scholarly journals Brevican-Deficient Mice Display Impaired Hippocampal CA1 Long-Term Potentiation but Show No Obvious Deficits in Learning and Memory

2002 ◽  
Vol 22 (21) ◽  
pp. 7417-7427 ◽  
Author(s):  
Cord Brakebusch ◽  
Constanze I. Seidenbecher ◽  
Fredrik Asztely ◽  
Uwe Rauch ◽  
Henry Matthies ◽  
...  
Keyword(s):  
Learning And Memory ◽  
Long Term Potentiation ◽  
Brain Anatomy ◽  
Perineuronal Nets ◽  
Functional Roles ◽  
Term Potentiation ◽  
And Function ◽  
Deficient Mice

ABSTRACT Brevican is a brain-specific proteoglycan which is found in specialized extracellular matrix structures called perineuronal nets. Brevican increases the invasiveness of glioma cells in vivo and has been suggested to play a role in central nervous system fiber tract development. To study the role of brevican in the development and function of the brain, we generated mice lacking a functional brevican gene. These mice are viable and fertile and have a normal life span. Brain anatomy was normal, although alterations in the expression of neurocan were detected. Perineuronal nets formed but appeared to be less prominent in mutant than in wild-type mice. Brevican-deficient mice showed significant deficits in the maintenance of hippocampal long-term potentiation (LTP). However, no obvious impairment of excitatory and inhibitory synaptic transmission was found, suggesting a complex cause for the LTP defect. Detailed behavioral analysis revealed no statistically significant deficits in learning and memory. These data indicate that brevican is not crucial for brain development but has restricted structural and functional roles.

Enhanced long-term potentiation in vivo in dentate gyrus of NELL2-deficient mice

Neuroreport ◽  
2004 ◽  
Vol 15 (3) ◽  
pp. 417-420 ◽  
Author(s):  
Shogo Matsuyama ◽  
Koutoku Aihara ◽  
Naoki Nishino ◽  
Satoshi Takeda ◽  
Katsuyuki Tanizawa ◽  
...  
Keyword(s):  
Dentate Gyrus ◽  
Long Term Potentiation ◽  
Term Potentiation ◽  
Deficient Mice

Increased network excitability and impaired induction of long-term potentiation in the dentate gyrus of collybistin-deficient mice in vivo

2009 ◽  
Vol 41 (1) ◽  
pp. 94-100 ◽  
Author(s):  
Peter Jedlicka ◽  
Theofilos Papadopoulos ◽  
Thomas Deller ◽  
Heinrich Betz ◽  
Stephan W. Schwarzacher
Keyword(s):  
Dentate Gyrus ◽  
Long Term Potentiation ◽  
Term Potentiation ◽  
Deficient Mice

scholarly journals Long-term potentiation in the hippocampus: discovery, mechanisms and function

Neuroforum ◽  
2018 ◽  
Vol 24 (3) ◽  
pp. A103-A120 ◽  
Author(s):  
Tim V.P. Bliss ◽  
Graham L. Collingridge ◽  
Richard G.M. Morris ◽  
Klaus G. Reymann
Keyword(s):  
Learning And Memory ◽  
Long Term Potentiation ◽  
Term Potentiation ◽  
And Function

Abstract In this review we reflect upon our contributions to the study of the properties and mechanisms of long-term potentiation (LTP) and describe some of the major influences on our work. We then go on to consider whether LTP has fulfilled its early promise of providing a compelling account of the synaptic basis of learning and memory.

scholarly journals Neurocan Is Dispensable for Brain Development

2001 ◽  
Vol 21 (17) ◽  
pp. 5970-5978 ◽  
Author(s):  
Xiao-Hong Zhou ◽  
Cord Brakebusch ◽  
Henry Matthies ◽  
Toshitaka Oohashi ◽  
Emilio Hirsch ◽  
...  
Keyword(s):  
Brain Development ◽  
Late Phase ◽  
Neurite Growth ◽  
Long Term Potentiation ◽  
Brain Anatomy ◽  
Term Potentiation

ABSTRACT Neurocan is a component of the extracellular matrix in brain. Due to its inhibition of neuronal adhesion and outgrowth in vitro and its expression pattern in vivo it was suggested to play an important role in axon guidance and neurite growth. To study the role of neurocan in brain development we generated neurocan-deficient mice by targeted disruption of the neurocan gene. These mice are viable and fertile and have no obvious deficits in reproduction and general performance. Brain anatomy, morphology, and ultrastructure are similar to those of wild-type mice. Perineuronal nets surrounding neurons appear largely normal. Mild deficits in synaptic plasticity may exist, as maintenance of late-phase hippocampal long-term potentiation is reduced. These data indicate that neurocan has either a redundant or a more subtle function in the development of the brain.

scholarly journals Impairment of in vivo theta-burst long-term potentiation and network excitability in the dentate gyrus of synaptopodin-deficient mice lacking the spine apparatus and the cisternal organelle

Hippocampus ◽  
2009 ◽  
Vol 19 (2) ◽  
pp. 130-140 ◽  
Author(s):  
Peter Jedlicka ◽  
Stephan W. Schwarzacher ◽  
Raphael Winkels ◽  
Friederike Kienzler ◽  
Michael Frotscher ◽  
...  
Keyword(s):  
Dentate Gyrus ◽  
Long Term Potentiation ◽  
Term Potentiation ◽  
Spine Apparatus ◽  
Theta Burst ◽  
Deficient Mice

