Genetically Induced Retrograde Amnesia of Associative Memories After Neuroplastin Ablation

Bhattacharya, Soumee; Herrera-Molina, Rodrigo; Sabanov, Victor; Ahmed, Tariq; Iscru, Emilia; Stöber, Franziska; Richter, Karin; Fischer, Klaus; Angenstein, Frank; Goldschmidt, Jürgen; Beesley, Philip; Balschun, Detlef; Smalla, Karl Heinz; Gundelfinger, Eckart D.; Montag, Dirk

doi:10.1016/j.biopsych.2016.03.2107

Cited by 42 publications

(124 citation statements)

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“…Long-term potentiation in the hippocampal CA1 region is a better model for studying synaptic plasticity. In this study, we first confirmed that Np65 KO mice exhibited impaired maintenance of LTP, consistent with previous reports in which incubation with Np65-Fc fusion protein or Np65 antibody in hippocampal slices impairs the maintenance of LTP or impaired LTP in Nptn-deficient mice [6,24]. Furthermore, previous reports show that Np65 exerts multiple effects on glutamatergic and GABAergic synapses [7,8].…”

Section: Discussionsupporting

confidence: 91%

“…Finally, Np65 KO mice exhibited [25] reported that Nptn ablation in glutamatergic neurons (Nptn lox/lox Emx1Cre mice) did not disturb formation of spatial memory but showed the discontinuity of swimming action with repetitive pause-swimming cycles and the swimming strategy in reversal probe test. They also reported reduced PMCAs in Nptn À/À mice, inducible Nptn KO mice and Nptn lox/lox Emx1Cre mice, which may be correlated with the altered behaviors [24,25]. The behavioral differences between Np65 KO and Nptn KO mice may be due to these two mouse models having different genetic deletions.…”

Section: Discussionmentioning

confidence: 91%

“…memory as measured by the probe test and reversal probe test of the MWM and NOR tests. Bhattacharya et al[24] recently reported that Nptn À/À mice (with constitutive deletion of Np65 and Np55) and inducible Nptn KO mice exhibited reduced anxiety-like behavior and social interaction, and increased depressive-like behavior, and aberrant swimming behavior (diving) in the MWM test. Besides, Herrera-Molina et al…”

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confidence: 99%

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Neuroplastin 65 modulates anxiety‐ and depression‐like behavior likely through adult hippocampal neurogenesis and central 5‐HT activity

Liu

Gao

et al. 2019

The FEBS Journal

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Neuroplastin 65 (Np65) is a brain‐specific cell adhesion molecule that is highly expressed in the hippocampus, amygdala, and cortex, regions of the brain that are associated with memory and emotions. However, the role of Np65 in regulation of emotional behavior is still unclear. In the present study, we show that Np65 knock‐out (Np65 KO) mice display enhanced anxiety‐like behavior, a reduction in some aspects of depressive‐like behaviors, and increased sociability and memory. Biochemical investigations revealed that Np65 KO mice show increased adult‐born neurons and proliferation in the hippocampus. In addition, the level of 5‐hydroxytryptamine (5‐HT) in the hippocampus was reduced. The expression of tryptophan hydroxylase 2 in the brainstem and the expression of the 5‐HT3A receptor were also decreased. Electrophysiological recordings confirmed an impaired maintenance of long‐term potentiation in the hippocampus of Np65 KO mice. Together, our findings uncover a role for Np65 in regulating anxiety‐ and depressive‐like behaviors and suggest that Np65 may be essential for the maintenance of emotional stability, indicating that it might be an attractive potential target for treatment of psychiatric disorders.

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Section: Discussionsupporting

confidence: 91%

Section: Discussionmentioning

confidence: 91%

mentioning

confidence: 99%

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Neuroplastin 65 modulates anxiety‐ and depression‐like behavior likely through adult hippocampal neurogenesis and central 5‐HT activity

Liu

Gao

et al. 2019

The FEBS Journal

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“…Two isoforms of neuroplastin, Np55 and brain‐specific Np65, have been described . Neuroplastin functions in several vital processes in the mammalian central nervous system including neurite outgrowth, regulation of synaptic plasticity, long‐term potentiation, maintaining balance between the excitatory and inhibitory pathways and the formation of associative memory . Data from mice and rats have allowed us to determine that neuroplastin has a high preference for the hippocampus and cerebellum, but only two studies have systematically analysed Np expression in human brains .…”

