Neuroprotective effects of vinpocetine, as a phosphodiesterase 1 inhibitor, on long-term potentiation in a rat model of Alzheimer’s disease

Background Vinpocetine (Vin) is known as a phosphodiesterase 1 inhibitor (PDE1-I) drug with multilateral effects, including antioxidant and anti-inflammatory activity. In this research, we investigated the neuroprotective and therapeutic effects of Vin through hippocampal synaptic plasticity on a ra...

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Vydáno v:BMC neuroscience Ročník 24; číslo 1; s. 20 - 10
Hlavní autoři: Shekarian, Meysam, Salehi, Iraj, Raoufi, Safoura, Asadbegi, Masoumeh, Kourosh-Arami, Masoumeh, Komaki, Alireza
Médium: Journal Article
Jazyk:angličtina
Vydáno: London BioMed Central 16.03.2023
BioMed Central Ltd
Springer Nature B.V
BMC
Témata:
Alzheimer Disease - metabolism
Alzheimer's disease
Amyloid beta-Peptides - metabolism
Animal cognition
Animal Models
Animals
Anti-inflammatory agents
Beta-amyloid
Biomedical and Life Sciences
Biomedicine
Brain
Care and treatment
Dentate gyrus
Development and progression
Drug dosages
Electrodes
Excitatory postsynaptic potentials
Hippocampal plasticity
Hippocampus
Hippocampus - metabolism
Inflammation
Kinases
Long-Term Potentiation
Male
Memory
Neurobiology
Neurodegenerative diseases
Neuroprotection
Neuroprotective agents
Neuroprotective Agents - pharmacology
Neurosciences
Oral administration
Oxidative stress
Peptide Fragments - pharmacology
Peptides
Phosphodiesterase
Phosphodiesterase1 inhibitor
Phosphoric Diester Hydrolases - adverse effects
Phosphoric Diester Hydrolases - metabolism
Proteins
Rats
Rats, Wistar
Stereotaxic surgery
Surveillance
Synaptic plasticity
Testing
Vinpocetine
β-Amyloid
Iran
United States > US
Phosphodiesterase1 inhibitor
Alzheimer’s disease
Long-term potentiation
Hippocampus
Beta-amyloid
Vinpocetine
ISSN:1471-2202, 1471-2202
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Abstract Background Vinpocetine (Vin) is known as a phosphodiesterase 1 inhibitor (PDE1-I) drug with multilateral effects, including antioxidant and anti-inflammatory activity. In this research, we investigated the neuroprotective and therapeutic effects of Vin through hippocampal synaptic plasticity on a rat’s model of Alzheimer’s disease (AD) induced by an intracerebroventricular (ICV) injection of beta-amyloid (Aβ). Methods Sixty adult male Wistar rats were randomly divided into six groups: 1. control, 2. sham, 3. Aβ, 4. pretreatment (Vin + Aβ): Vin (4 mg/kg, gavage) for 30 days and then, inducing an AD model by an ICV injection of Aβ(1–42), 5. treatment (Aβ + Vin): inducing an AD model and then receiving Vin for 30 days by gavage, and 7. pretreatment + treatment (Vin + Aβ + Vin): receiving Vin by gavage for 30 days before and 30 days after the induction of an AD model. After these procedures, via stereotaxic surgery, the stimulating electrodes were placed at the perforant pathway (PP) and the recording electrodes were implanted in the dentate gyrus. Results Excitatory postsynaptic potential (EPSP) slope and population spike (PS) amplitude in the Aβ group meaningfully diminished compared to the control group after the induction of long-term potentiation (LTP). Conclusions Vin could significantly prevent the Aβ effects on LTP. It can be concluded that pretreatment and treatment with Vin can be neuroprotective against harmful consequences of Aβ on hippocampal synaptic plasticity.
AbstractList Vinpocetine (Vin) is known as a phosphodiesterase 1 inhibitor (PDE1-I) drug with multilateral effects, including antioxidant and anti-inflammatory activity. In this research, we investigated the neuroprotective and therapeutic effects of Vin through hippocampal synaptic plasticity on a rat's model of Alzheimer's disease (AD) induced by an intracerebroventricular (ICV) injection of beta-amyloid (Aβ). Sixty adult male Wistar rats were randomly divided into six groups: 1. control, 2. sham, 3. Aβ, 4. pretreatment (Vin + Aβ): Vin (4 mg/kg, gavage) for 30 days and then, inducing an AD model by an ICV injection of Aβ(1-42), 5. treatment (Aβ + Vin): inducing an AD model and then receiving Vin for 30 days by gavage, and 7. pretreatment + treatment (Vin + Aβ + Vin): receiving Vin by gavage for 30 days before and 30 days after the induction of an AD model. After these procedures, via stereotaxic surgery, the stimulating electrodes were placed at the perforant pathway (PP) and the recording electrodes were implanted in the dentate gyrus. Excitatory postsynaptic potential (EPSP) slope and population spike (PS) amplitude in the Aβ group meaningfully diminished compared to the control group after the induction of long-term potentiation (LTP). Vin could significantly prevent the Aβ effects on LTP. It can be concluded that pretreatment and treatment with Vin can be neuroprotective against harmful consequences of Aβ on hippocampal synaptic plasticity.
