs did not alter pain perception. Also, 24 h TSD or RSD attenuated Memory Acquisition with no effect on locomotor activity and only TSD induced an analgesic effect. Intra-CA1 administration of subthreshold dose of nicotine (0.0001 µg/rat) and mecamylamine (0.001 µg/rat) did not alter Memory Acquisition, pain perception and locomotor activity in sham of TSD/RSD rats. Both drugs reversed all behavioral changes induced by TSD. Furthermore, both drugs reversed the effect of RSD on Memory Acquisition, while only mecamylamine reversed the effect of RSD on locomotor activity. In conclusion, CA1 nicotinic receptors play a significant role in TSD/RSD-induced behavioral changes.

  • the role of 5 ht4 serotonin receptors in the ca1 hippocampal region on Memory Acquisition impairment induced by total tsd and rem sleep deprivation rsd
    Physiology & Behavior, 2020
    Co-Authors: Zainab Eydipour, Mohammad Nasehi, Salar Vaseghi, Seyed Hamid Jamaldini, Mohammad-reza Zarrindast
    Abstract:

    Sleep is a circadian rhythm that is modulated by endogenous circadian clock located in the suprachiasmatic nucleus (SCN). Sleep modulates Memory Acquisition and promotes Memory consolidation. Studies have shown that sleep deprivation (SD) impairs different types of Memory including passive avoidance. Furthermore, the hippocampus plays a significant role in modulating passive avoidance Memory. On the other hand, 5-HT4 receptors are expressed in the hippocampus and involved in learning and Memory processes. In this study, we aimed to investigate the role of CA1 hippocampal 5-HT4 receptors in Memory Acquisition impairment induced by total sleep deprivation (TSD: 24 h) and REM sleep deprivation (RSD: 24 h). The water box apparatus was used to induce TSD, while multi-platform apparatus was applied to induce RSD. Passive avoidance Memory test was also used to evaluate Memory Acquisition. The results showed that, intra-CA1 pre-training injection of RS67333 (5-HT4 agonist) and RS23597 (5-HT4 antagonist) at the doses of 0.01 and 0.1 µg/rat decreased Memory Acquisition, but did not alter pain perception and locomotor activity. Furthermore, TSD and RSD decreased Memory Acquisition; however, only TSD decreased locomotor activity and induced analgesic effect. The sub-threshold doses of RS67333 and RS23597, 0.001 and 0.0001 µg/rat, respectively, reversed the effect of TSD on Memory Acquisition and locomotor activity. In addition, only RS23597 reversed TSD-induced analgesia. In RSD condition, the subthreshold dose of RS23597 improved RSD-induced Memory Acquisition deficit. In conclusion, CA1 hippocampal 5-HT4 receptors play an important role in TSD/RSD-induced cognitive alterations.

  • critical role of ca1 nicotinic receptors on Memory Acquisition deficit under induction of total sleep deprivation and rem sleep deprivation
    International Clinical Neuroscience Journal, 2018
    Co-Authors: Bibi Zahra Javadmoosavi, Mohammad Nasehi, Gholamhassan Vaezi, Seyed Ali Haeri Rouhani, Mohammad-reza Zarrindast
    Abstract:

    Objective : Sleep disorder or sleep deprivation (SD) is a common issue in today’s society. Numerous evidences show that sleep is essential for proper brain performance and cognitive processes; on the other hand, cognitive functions have a broad range with learning and long-term Memory as the most important ones related to attention. Since many studies show that cholinergic system has a significant role in sleep, learning, and Memory, this study aims to investigate the impacts of CA1 Cholinergic Nicotinic Receptors on Memory Acquisition deficit which is stimulated by total sleep deprivation (TSD) and REM sleep deprivation (RSD). Methodology : In this study a water box or a multi-platform apparatus was used in order to induce total sleep deprivation (TSD) or REM sleep deprivation (RSD). In order to investigate interactions of cholinergic system and hippocampus-dependent Memory, nicotinic receptor agonist (nicotine) or nicotinic receptor antagonist (mecamylamine) was injected in hippocampal CA1. Results : According to the results of this study, 24 hours TSD or RSD decreased Memory Acquisition and injection of nicotine (0.0001  or mecamylamine (0.001  in TSD and RSD sham groups didn’t change Memory Acquisition. However, injection of sub-threshold dose of nicotine (0.0001  and mecamylamine (0.001  could reduce negative effects of SD in both TSD and RSD. Discussion ; According to the present study, cholinergic nicotinic receptors are effective in learning and Memory improvement.