Section: Introductionmentioning

confidence: 99%

“…long-term potentiation, 7,8 maintaining balance between the excitatory and inhibitory pathways 9 and the formation of associative memory. 10 Data from mice and rats have allowed us to determine that neuroplastin has a high preference for the hippocampus and cerebellum, 11,12 but only two studies have systematically analysed Np expression in human brains. 3,11 As with other CAMs, it is presumed that Np is involved in the molecular events which underlay the structural and functional processes of brain development, ageing, and neurodegeneration.…”

mentioning

confidence: 99%

Hippocampal expression of cell‐adhesion glycoprotein neuroplastin is altered in Alzheimer's disease

Ilić

Mlinac-Jerkovic

Jovanov-Milošević

et al. 2018

J Cellular Molecular Medi

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Cell‐adhesion glycoprotein neuroplastin (Np) is involved in the regulation of synaptic plasticity and balancing hippocampal excitatory/inhibitory inputs which aids in the process of associative memory formation and learning. Our recent findings show that neuroplastin expression in the adult human hippocampus is specifically associated with major hippocampal excitatory pathways and is related to neuronal calcium regulation. Here, we investigated the hippocampal expression of brain‐specific neuroplastin isoform (Np65), its relationship with amyloid and tau pathology in Alzheimer's disease (AD), and potential involvement of neuroplastin in tissue response during the disease progression. Np65 expression and localization was analysed in six human hippocampi with confirmed AD neuropathology, and six age‐/gender‐matched control hippocampi by imunohistochemistry. In AD cases with shorter disease duration, the Np65 immunoreactivity was significantly increased in the dentate gyrus (DG), Cornu Ammonis 2/3 (CA2/3), and subiculum, with the highest level of Np expression being located on the dendrites of granule cells and subicular pyramidal neurons. Changes in the expression of neuroplastin in AD hippocampal areas seem to be related to the progression of disease. Our study suggests that cell‐adhesion protein neuroplastin is involved in tissue reorganization and is a potential molecular marker of plasticity response in the early neurodegeneration process of AD.

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Gender‐related variation expressions of neuroplastin TRAF6, GluA1, GABA(A) receptor, and PMCA in cortex, hippocampus, and brainstem in an experimental epilepsy model

Doğanyiğit,

Okan,

Yılmaz

et al. 2024

Synapse

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Epileptic seizures are seen as a result of changing excitability balance depending on the deterioration in synaptic plasticity in the brain. Neuroplastin, and its related molecules which are known to play a role in synaptic plasticity, neurotransmitter activities that provide balance of excitability and, different neurological diseases, have not been studied before in epilepsy.In this study, a total of 34 Sprague–Dawley male and female rats, 2 months old, weighing 250–300 g were used. The epilepsy model in rats was made via pentylenetetrazole (PTZ). After the completion of the experimental procedure, the brain tissue of the rats were taken and the histopathological changes in the hippocampus and cortex parts and the brain stem were investigated, as well as the immunoreactivity of the proteins related to the immunohistochemical methods.As a result of the histopathological evaluation, it was determined that neuron degeneration and the number of dilated blood vessels in the hippocampus, frontal cortex, and brain stem were higher in the PTZ status epilepticus (SE) groups than in the control groups. It was observed that neuroplastin and related proteins TNF receptor‐associated factor 6 (TRAF6), Gamma amino butyric acid type A receptors [(GABA(A)], and plasma membrane Ca2+ ATPase (PMCA) protein immunoreactivity levels increased especially in the male hippocampus, and only AMPA receptor subunit type 1 (GluA1) immunoreactivity decreased, unlike other proteins.We believe this may be caused by a problem in the mechanisms regulating the interaction of neuroplastin and GluA1 and may cause problems in synaptic plasticity in the experimental epilepsy model. It may be useful to elucidate this mechanism and target GluA1 when determining treatment strategies.

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Genetically Induced Retrograde Amnesia of Associative Memories After Neuroplastin Ablation

Cited by 42 publications

References 44 publications

Neuroplastin 65 modulates anxiety‐ and depression‐like behavior likely through adult hippocampal neurogenesis and central 5‐HT activity

Neuroplastin 65 modulates anxiety‐ and depression‐like behavior likely through adult hippocampal neurogenesis and central 5‐HT activity

Hippocampal expression of cell‐adhesion glycoprotein neuroplastin is altered in Alzheimer's disease

Gender‐related variation expressions of neuroplastin TRAF6, GluA1, GABA(A) receptor, and PMCA in cortex, hippocampus, and brainstem in an experimental epilepsy model

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