Vinpocetine (Vin) is known as a phosphodiesterase 1 inhibitor (PDE1-I) drug with multilateral effects, including antioxidant and anti-inflammatory activity. In this research, we investigated the neuroprotective and therapeutic effects of Vin through hippocampal synaptic plasticity on a rat's model of Alzheimer's disease (AD) induced by an intracerebroventricular (ICV) injection of beta-amyloid (Aβ).BACKGROUNDVinpocetine (Vin) is known as a phosphodiesterase 1 inhibitor (PDE1-I) drug with multilateral effects, including antioxidant and anti-inflammatory activity. In this research, we investigated the neuroprotective and therapeutic effects of Vin through hippocampal synaptic plasticity on a rat's model of Alzheimer's disease (AD) induced by an intracerebroventricular (ICV) injection of beta-amyloid (Aβ).Sixty adult male Wistar rats were randomly divided into six groups: 1. control, 2. sham, 3. Aβ, 4. pretreatment (Vin + Aβ): Vin (4 mg/kg, gavage) for 30 days and then, inducing an AD model by an ICV injection of Aβ(1-42), 5. treatment (Aβ + Vin): inducing an AD model and then receiving Vin for 30 days by gavage, and 7. pretreatment + treatment (Vin + Aβ + Vin): receiving Vin by gavage for 30 days before and 30 days after the induction of an AD model. After these procedures, via stereotaxic surgery, the stimulating electrodes were placed at the perforant pathway (PP) and the recording electrodes were implanted in the dentate gyrus.METHODSSixty adult male Wistar rats were randomly divided into six groups: 1. control, 2. sham, 3. Aβ, 4. pretreatment (Vin + Aβ): Vin (4 mg/kg, gavage) for 30 days and then, inducing an AD model by an ICV injection of Aβ(1-42), 5. treatment (Aβ + Vin): inducing an AD model and then receiving Vin for 30 days by gavage, and 7. pretreatment + treatment (Vin + Aβ + Vin): receiving Vin by gavage for 30 days before and 30 days after the induction of an AD model. After these procedures, via stereotaxic surgery, the stimulating electrodes were placed at the perforant pathway (PP) and the recording electrodes were implanted in the dentate gyrus.Excitatory postsynaptic potential (EPSP) slope and population spike (PS) amplitude in the Aβ group meaningfully diminished compared to the control group after the induction of long-term potentiation (LTP).RESULTSExcitatory postsynaptic potential (EPSP) slope and population spike (PS) amplitude in the Aβ group meaningfully diminished compared to the control group after the induction of long-term potentiation (LTP).Vin could significantly prevent the Aβ effects on LTP. It can be concluded that pretreatment and treatment with Vin can be neuroprotective against harmful consequences of Aβ on hippocampal synaptic plasticity.CONCLUSIONSVin could significantly prevent the Aβ effects on LTP. It can be concluded that pretreatment and treatment with Vin can be neuroprotective against harmful consequences of Aβ on hippocampal synaptic plasticity.