  • Role of CA1 GABAA and GABAB receptors on learning deficit induced by D-AP5 in passive avoidance step-through task.
    Brain research, 2017
    Co-Authors: Mohaddeseh Ebrahimi-ghiri, Mohammad Nasehi, Masoumeh Rostampour, Mehdi Jamshidi-mehr, Mohammad-reza Zarrindast
    Abstract:

    Abstract To investigate the interaction between hippocampal γ-aminobutyric acid GABA A receptor (GABA A R) or GABA B receptor (GABA B R) and N-methyl-D-aspartate receptor (NMDAR) in the Acquisition of passive avoidance Memory in rats, we used GABA A or GABA B agents, D-AP5 (as a NMDAR antagonist), and a combination of the mentioned drugs in a step-through task. All agents were microinjected into the intra-CA1 regions at a volume of 1 µl/rat, prior to training. GABA A R agonist muscimol (0.2 µg/rat), selective GABA B R agonist baclofen (0.5 µg/rat) or NMDAR antagonist D-AP5 (0.25 µg/rat) decreased step-through latency, indicating a Memory retention impairment. Neither GABA A R antagonist bicuculline (0.0625–0.25 µg/rat) nor GABA B R antagonist phaclofen (0.1–0.5 µg/rat) altered Memory retrieval by itself. Moreover, the lower dose of muscimol (0.05 µg/rat) decreased D-AP5 (0.125 µg/rat) response on Memory Acquisition, but bicuculline did not alter the D-AP5 response. Furthermore, baclofen and phaclofen at the dose of 0.1 µg/rat potentiated D-AP5 response at the doses of 0.0625 and 0.125 µg/rat, but abolished Memory impairment induced by D-AP5 at the higher dose (0.25 µg/rat). The results suggest that the microinjection of GABA A and GABA B agents into the CA1 region differently affects Memory Acquisition deficit induced by D-AP5. The activation of GABA A Rs increased the impairment effect of D-AP5 on passive avoidance Memory, but their blockade did not have an effect. Also, the activation or blockade of GABA B Rs induced a similar and dual effect.

  • critical role of ca1 muscarinic receptors on Memory Acquisition deficit induced by total tsd and rem sleep deprivation rsd
    Progress in Neuro-psychopharmacology & Biological Psychiatry, 2017
    Co-Authors: Bibi Zahra Javadmoosavi, Mohammad Nasehi, Gholamhassan Vaezi, Seyedali Haerirouhani, Mohammad-reza Zarrindast
    Abstract:

    Abstract Aim Despite different theories regarding sleep physiological function, an overall census indicates that sleep is useful for neural plasticity which eventually strengthens cognition and brain performance. Different studies show that sleep deprivation (SD) leads to impaired learning and hippocampus dependent Memory. According to some studies, cholinergic system plays an important role in sleep (particularly REM sleep), learning, Memory, and its retrieval. So this study has been designed to investigate the effect of CA1 Cholinergic Muscarinic Receptors on Memory Acquisition deficit induced by total sleep deprivation (TSD) and REM sleep deprivation (RSD). Method A modified water box (locomotor activity may be provide a limiting factor in this method of SD) or multiple platforms were used for induction of TSD or RSD, respectively. Inhibitory passive avoidance apparatus has been used to determine the effects of SD and its changes by physostigmine (as cholinesterase inhibitor) or scopolamine (muscarinic receptor antagonist) on Memory formation. Because locomotor activity and pain perception induce critical roles in passive avoidance Memory formation, we also measured these factors by open field and hot-plate instruments, respectively. Results The results showed that TSD and RSD for 24 hours impaired Memory formation but they did not alter locomotor activity. TSD also induced analgesia effect, but RSD did not alter it. Intra-CA1 injection of physostigmine (0.0001 μg/rat) and scopolamine (0.01 μg/rat) did not alter Memory Acquisition in the sham-TSD or sham-RSD, by themselves. Moreover, intra-CA1 injection of sub-threshold dose of physostigmine (0.0001 μg/rat) and scopolamine (0.01 μg/rat) could restore the Memory Acquisition deficit induced by RSD, while scopolamine could restore TSD-induced amnesia. Both drugs reversed analgesia induced by TSD. None of previous interventions altered locomotor activity. Conclusion According to this study, CA1 cholinergic muscarinic receptors play an important role in amnesia induced by both TSD and RSD. However further studies are needed for showing cellular and molecular mechanisms of surprising result of similar pharmacological effects using compounds with opposite profiles.