Brivaracetam Prevents the Over-expression of Synaptic Vesicle Protein 2A and Rescues the Deficits of Hippocampal Long-term Potentiation In Vivo in Chronic Temporal Lobe Epilepsy Rats

2020 ◽  
Vol 17 (4) ◽  
pp. 354-360 ◽  
Author(s):  
Yu-Xing Ge ◽  
Ying-Ying Lin ◽  
Qian-Qian Bi ◽  
Yu-Juan Chen
Keyword(s):  
Synaptic Plasticity ◽  
Temporal Lobe Epilepsy ◽  
Synaptic Vesicle ◽  
Long Term Potentiation ◽  
Synaptic Dysfunction ◽  
Over Expression ◽  
Term Potentiation ◽  
Synaptic Vesicle Protein 2A

Background: Patients with temporal lobe epilepsy (TLE) usually suffer from cognitive deficits and recurrent seizures. Brivaracetam (BRV) is a novel anti-epileptic drug (AEDs) recently used for the treatment of partial seizures with or without secondary generalization. Different from other AEDs, BRV has some favorable properties on synaptic plasticity. However, the underlying mechanisms remain elusive. Objective: The aim of this study was to explore the neuroprotective mechanism of BRV on synaptic plasticity in experimental TLE rats. Methods: The effect of chronic treatment with BRV (10 mg/kg) was assessed on Pilocarpine induced TLE model through measurement of the field excitatory postsynaptic potentials (fEPSPs) in vivo. Differentially expressed synaptic vesicle protein 2A (SV2A) were identified with immunoblot. Then, fast phosphorylation of synaptosomal-associated protein 25 (SNAP-25) during long-term potentiation (LTP) induction was performed to investigate the potential roles of BRV on synaptic plasticity in the TLE model. Results: An increased level of SV2A accompanied by a depressed LTP in the hippocampus was shown in epileptic rats. Furthermore, BRV treatment continued for more than 30 days improved the over-expression of SV2A and reversed the synaptic dysfunction in epileptic rats. Additionally, BRV treatment alleviates the abnormal SNAP-25 phosphorylation at Ser187 during LTP induction in epileptic ones, which is relevant to the modulation of synaptic vesicles exocytosis and voltagegated calcium channels. Conclusion: BRV treatment ameliorated the over-expression of SV2A in the hippocampus and rescued the synaptic dysfunction in epileptic rats. These results identify the neuroprotective effect of BRV on TLE model.

scholarly journals Aη-α and Aη-β peptides impair LTP ex vivo within the low nanomolar range and impact neuronal activity in vivo

2021 ◽  
Vol 13 (1) ◽  
Author(s):  
Maria Mensch ◽  
Jade Dunot ◽  
Sandy M. Yishan ◽  
Samuel S. Harris ◽  
Aline Blistein ◽  
...  
Keyword(s):  
Neuronal Activity ◽  
Ex Vivo ◽  
Long Term Potentiation ◽  
Network Activity ◽  
Strongly Correlated ◽  
App Processing ◽  
Term Potentiation ◽  
Hippocampal Network

Abstract Background Amyloid precursor protein (APP) processing is central to Alzheimer’s disease (AD) etiology. As early cognitive alterations in AD are strongly correlated to abnormal information processing due to increasing synaptic impairment, it is crucial to characterize how peptides generated through APP cleavage modulate synapse function. We previously described a novel APP processing pathway producing η-secretase-derived peptides (Aη) and revealed that Aη–α, the longest form of Aη produced by η-secretase and α-secretase cleavage, impaired hippocampal long-term potentiation (LTP) ex vivo and neuronal activity in vivo. Methods With the intention of going beyond this initial observation, we performed a comprehensive analysis to further characterize the effects of both Aη-α and the shorter Aη-β peptide on hippocampus function using ex vivo field electrophysiology, in vivo multiphoton calcium imaging, and in vivo electrophysiology. Results We demonstrate that both synthetic peptides acutely impair LTP at low nanomolar concentrations ex vivo and reveal the N-terminus to be a primary site of activity. We further show that Aη-β, like Aη–α, inhibits neuronal activity in vivo and provide confirmation of LTP impairment by Aη–α in vivo. Conclusions These results provide novel insights into the functional role of the recently discovered η-secretase-derived products and suggest that Aη peptides represent important, pathophysiologically relevant, modulators of hippocampal network activity, with profound implications for APP-targeting therapeutic strategies in AD.

Arousing the LTP and learning debate

1997 ◽  
Vol 20 (4) ◽  
pp. 622-623 ◽  
Author(s):  
Stephen Maren
Keyword(s):  
Learning And Memory ◽  
Long Term Potentiation ◽  
Term Potentiation ◽  
Arousal Mechanism

Shors & Matzel provide compelling arguments against a role for hippocampal long-term potentiation (LTP) in mammalian learning and memory. As an alternative, they suggest that LTP is an arousal mechanism. I will argue that this view is not a satisfactory alternative to current conceptions of LTP function.

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