BIOMAT Database Logo BIOMAT Database Logo

Serotonin type 6 receptor antagonist attenuates the impairment of long-term potentiation and memory induced by Abeta. 2019

Siamak Shahidi, and Nasrin Hashemi-Firouzi, and Sara Soleimani Asl, and Alireza Komaki
Neurophysiology Research Center, Hamadan University of Medical Sciences, Hamadan, Iran.

Alzheimer's disease (AD) is the most common cause of dementia, characterized by memory impairment and synaptic loss. Long-term potentiation (LTP), a type of synaptic plasticity, is impaired during AD. Serotonin type 6 receptor (5-HT6R) inactivation is proposed as a therapeutic target for AD. This study examined the effects of chronic administration of the 5-HT6R antagonist, SB-258585, on cognitive, memory, and hippocampal plasticity in a rat model of AD. Abeta neurotoxicity was induced in rats using Aβ (1.35 pmol intracerebroventricular [ICV] injection). The following groups were formed: control sustained surgery and saline-treated, Aβ+saline (1 μL ICV for 30 days), and Aβ+SB-258585 (0.024 mg/kg, ICV for 30 days). The learning and memory were tested using the novel object recognition and passive avoidance tests. Next, anesthetized rats were placed in a stereotaxic apparatus. The population spike (PS) amplitude and the slope of the excitatory postsynaptic potentials (fEPSPs) of the LTP were measured following high-frequency stimulation in the dentate gyrus. The Aβ injection reduced step-through latency in the passive avoidance test and decreased the discrimination index in the novel object test. Aβ diminished both the amplitude of hippocampal neuron population spikes and the slope of excitatory postsynaptic potentials, compared to the control group. The administration of SB-258585 in rats receiving Aβ attenuated the Aβ-induced deficits in cognition, memory, and LTP in comparison with the Aβ group. It can be concluded that chronic treatment with SB-258585 antagonist can prevent Aβ-related deficiencies in learning and memory performance by improving neuronal plasticity. SB-258585 can prevent the progression of AD.

UI MeSH Term Description Entries
D008297 Male Males
D008568 Memory Complex mental function having four distinct phases: (1) memorizing or learning, (2) retention, (3) recall, and (4) recognition. Clinically, it is usually subdivided into immediate, recent, and remote memory.
D009473 Neuronal Plasticity The capacity of the NERVOUS SYSTEM to change its reactivity as the result of successive activations. Brain Plasticity,Plasticity, Neuronal,Axon Pruning,Axonal Pruning,Dendrite Arborization,Dendrite Pruning,Dendritic Arborization,Dendritic Pruning,Dendritic Remodeling,Neural Plasticity,Neurite Pruning,Neuronal Arborization,Neuronal Network Remodeling,Neuronal Pruning,Neuronal Remodeling,Neuroplasticity,Synaptic Plasticity,Synaptic Pruning,Arborization, Dendrite,Arborization, Dendritic,Arborization, Neuronal,Arborizations, Dendrite,Arborizations, Dendritic,Arborizations, Neuronal,Axon Prunings,Axonal Prunings,Brain Plasticities,Dendrite Arborizations,Dendrite Prunings,Dendritic Arborizations,Dendritic Prunings,Dendritic Remodelings,Network Remodeling, Neuronal,Network Remodelings, Neuronal,Neural Plasticities,Neurite Prunings,Neuronal Arborizations,Neuronal Network Remodelings,Neuronal Plasticities,Neuronal Prunings,Neuronal Remodelings,Neuroplasticities,Plasticities, Brain,Plasticities, Neural,Plasticities, Neuronal,Plasticities, Synaptic,Plasticity, Brain,Plasticity, Neural,Plasticity, Synaptic,Pruning, Axon,Pruning, Axonal,Pruning, Dendrite,Pruning, Dendritic,Pruning, Neurite,Pruning, Neuronal,Pruning, Synaptic,Prunings, Axon,Prunings, Axonal,Prunings, Dendrite,Prunings, Dendritic,Prunings, Neurite,Prunings, Neuronal,Prunings, Synaptic,Remodeling, Dendritic,Remodeling, Neuronal,Remodeling, Neuronal Network,Remodelings, Dendritic,Remodelings, Neuronal,Remodelings, Neuronal Network,Synaptic Plasticities,Synaptic Prunings
D009474 Neurons The basic cellular units of nervous tissue. Each neuron consists of a body, an axon, and dendrites. Their purpose is to receive, conduct, and transmit impulses in the NERVOUS SYSTEM. Nerve Cells,Cell, Nerve,Cells, Nerve,Nerve Cell,Neuron
D010446 Peptide Fragments Partial proteins formed by partial hydrolysis of complete proteins or generated through PROTEIN ENGINEERING techniques. Peptide Fragment,Fragment, Peptide,Fragments, Peptide
D010879 Piperazines Compounds that are derived from PIPERAZINE.
D011985 Receptors, Serotonin Cell-surface proteins that bind SEROTONIN and trigger intracellular changes which influence the behavior of cells. Several types of serotonin receptors have been recognized which differ in their pharmacology, molecular biology, and mode of action. 5-HT Receptor,5-HT Receptors,5-Hydroxytryptamine Receptor,5-Hydroxytryptamine Receptors,Receptors, Tryptamine,Serotonin Receptor,Serotonin Receptors,Tryptamine Receptor,Tryptamine Receptors,Receptors, 5-HT,Receptors, 5-Hydroxytryptamine,5 HT Receptor,5 HT Receptors,5 Hydroxytryptamine Receptor,5 Hydroxytryptamine Receptors,Receptor, 5-HT,Receptor, 5-Hydroxytryptamine,Receptor, Serotonin,Receptor, Tryptamine,Receptors, 5 HT,Receptors, 5 Hydroxytryptamine
D004195 Disease Models, Animal Naturally-occurring or experimentally-induced animal diseases with pathological processes analogous to human diseases. Animal Disease Model,Animal Disease Models,Disease Model, Animal
D006624 Hippocampus A curved elevation of GRAY MATTER extending the entire length of the floor of the TEMPORAL HORN of the LATERAL VENTRICLE (see also TEMPORAL LOBE). The hippocampus proper, subiculum, and DENTATE GYRUS constitute the hippocampal formation. Sometimes authors include the ENTORHINAL CORTEX in the hippocampal formation. Ammon Horn,Cornu Ammonis,Hippocampal Formation,Subiculum,Ammon's Horn,Hippocampus Proper,Ammons Horn,Formation, Hippocampal,Formations, Hippocampal,Hippocampal Formations,Hippocampus Propers,Horn, Ammon,Horn, Ammon's,Proper, Hippocampus,Propers, Hippocampus,Subiculums
D000544 Alzheimer Disease A degenerative disease of the BRAIN characterized by the insidious onset of DEMENTIA. Impairment of MEMORY, judgment, attention span, and problem solving skills are followed by severe APRAXIAS and a global loss of cognitive abilities. The condition primarily occurs after age 60, and is marked pathologically by severe cortical atrophy and the triad of SENILE PLAQUES; NEUROFIBRILLARY TANGLES; and NEUROPIL THREADS. (From Adams et al., Principles of Neurology, 6th ed, pp1049-57) Acute Confusional Senile Dementia,Alzheimer's Diseases,Dementia, Alzheimer Type,Dementia, Senile,Presenile Alzheimer Dementia,Senile Dementia, Alzheimer Type,Alzheimer Dementia,Alzheimer Disease, Early Onset,Alzheimer Disease, Late Onset,Alzheimer Sclerosis,Alzheimer Syndrome,Alzheimer Type Senile Dementia,Alzheimer's Disease,Alzheimer's Disease, Focal Onset,Alzheimer-Type Dementia (ATD),Dementia, Presenile,Dementia, Primary Senile Degenerative,Early Onset Alzheimer Disease,Familial Alzheimer Disease (FAD),Focal Onset Alzheimer's Disease,Late Onset Alzheimer Disease,Primary Senile Degenerative Dementia,Senile Dementia, Acute Confusional,Alzheimer Dementias,Alzheimer Disease, Familial (FAD),Alzheimer Diseases,Alzheimer Type Dementia,Alzheimer Type Dementia (ATD),Alzheimers Diseases,Dementia, Alzheimer,Dementia, Alzheimer-Type (ATD),Familial Alzheimer Diseases (FAD),Presenile Dementia,Sclerosis, Alzheimer,Senile Dementia