Jos Prickaerts - One of the best experts on this subject based on the ideXlab platform.

  • Dissociable effects of acetylcholinesterase inhibitors and phosphodiesterase type 5 inhibitors on object recognition Memory: Acquisition versus consolidation
    Psychopharmacology, 2005
    Co-Authors: Jos Prickaerts, Ayhan şik, Jan De Vente, Franz Josef Staay, Arjan Blokland
    Abstract:

    Rationale Phosphodiesterase enzyme type 5 (PDE5) inhibitors and acetylcholinesterase (AChE) inhibitors have cognition-enhancing properties. However, it is not known whether these drug classes affect the same Memory processes. Objective We investigated the Memory-enhancing effects of the PDE5 inhibitor sildenafil and AChE inhibitors metrifonate and donepezil in the object recognition task to find out whether Acquisition or consolidation processes were affected by these drugs. Methods The object recognition task measures whether rats remembered an object they have explored in a previous learning trial. All drugs were given orally 30 min before or immediately after learning to study Acquisition and consolidation, respectively. Results Sildenafil given immediately after the first trial improved the Memory performance after 24 h and resulted in an inverted U-shaped dose–effect curve with the peak dose at 3 mg/kg. When given before the first trial, sildenafil also improved the Memory performance. However, the dose needed for the best performance under this condition was 10 mg/kg, suggesting that the dose–effect curve shifted to the right. This can be explained by the metabolic clearance of the high dose of sildenafil. Donepezil had no Memory improving effect when given after the first trial. However, when given before the first trial, a gradually increasing dose–effect curve was found which had its maximum effect at the highest dose tested (1 mg/kg). Likewise, only when metrifonate (30 mg/kg) was given before the first trial did rats show an improved Memory performance. Conclusion Our data strongly suggest that PDE5 inhibitors improve processes of consolidation of object information, whereas AChE inhibitors improve processes of Acquisition of object information.

  • dissociable effects of acetylcholinesterase inhibitors and phosphodiesterase type 5 inhibitors on object recognition Memory Acquisition versus consolidation
    Psychopharmacology, 2005
    Co-Authors: Jos Prickaerts, Ayhan şik, Franz Josef Van Der Staay, Jan De Vente, Arjan Blokland
    Abstract:

    Rationale Phosphodiesterase enzyme type 5 (PDE5) inhibitors and acetylcholinesterase (AChE) inhibitors have cognition-enhancing properties. However, it is not known whether these drug classes affect the same Memory processes.

Arjan Blokland - One of the best experts on this subject based on the ideXlab platform.

  • Dissociable effects of acetylcholinesterase inhibitors and phosphodiesterase type 5 inhibitors on object recognition Memory: Acquisition versus consolidation
    Psychopharmacology, 2005
    Co-Authors: Jos Prickaerts, Ayhan şik, Jan De Vente, Franz Josef Staay, Arjan Blokland
    Abstract:

