Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Cholecystokinin from the entorhinal cortex enables neural plasticity in the auditory cortex.

ABSTRACT: Patients with damage to the medial temporal lobe show deficits in forming new declarative memories but can still recall older memories, suggesting that the medial temporal lobe is necessary for encoding memories in the neocortex. Here, we found that cortical projection neurons in the perirhinal and entorhinal cortices were mostly immunopositive for cholecystokinin (CCK). Local infusion of CCK in the auditory cortex of anesthetized rats induced plastic changes that enabled cortical neurons to potentiate their responses or to start responding to an auditory stimulus that was paired with a tone that robustly triggered action potentials. CCK infusion also enabled auditory neurons to start responding to a light stimulus that was paired with a noise burst. In vivo intracellular recordings in the auditory cortex showed that synaptic strength was potentiated after two pairings of presynaptic and postsynaptic activity in the presence of CCK. Infusion of a CCKB antagonist in the auditory cortex prevented the formation of a visuo-auditory association in awake rats. Finally, activation of the entorhinal cortex potentiated neuronal responses in the auditory cortex, which was suppressed by infusion of a CCKB antagonist. Together, these findings suggest that the medial temporal lobe influences neocortical plasticity via CCK-positive cortical projection neurons in the entorhinal cortex.

SUBMITTER: Li X

PROVIDER: S-EPMC3945883 | biostudies-other | 2014 Mar

REPOSITORIES: biostudies-other

ACCESS DATA

Json Xml

Similar Datasets

Heterosynaptic plasticity of the visuo-auditory projection requires cholecystokinin released from entorhinal cortex afferents.

Project description:The entorhinal cortex is involved in establishing enduring visuo-auditory associative memory in the neocortex. Here we explored the mechanisms underlying this synaptic plasticity related to projections from the visual and entorhinal cortices to the auditory cortex in mice using optogenetics of dual pathways. High-frequency laser stimulation (HFS laser) of the visuo-auditory projection did not induce long-term potentiation. However, after pairing with sound stimulus, the visuo-auditory inputs were potentiated following either infusion of cholecystokinin (CCK) or HFS laser of the entorhino-auditory CCK-expressing projection. Combining retrograde tracing and RNAscope in situ hybridization, we show that Cck expression is higher in entorhinal cortex neurons projecting to the auditory cortex than in those originating from the visual cortex. In the presence of CCK, potentiation in the neocortex occurred when the presynaptic input arrived 200 ms before postsynaptic firing, even after just five trials of pairing. Behaviorally, inactivation of the CCK+ projection from the entorhinal cortex to the auditory cortex blocked the formation of visuo-auditory associative memory. Our results indicate that neocortical visuo-auditory association is formed through heterosynaptic plasticity, which depends on release of CCK in the neocortex mostly from entorhinal afferents.

| S-EPMC10954309 | biostudies-literature

Sensory cortex plasticity supports auditory social learning.

Project description:Social learning (SL) through experience with conspecifics can facilitate the acquisition of many behaviors. Thus, when Mongolian gerbils are exposed to a demonstrator performing an auditory discrimination task, their subsequent task acquisition is facilitated, even in the absence of visual cues. Here, we show that transient inactivation of auditory cortex (AC) during exposure caused a significant delay in task acquisition during the subsequent practice phase, suggesting that AC activity is necessary for SL. Moreover, social exposure induced an improvement in AC neuron sensitivity to auditory task cues. The magnitude of neural change during exposure correlated with task acquisition during practice. In contrast, exposure to only auditory task cues led to poorer neurometric and behavioral outcomes. Finally, social information during exposure was encoded in the AC of observer animals. Together, our results suggest that auditory SL is supported by AC neuron plasticity occurring during social exposure and prior to behavioral performance.

| S-EPMC10511464 | biostudies-literature

Modeling Neural Adaptation in Auditory Cortex.

Project description:Neural responses recorded from auditory cortex exhibit adaptation, a stimulus-specific decrease that occurs when the same sound is presented repeatedly. Stimulus-specific adaptation is thought to facilitate perception in noisy environments. Although adaptation is assumed to arise independently from cortex, this has been difficult to validate directly in vivo. In this study, we used a neural network model of auditory cortex with multicompartmental cell modeling to investigate cortical adaptation. We found that repetitive, non-adapted inputs to layer IV neurons in the model elicited frequency-specific decreases in simulated single neuron, population-level and local field potential (LFP) activity, consistent with stimulus-specific cortical adaptation. Simulated recordings of LFPs, generated solely by excitatory post-synaptic inputs and recorded from layers II/III in the model, showed similar waveform morphologies and stimulus probability effects as auditory evoked responses recorded from human cortex. We tested two proposed mechanisms of cortical adaptation, neural fatigue and neural sharpening, by varying the strength and type of inter- and intra-layer synaptic connections (excitatory, inhibitory). Model simulations showed that synaptic depression modeled in excitatory (AMPA) synapses was sufficient to elicit a reduction in neural firing rate, consistent with neural fatigue. However, introduction of lateral inhibition from local layer II/III interneurons resulted in a reduction in the number of responding neurons, but not their firing rates, consistent with neural sharpening. These modeling results demonstrate that adaptation can arise from multiple neural mechanisms in auditory cortex.

| S-EPMC6133953 | biostudies-literature

Long-term exposure to moderate noise induces neural plasticity in the infant rat primary auditory cortex.