Background Vinpocetine (Vin) is known as a phosphodiesterase 1 inhibitor (PDE1-I) drug with multilateral effects, including antioxidant and anti-inflammatory activity. In this research, we investigated the neuroprotective and therapeutic effects of Vin through hippocampal synaptic plasticity on a rat's model of Alzheimer's disease (AD) induced by an intracerebroventricular (ICV) injection of beta-amyloid (A[beta]). Methods Sixty adult male Wistar rats were randomly divided into six groups: 1. control, 2. sham, 3. A[beta], 4. pretreatment (Vin + A[beta]): Vin (4 mg/kg, gavage) for 30 days and then, inducing an AD model by an ICV injection of A[beta](1-42), 5. treatment (A[beta] + Vin): inducing an AD model and then receiving Vin for 30 days by gavage, and 7. pretreatment + treatment (Vin + A[beta] + Vin): receiving Vin by gavage for 30 days before and 30 days after the induction of an AD model. After these procedures, via stereotaxic surgery, the stimulating electrodes were placed at the perforant pathway (PP) and the recording electrodes were implanted in the dentate gyrus. Results Excitatory postsynaptic potential (EPSP) slope and population spike (PS) amplitude in the A[beta] group meaningfully diminished compared to the control group after the induction of long-term potentiation (LTP). Conclusions Vin could significantly prevent the A[beta] effects on LTP. It can be concluded that pretreatment and treatment with Vin can be neuroprotective against harmful consequences of A[beta] on hippocampal synaptic plasticity. Keywords: Alzheimer's disease, Beta-amyloid, Vinpocetine, Phosphodiesterase1 inhibitor, Hippocampus, Long-term potentiation
Background Vinpocetine (Vin) is known as a phosphodiesterase 1 inhibitor (PDE1-I) drug with multilateral effects, including antioxidant and anti-inflammatory activity. In this research, we investigated the neuroprotective and therapeutic effects of Vin through hippocampal synaptic plasticity on a rat’s model of Alzheimer’s disease (AD) induced by an intracerebroventricular (ICV) injection of beta-amyloid (Aβ). Methods Sixty adult male Wistar rats were randomly divided into six groups: 1. control, 2. sham, 3. Aβ, 4. pretreatment (Vin + Aβ): Vin (4 mg/kg, gavage) for 30 days and then, inducing an AD model by an ICV injection of Aβ(1–42), 5. treatment (Aβ + Vin): inducing an AD model and then receiving Vin for 30 days by gavage, and 7. pretreatment + treatment (Vin + Aβ + Vin): receiving Vin by gavage for 30 days before and 30 days after the induction of an AD model. After these procedures, via stereotaxic surgery, the stimulating electrodes were placed at the perforant pathway (PP) and the recording electrodes were implanted in the dentate gyrus. Results Excitatory postsynaptic potential (EPSP) slope and population spike (PS) amplitude in the Aβ group meaningfully diminished compared to the control group after the induction of long-term potentiation (LTP). Conclusions Vin could significantly prevent the Aβ effects on LTP. It can be concluded that pretreatment and treatment with Vin can be neuroprotective against harmful consequences of Aβ on hippocampal synaptic plasticity.
Vinpocetine (Vin) is known as a phosphodiesterase 1 inhibitor (PDE1-I) drug with multilateral effects, including antioxidant and anti-inflammatory activity. In this research, we investigated the neuroprotective and therapeutic effects of Vin through hippocampal synaptic plasticity on a rat's model of Alzheimer's disease (AD) induced by an intracerebroventricular (ICV) injection of beta-amyloid (A[beta]). Sixty adult male Wistar rats were randomly divided into six groups: 1. control, 2. sham, 3. A[beta], 4. pretreatment (Vin + A[beta]): Vin (4 mg/kg, gavage) for 30 days and then, inducing an AD model by an ICV injection of A[beta](1-42), 5. treatment (A[beta] + Vin): inducing an AD model and then receiving Vin for 30 days by gavage, and 7. pretreatment + treatment (Vin + A[beta] + Vin): receiving Vin by gavage for 30 days before and 30 days after the induction of an AD model. After these procedures, via stereotaxic surgery, the stimulating electrodes were placed at the perforant pathway (PP) and the recording electrodes were implanted in the dentate gyrus. Excitatory postsynaptic potential (EPSP) slope and population spike (PS) amplitude in the A[beta] group meaningfully diminished compared to the control group after the induction of long-term potentiation (LTP). Vin could significantly prevent the A[beta] effects on LTP. It can be concluded that pretreatment and treatment with Vin can be neuroprotective against harmful consequences of A[beta] on hippocampal synaptic plasticity.
Abstract Background Vinpocetine (Vin) is known as a phosphodiesterase 1 inhibitor (PDE1-I) drug with multilateral effects, including antioxidant and anti-inflammatory activity. In this research, we investigated the neuroprotective and therapeutic effects of Vin through hippocampal synaptic plasticity on a rat’s model of Alzheimer’s disease (AD) induced by an intracerebroventricular (ICV) injection of beta-amyloid (Aβ). Methods Sixty adult male Wistar rats were randomly divided into six groups: 1. control, 2. sham, 3. Aβ, 4. pretreatment (Vin + Aβ): Vin (4 mg/kg, gavage) for 30 days and then, inducing an AD model by an ICV injection of Aβ(1–42), 5. treatment (Aβ + Vin): inducing an AD model and then receiving Vin for 30 days by gavage, and 7. pretreatment + treatment (Vin + Aβ + Vin): receiving Vin by gavage for 30 days before and 30 days after the induction of an AD model. After these procedures, via stereotaxic surgery, the stimulating electrodes were placed at the perforant pathway (PP) and the recording electrodes were implanted in the dentate gyrus. Results Excitatory postsynaptic potential (EPSP) slope and population spike (PS) amplitude in the Aβ group meaningfully diminished compared to the control group after the induction of long-term potentiation (LTP). Conclusions Vin could significantly prevent the Aβ effects on LTP. It can be concluded that pretreatment and treatment with Vin can be neuroprotective against harmful consequences of Aβ on hippocampal synaptic plasticity.