Related Publications

Siamak Shahidi, and Nasrin Hashemi-Firouzi, and Sara Soleimani Asl, and Alireza Komaki
Lithium attenuates stress-induced impairment of long-term potentiation induction.
September 2005, Neuroreport,
Siamak Shahidi, and Nasrin Hashemi-Firouzi, and Sara Soleimani Asl, and Alireza Komaki
Nicotine alleviates alcohol-induced memory and long-term potentiation impairment.
August 2022, Neuroscience letters,
Siamak Shahidi, and Nasrin Hashemi-Firouzi, and Sara Soleimani Asl, and Alireza Komaki
Opioid antagonist eliminates the stress-induced impairment of long-term potentiation (LTP).
January 1990, Brain research,
Siamak Shahidi, and Nasrin Hashemi-Firouzi, and Sara Soleimani Asl, and Alireza Komaki
Sulforaphane enhances long-term potentiation and ameliorate scopolamine-induced memory impairment.
September 2021, Physiology & behavior,
Siamak Shahidi, and Nasrin Hashemi-Firouzi, and Sara Soleimani Asl, and Alireza Komaki
Tanshinone IIA attenuates neuronal damage and the impairment of long-term potentiation induced by hydrogen peroxide.
March 2011, Journal of ethnopharmacology,
Siamak Shahidi, and Nasrin Hashemi-Firouzi, and Sara Soleimani Asl, and Alireza Komaki
Impairment of long-term potentiation and spatial memory in leptin receptor-deficient rodents.
January 2002, Neuroscience,
Siamak Shahidi, and Nasrin Hashemi-Firouzi, and Sara Soleimani Asl, and Alireza Komaki
Retrograde amnesia for spatial memory induced by NMDA receptor-mediated long-term potentiation.
January 2001, The Journal of neuroscience : the official journal of the Society for Neuroscience,
Siamak Shahidi, and Nasrin Hashemi-Firouzi, and Sara Soleimani Asl, and Alireza Komaki
Dopaminergic neurotransmission dysfunction induced by amyloid-β transforms cortical long-term potentiation into long-term depression and produces memory impairment.
May 2016, Neurobiology of aging,
Siamak Shahidi, and Nasrin Hashemi-Firouzi, and Sara Soleimani Asl, and Alireza Komaki
Aluminium-maltolate-induced impairment of learning, memory and hippocampal long-term potentiation in rats.
January 2012, Industrial health,
Siamak Shahidi, and Nasrin Hashemi-Firouzi, and Sara Soleimani Asl, and Alireza Komaki
Abeta oligomer-mediated long-term potentiation impairment involves protein phosphatase 1-dependent mechanisms.
July 2007, The Journal of neuroscience : the official journal of the Society for Neuroscience,
Copied contents to your clipboard!