Faculty Opinions recommendation of Neural ensemble dynamics underlying a long-term associative memory.

AbstractSpontaneous recognition tests, which utilize rodents’ innate tendency to explore novelty, can evaluate not only simple non-associative recognition memory but also more complex associative memory in animals. In the present study, we investigated whether the length of the object familiarization period (sample phase) improved subsequent novelty discrimination in the spontaneous object, place, and object-place-context (OPC) recognition tests in rats. In the OPC test, rats showed a significant novelty preference only when the familiarization period was 30 min but not when it was 5 min or 15 min. However, the rats exhibited a successful discrimination between the stayed and replaced objects under 15 min and 30 min familiarization period conditions in the place recognition test and between the novel and familiar objects under all conditions of 5, 15 and 30 min in the object recognition test. Our results suggest that the extension of the familiarization period improves performance in the spontaneous recognition paradigms, and a longer familiarization period is necessary for long-term associative recognition memory than for non-associative memory.

Download Full-text

LTP and memory impairment caused by extracellular Aβ and Tau oligomers is APP-dependent

eLife ◽

10.7554/elife.26991 ◽

2017 ◽

Vol 6 ◽

Cited By ~ 48

Author(s):

Daniela Puzzo ◽

Roberto Piacentini ◽

Mauro Fá ◽

Walter Gulisano ◽

Domenica D Li Puma ◽

...

Keyword(s):

Associative Memory ◽

Memory Impairment ◽

Long Term Potentiation ◽

Neuronal Uptake ◽

Common Mechanism ◽

Tau Oligomers ◽

Term Potentiation ◽

Induced Defects ◽

Oligomeric Forms

The concurrent application of subtoxic doses of soluble oligomeric forms of human amyloid-beta (oAβ) and Tau (oTau) proteins impairs memory and its electrophysiological surrogate long-term potentiation (LTP), effects that may be mediated by intra-neuronal oligomers uptake. Intrigued by these findings, we investigated whether oAβ and oTau share a common mechanism when they impair memory and LTP in mice. We found that as already shown for oAβ, also oTau can bind to amyloid precursor protein (APP). Moreover, efficient intra-neuronal uptake of oAβ and oTau requires expression of APP. Finally, the toxic effect of both extracellular oAβ and oTau on memory and LTP is dependent upon APP since APP-KO mice were resistant to oAβ- and oTau-induced defects in spatial/associative memory and LTP. Thus, APP might serve as a common therapeutic target against Alzheimer's Disease (AD) and a host of other neurodegenerative diseases characterized by abnormal levels of Aβ and/or Tau.

Download Full-text

Cholecystokinin release triggered by NMDA receptors produces LTP and sound–sound associative memory

Proceedings of the National Academy of Sciences ◽

10.1073/pnas.1816833116 ◽

2019 ◽

Vol 116 (13) ◽

pp. 6397-6406 ◽

Cited By ~ 3

Author(s):

Xi Chen ◽

Xiao Li ◽

Yin Ting Wong ◽

Xuejiao Zheng ◽

Haitao Wang ◽

...

Keyword(s):

Associative Learning ◽

Associative Memory ◽

High Frequency ◽

Low Frequency ◽

Long Term Potentiation ◽

High Frequency Stimulation ◽

Low Frequency Stimulation ◽

Term Potentiation ◽

Frequency Stimulation

Memory is stored in neural networks via changes in synaptic strength mediated in part by NMDA receptor (NMDAR)-dependent long-term potentiation (LTP). Here we show that a cholecystokinin (CCK)-B receptor (CCKBR) antagonist blocks high-frequency stimulation-induced neocortical LTP, whereas local infusion of CCK induces LTP. CCK−/−mice lacked neocortical LTP and showed deficits in a cue–cue associative learning paradigm; and administration of CCK rescued associative learning deficits. High-frequency stimulation-induced neocortical LTP was completely blocked by either the NMDAR antagonist or the CCKBR antagonist, while application of either NMDA or CCK induced LTP after low-frequency stimulation. In the presence of CCK, LTP was still induced even after blockade of NMDARs. Local application of NMDA induced the release of CCK in the neocortex. These findings suggest that NMDARs control the release of CCK, which enables neocortical LTP and the formation of cue–cue associative memory.

Download Full-text