    Rationale Phosphodiesterase enzyme type 5 (PDE5) inhibitors and acetylcholinesterase (AChE) inhibitors have cognition-enhancing properties. However, it is not known whether these drug classes affect the same Memory processes. Objective We investigated the Memory-enhancing effects of the PDE5 inhibitor sildenafil and AChE inhibitors metrifonate and donepezil in the object recognition task to find out whether Acquisition or consolidation processes were affected by these drugs. Methods The object recognition task measures whether rats remembered an object they have explored in a previous learning trial. All drugs were given orally 30 min before or immediately after learning to study Acquisition and consolidation, respectively. Results Sildenafil given immediately after the first trial improved the Memory performance after 24 h and resulted in an inverted U-shaped dose–effect curve with the peak dose at 3 mg/kg. When given before the first trial, sildenafil also improved the Memory performance. However, the dose needed for the best performance under this condition was 10 mg/kg, suggesting that the dose–effect curve shifted to the right. This can be explained by the metabolic clearance of the high dose of sildenafil. Donepezil had no Memory improving effect when given after the first trial. However, when given before the first trial, a gradually increasing dose–effect curve was found which had its maximum effect at the highest dose tested (1 mg/kg). Likewise, only when metrifonate (30 mg/kg) was given before the first trial did rats show an improved Memory performance. Conclusion Our data strongly suggest that PDE5 inhibitors improve processes of consolidation of object information, whereas AChE inhibitors improve processes of Acquisition of object information.

  • dissociable effects of acetylcholinesterase inhibitors and phosphodiesterase type 5 inhibitors on object recognition Memory Acquisition versus consolidation
    Psychopharmacology, 2005
    Co-Authors: Jos Prickaerts, Ayhan şik, Franz Josef Van Der Staay, Jan De Vente, Arjan Blokland
    Abstract:

    Rationale Phosphodiesterase enzyme type 5 (PDE5) inhibitors and acetylcholinesterase (AChE) inhibitors have cognition-enhancing properties. However, it is not known whether these drug classes affect the same Memory processes.

Bibi Zahra Javadmoosavi - One of the best experts on this subject based on the ideXlab platform.

  • activation and inactivation of nicotinic receptnors in the dorsal hippocampal region restored negative effects of total tsd and rem sleep deprivation rsd on Memory Acquisition locomotor activity and pain perception
    Neuroscience, 2020
    Co-Authors: Bibi Zahra Javadmoosavi, Mohammad Nasehi, Salar Vaseghi, Seyed Hamid Jamaldini, Mohammad-reza Zarrindast
    Abstract:

    Abstract Sleep deprivation (SD) is a common issue in today’s society. Sleep is essential for proper cognitive functions, including learning and Memory. Furthermore, sleep disorders can alter pain information processing. Meanwhile, hippocampal nicotinic receptors have a role in modulating pain and Memory. The goal of this study is to investigate the effect of dorsal hippocampal (CA1) nicotinic receptors on behavioral changes induced by Total (TSD) and REM Sleep Deprivation (RSD). A modified water box and multi-platform apparatus were used to induce TSD and RSD, respectively. To investigate the interaction between nicotinic receptors and hippocampus-dependent Memory, nicotinic receptor agonist (nicotine) or antagonist (mecamylamine) was injected into the CA1 region. The results showed, nicotine at the doses of 0.001 and 0.1 µg/rat and mecamylamine at the doses of 0.01 and 0.1 µg/rat decreased Memory Acquisition, while both at the doses of 0.01 and 0.1 µg/rat enhanced locomotor activity. Additionally, all doses used for both drugs did not alter pain perception. Also, 24 h TSD or RSD attenuated Memory Acquisition with no effect on locomotor activity and only TSD induced an analgesic effect. Intra-CA1 administration of subthreshold dose of nicotine (0.0001 µg/rat) and mecamylamine (0.001 µg/rat) did not alter Memory Acquisition, pain perception and locomotor activity in sham of TSD/RSD rats. Both drugs reversed all behavioral changes induced by TSD. Furthermore, both drugs reversed the effect of RSD on Memory Acquisition, while only mecamylamine reversed the effect of RSD on locomotor activity. In conclusion, CA1 nicotinic receptors play a significant role in TSD/RSD-induced behavioral changes.