BackgroundVinpocetine (Vin) is known as a phosphodiesterase 1 inhibitor (PDE1-I) drug with multilateral effects, including antioxidant and anti-inflammatory activity. In this research, we investigated the neuroprotective and therapeutic effects of Vin through hippocampal synaptic plasticity on a rat’s model of Alzheimer’s disease (AD) induced by an intracerebroventricular (ICV) injection of beta-amyloid (Aβ).MethodsSixty adult male Wistar rats were randomly divided into six groups: 1. control, 2. sham, 3. Aβ, 4. pretreatment (Vin + Aβ): Vin (4 mg/kg, gavage) for 30 days and then, inducing an AD model by an ICV injection of Aβ(1–42), 5. treatment (Aβ + Vin): inducing an AD model and then receiving Vin for 30 days by gavage, and 7. pretreatment + treatment (Vin + Aβ + Vin): receiving Vin by gavage for 30 days before and 30 days after the induction of an AD model. After these procedures, via stereotaxic surgery, the stimulating electrodes were placed at the perforant pathway (PP) and the recording electrodes were implanted in the dentate gyrus.ResultsExcitatory postsynaptic potential (EPSP) slope and population spike (PS) amplitude in the Aβ group meaningfully diminished compared to the control group after the induction of long-term potentiation (LTP).ConclusionsVin could significantly prevent the Aβ effects on LTP. It can be concluded that pretreatment and treatment with Vin can be neuroprotective against harmful consequences of Aβ on hippocampal synaptic plasticity.
ArticleNumber 20
Audience Academic
Author Kourosh-Arami, Masoumeh
Salehi, Iraj
Komaki, Alireza
Asadbegi, Masoumeh
Shekarian, Meysam
Raoufi, Safoura
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  surname: Komaki
  fullname: Komaki, Alireza
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  organization: Department of Physiology, School of Medicine, Hamadan University of Medical Sciences, Department of Neuroscience, School of Science and Advanced Technologies in Medicine, Hamadan University of Medical Sciences
BackLink https://www.ncbi.nlm.nih.gov/pubmed/36927298$$D View this record in MEDLINE/PubMed
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Issue 1
Keywords Phosphodiesterase1 inhibitor
Alzheimer’s disease
Long-term potentiation
Hippocampus
Beta-amyloid
Vinpocetine
Language English
License 2023. The Author(s).
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Snippet Background Vinpocetine (Vin) is known as a phosphodiesterase 1 inhibitor (PDE1-I) drug with multilateral effects, including antioxidant and anti-inflammatory...
Vinpocetine (Vin) is known as a phosphodiesterase 1 inhibitor (PDE1-I) drug with multilateral effects, including antioxidant and anti-inflammatory activity. In...
Background Vinpocetine (Vin) is known as a phosphodiesterase 1 inhibitor (PDE1-I) drug with multilateral effects, including antioxidant and anti-inflammatory...
BackgroundVinpocetine (Vin) is known as a phosphodiesterase 1 inhibitor (PDE1-I) drug with multilateral effects, including antioxidant and anti-inflammatory...
Abstract Background Vinpocetine (Vin) is known as a phosphodiesterase 1 inhibitor (PDE1-I) drug with multilateral effects, including antioxidant and...
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SubjectTerms Alzheimer Disease - metabolism
Alzheimer's disease
Amyloid beta-Peptides - metabolism
Animal cognition
Animal Models
Animals
Anti-inflammatory agents
Beta-amyloid
Biomedical and Life Sciences
Biomedicine
Brain
Care and treatment
Dentate gyrus
Development and progression
Drug dosages
Electrodes
Excitatory postsynaptic potentials
Hippocampal plasticity
Hippocampus
Hippocampus - metabolism
Inflammation
Kinases
Long-Term Potentiation
Male
Memory
Neurobiology
Neurodegenerative diseases
Neuroprotection
Neuroprotective agents
Neuroprotective Agents - pharmacology
Neurosciences
Oral administration
Oxidative stress
Peptide Fragments - pharmacology
Peptides
Phosphodiesterase
Phosphodiesterase1 inhibitor
Phosphoric Diester Hydrolases - adverse effects
Phosphoric Diester Hydrolases - metabolism
Proteins
Rats
Rats, Wistar
Stereotaxic surgery
Surveillance
Synaptic plasticity
Testing
Vinpocetine
β-Amyloid
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Title Neuroprotective effects of vinpocetine, as a phosphodiesterase 1 inhibitor, on long-term potentiation in a rat model of Alzheimer’s disease
URI https://link.springer.com/article/10.1186/s12868-023-00790-8
https://www.ncbi.nlm.nih.gov/pubmed/36927298
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