NS.4.2 - PRAMIPEXOLE DISRUPTS SYNAPTIC PLASTICITY IN THE CA1 AREA OF THE HIPOCAMPUS OF RATS THAT DEVELOP CONTRAFREELOADING FOR WATER, AN ANIMAL MODEL OF COMPULSIVE BEHAVIOR

Diabetes mellitus (DM) is a multisystem endocrine disorder affecting the brain. Mesenchymal stem cells (MSCs) pretreated with Melatonin have been shown to increase the potency of MSCs. This work aimed to compare Melatonin, stem cells, and stem cells pretreated with Melatonin on the cognitive functions and markers of synaptic plasticity in an animal model of type I diabetes mellitus (TIDM). Thirty-six rats represented the animal model; six rats for isolation of MSCs and 30 rats were divided into five groups: control, TIDM, TIDM + Melatonin, TIDM + Stem cells, and TIDM + Stem ex vivo Melatonin. Functional assessment was performed with Y-maze, forced swimming test and novel object recognition. Histological and biochemical evaluation of hippocampal Neuroligin 1, Sortilin, Brain-Derived Neurotrophic Factor (BDNF), inducible nitric oxide synthase (iNOS), toll-like receptor 2 (TLR2), Tumor necrosis factor-alpha (TNF-α), and Growth Associated Protein 43 (GAP43). The TIDM group showed a significant decrease of hippocampal Neuroligin, Sortilin, and BDNF and a significant increase in iNOS, TNF-α, TLR2, and GAP43. Melatonin or stem cells groups showed improvement compared to the diabetic group but not compared to the control group. TIDM + Stem ex vivo Melatonin group showed a significant improvement, and some values were restored to normal. Ex vivo melatonin-treated stem cells had improved spatial working and object recognition memory and depression, with positive effects on glucose homeostasis, inflammatory markers levels and synaptic plasticity markers expression.

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Probiotic treatment improves the impaired spatial cognitive performance and restores synaptic plasticity in an animal model of Alzheimer's disease

Behavioural Brain Research ◽

10.1016/j.bbr.2019.112183 ◽

2019 ◽

Vol 376 ◽

pp. 112183 ◽

Cited By ~ 8

Author(s):

Zahra Rezaei Asl ◽

Gholamreza Sepehri ◽

Mahmoud Salami

Keyword(s):

Alzheimer’S Disease ◽

Alzheimer's Disease ◽

Animal Model ◽

Synaptic Plasticity ◽

Cognitive Performance ◽

Model Of Alzheimer’S Disease ◽

Probiotic Treatment

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Differential effect of FHM2 mutation on synaptic plasticity in distinct hippocampal regions

Cephalalgia ◽

10.1177/0333102419839967 ◽

2019 ◽

Vol 39 (10) ◽

pp. 1333-1338 ◽

Cited By ~ 3

Author(s):

Antonio de Iure ◽

Petra Mazzocchetti ◽

Guendalina Bastioli ◽

Barbara Picconi ◽

Cinzia Costa ◽

...

Keyword(s):

Synaptic Plasticity ◽

Long Term Potentiation ◽

Familial Hemiplegic Migraine ◽

Loss Of Function ◽

Hemiplegic Migraine ◽

Term Potentiation ◽

Atp1a2 Gene ◽

Ca1 Area ◽

Reduced Rate

Introduction Familial hemiplegic migraine 2 is a pathology linked to mutation of the ATP1A2 gene producing loss of function of the α2 Na+/K+-ATPase (NKA). W887R/+ knock-in (KI) mice are used to model the familial hemiplegic migraine 2 condition and are characterized by 50% reduced NKA expression in the brain and reduced rate of K+ and glutamate clearance by astrocytes. These alterations might, in turn, produce synaptic changes in synaptic transmission and plasticity. Memory and learning deficits observed in familial hemiplegic migraine patients could be ascribed to a possible alteration of hippocampal neuronal plasticity and measuring possible changes of long-term potentiation in familial hemiplegic migraine 2 KI mice might provide insights to strengthen this link. Results Here we have investigated synaptic plasticity in distinct hippocampal regions in familial hemiplegic migraine 2 KI mice. We show that the dentate gyrus long-term potentiation of familial hemiplegic migraine 2 mice is abnormally increased in comparison with control animals. Conversely, in the CA1 area, KI and WT mice express long-term potentiation of similar amplitude. Conclusions The familial hemiplegic migraine 2 KI mice show region-dependent hippocampal plasticity abnormality, which might underlie some of the memory deficits observed in familial migraine.

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Long-lasting changes in hippocampal synaptic plasticity and cognition in an animal model of NMDA receptor dysfunction in psychosis

Neuropharmacology ◽

10.1016/j.neuropharm.2013.01.001 ◽

2013 ◽

Vol 74 ◽

pp. 48-58 ◽

Cited By ~ 28

Author(s):

Valentina Wiescholleck ◽

Denise Manahan-Vaughan

Keyword(s):

Animal Model ◽

Synaptic Plasticity ◽

Nmda Receptor ◽

Hippocampal Synaptic Plasticity

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Valproate-Induced “Wet Dog Shakes” – A Reproducible Animal Model of Human Compulsive Behavior : Effect of Antidepressants

Annals of Neurosciences ◽

10.5214/ans.0972.7531.2007.140402 ◽

2007 ◽

Vol 14 (4) ◽

pp. 93-95

Author(s):

Prathibha E A Jose ◽

Joy David ◽

Vikram K Yeragani ◽

Chanda Kulkarni

Keyword(s):

Animal Model ◽

Compulsive Behavior ◽

Wet Dog Shakes

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Psychostimulant-Induced Behavior as an Animal Model of Obsessive-Compulsive Disorder: An Ethological Approach to the Form of Compulsive Rituals

CNS Spectrums ◽

10.1017/s109285290001004x ◽

2005 ◽

Vol 10 (3) ◽

pp. 191-202 ◽

Cited By ~ 56

Author(s):

David Eilam ◽

Henry Szechtman

Keyword(s):

Animal Model ◽

Obsessive Compulsive Disorder ◽

Rat Model ◽

Receptor Agonist ◽

Dopamine Receptor Agonist ◽

Compulsive Behavior ◽

Obsessive Compulsive ◽

Compulsive Disorder ◽

Dopaminergic Mechanisms ◽

Motor Acts

AbstractRats treated chronically with the D2/D3, dopamine receptor agonist quinpirole show a pattern of behavior that meets a set of ethologically derived criteria of compulsive behavior in obsessive-compulsive disorder (OCD). Moreover, in both quinpirole-treated rats and OCD patients, the structure of compulsive rituals appear similar in being composed of relatively few motor acts that are organized in a flexible yet recurrent manner. In addition, the development of compulsive behavior in quinpirole-treated rats is attenuated by the OCD pharmacotherapeutic drug clomipramine. These similarities support the validity of quinpirole-treated rats as a psychostimulant-induced animal model of OCD. Considering that the induction of compulsive behavior in the rat model involves chronic hyperstimulation of dopamine receptors, this raises the possibility that dopaminergic mechanisms may play a role in OCD, at least in some subtypes of this disorder.

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