  • critical role of ca1 nicotinic receptors on Memory Acquisition deficit under induction of total sleep deprivation and rem sleep deprivation
    International Clinical Neuroscience Journal, 2018
    Co-Authors: Bibi Zahra Javadmoosavi, Mohammad Nasehi, Gholamhassan Vaezi, Seyed Ali Haeri Rouhani, Mohammad-reza Zarrindast
    Abstract:

    Objective : Sleep disorder or sleep deprivation (SD) is a common issue in today’s society. Numerous evidences show that sleep is essential for proper brain performance and cognitive processes; on the other hand, cognitive functions have a broad range with learning and long-term Memory as the most important ones related to attention. Since many studies show that cholinergic system has a significant role in sleep, learning, and Memory, this study aims to investigate the impacts of CA1 Cholinergic Nicotinic Receptors on Memory Acquisition deficit which is stimulated by total sleep deprivation (TSD) and REM sleep deprivation (RSD). Methodology : In this study a water box or a multi-platform apparatus was used in order to induce total sleep deprivation (TSD) or REM sleep deprivation (RSD). In order to investigate interactions of cholinergic system and hippocampus-dependent Memory, nicotinic receptor agonist (nicotine) or nicotinic receptor antagonist (mecamylamine) was injected in hippocampal CA1. Results : According to the results of this study, 24 hours TSD or RSD decreased Memory Acquisition and injection of nicotine (0.0001  or mecamylamine (0.001  in TSD and RSD sham groups didn’t change Memory Acquisition. However, injection of sub-threshold dose of nicotine (0.0001  and mecamylamine (0.001  could reduce negative effects of SD in both TSD and RSD. Discussion ; According to the present study, cholinergic nicotinic receptors are effective in learning and Memory improvement.

  • critical role of ca1 muscarinic receptors on Memory Acquisition deficit induced by total tsd and rem sleep deprivation rsd
    Progress in Neuro-psychopharmacology & Biological Psychiatry, 2017
    Co-Authors: Bibi Zahra Javadmoosavi, Mohammad Nasehi, Gholamhassan Vaezi, Seyedali Haerirouhani, Mohammad-reza Zarrindast
    Abstract:

    Abstract Aim Despite different theories regarding sleep physiological function, an overall census indicates that sleep is useful for neural plasticity which eventually strengthens cognition and brain performance. Different studies show that sleep deprivation (SD) leads to impaired learning and hippocampus dependent Memory. According to some studies, cholinergic system plays an important role in sleep (particularly REM sleep), learning, Memory, and its retrieval. So this study has been designed to investigate the effect of CA1 Cholinergic Muscarinic Receptors on Memory Acquisition deficit induced by total sleep deprivation (TSD) and REM sleep deprivation (RSD). Method A modified water box (locomotor activity may be provide a limiting factor in this method of SD) or multiple platforms were used for induction of TSD or RSD, respectively. Inhibitory passive avoidance apparatus has been used to determine the effects of SD and its changes by physostigmine (as cholinesterase inhibitor) or scopolamine (muscarinic receptor antagonist) on Memory formation. Because locomotor activity and pain perception induce critical roles in passive avoidance Memory formation, we also measured these factors by open field and hot-plate instruments, respectively. Results The results showed that TSD and RSD for 24 hours impaired Memory formation but they did not alter locomotor activity. TSD also induced analgesia effect, but RSD did not alter it. Intra-CA1 injection of physostigmine (0.0001 μg/rat) and scopolamine (0.01 μg/rat) did not alter Memory Acquisition in the sham-TSD or sham-RSD, by themselves. Moreover, intra-CA1 injection of sub-threshold dose of physostigmine (0.0001 μg/rat) and scopolamine (0.01 μg/rat) could restore the Memory Acquisition deficit induced by RSD, while scopolamine could restore TSD-induced amnesia. Both drugs reversed analgesia induced by TSD. None of previous interventions altered locomotor activity. Conclusion According to this study, CA1 cholinergic muscarinic receptors play an important role in amnesia induced by both TSD and RSD. However further studies are needed for showing cellular and molecular mechanisms of surprising result of similar pharmacological effects using compounds with opposite profiles.