Project description:Previous studies have reported that rearing infant rat pups in continuous moderate-level noise delayed the formation of topographic representational order and the refinement of response selectivity in the primary auditory (A1) cortex. The present study further verified that exposure to long-term moderate-intensity white noise (70 dB sound pressure level) from postnatal day (P) 12 to P30 elevated the hearing thresholds of infant rats. Compared with age-matched control rats, noise exposure (NE) rats had elevated hearing thresholds ranging from low to high frequencies, accompanied by decreased amplitudes and increased latencies of the two initial auditory brainstem response waves. The power of raw local field potential oscillations and high-frequency β oscillation in the A1 cortex of NE rats were larger, whereas the power of high-frequency γ oscillation was smaller than that of control rats. In addition, the expression levels of five glutamate receptor (GluR) subunits in the A1 cortex of NE rats were decreased with laminar specificity. These results suggest that the altered neural excitability and decreased GluR expression may underlie the delay of functional maturation in the A1 cortex, and may have implications for the treatment of hearing impairment induced by environmental noise.

| S-EPMC6711034 | biostudies-literature

The entorhinal cortex modulates trace fear memory formation and neuroplasticity in the mouse lateral amygdala via cholecystokinin.

Project description:Although fear memory formation is essential for survival and fear-related mental disorders, the neural circuitry and mechanism are incompletely understood. Here, we utilized trace fear conditioning to study the formation of trace fear memory in mice. We identified the entorhinal cortex (EC) as a critical component of sensory signaling to the amygdala. We adopted both loss-of-function and gain-of-function experiments to demonstrate that release of the cholecystokinin (CCK) from the EC is required for trace fear memory formation. We discovered that CCK-positive neurons project from the EC to the lateral nuclei of the amygdala (LA), and inhibition of CCK-dependent signaling in the EC prevented long-term potentiation of the auditory response in the LA and formation of trace fear memory. In summary, high-frequency activation of EC neurons triggers the release of CCK in their projection terminals in the LA, potentiating auditory response in LA neurons. The neural plasticity in the LA leads to trace fear memory formation.

| S-EPMC8629425 | biostudies-literature

Auditory Neural Plasticity in Tinnitus Mechanisms and Management.

Project description:Tinnitus, which is the perception of sound in the absence of a corresponding external acoustic stimulus, including change of hearing and neural plasticity, has become an increasingly important ailment affecting the daily life of a considerable proportion of the population and causing significant burdens for both the affected individuals and society as a whole. Here, we briefly review the epidemiology and classification of tinnitus, and the currently available treatments are discussed in terms of the available evidence for their mechanisms and efficacy. The conclusion drawn from the available evidence is that there is no specific medication for tinnitus treatment at present, and tinnitus management might provide better solutions. Therapeutic interventions for tinnitus should be based on a comprehensive understanding of the etiology and features of individual cases of tinnitus, and more high quality and large-scale research studies are urgently needed to develop more efficacious medications.

| S-EPMC7349625 | biostudies-literature

Gating of hippocampal activity, plasticity, and memory by entorhinal cortex long-range inhibition.

Project description:The cortico-hippocampal circuit is critical for storage of associational memories. Most studies have focused on the role in memory storage of the excitatory projections from entorhinal cortex to hippocampus. However, entorhinal cortex also sends inhibitory projections, whose role in memory storage and cortico-hippocampal activity remains largely unexplored. We found that these long-range inhibitory projections enhance the specificity of contextual and object memory encoding. At the circuit level, these ?-aminobutyric acid (GABA)-releasing projections target hippocampal inhibitory neurons and thus act as a disinhibitory gate that transiently promotes the excitation of hippocampal CA1 pyramidal neurons by suppressing feedforward inhibition. This enhances the ability of CA1 pyramidal neurons to fire synaptically evoked dendritic spikes and to generate a temporally precise form of heterosynaptic plasticity. Long-range inhibition from entorhinal cortex may thus increase the precision of hippocampal-based long-term memory associations by assessing the salience of mnemonormation to the immediate sensory input.

| S-EPMC4920085 | biostudies-literature

Physical Exercise Promotes Novel Object Recognition Memory in Spontaneously Hypertensive Rats after Ischemic Stroke by Promoting Neural Plasticity in the Entorhinal Cortex.

Project description:Cerebral ischemia leads to memory impairment, and several studies have indicated that physical exercise (PE) has memory-improving effects after ischemia. This study was designed to further explore the specific role of PE in novel object recognition (NOR) memory after stroke and the exact cortical regions in which memory is restored by PE. Spontaneously hypertensive rats (SHR) were subjected to transient middle cerebral artery occlusion (tMCAO) or sham surgery, followed by 26 days of PE starting on day 3 post-tMCAO. Thereafter, infarct volume, neurobehavioral outcome and NOR memory were assessed. Immunofluorescence staining and Luxol Fast Blue (LFB) staining were performed in the prefrontal cortex, entorhinal cortex and corpus callosum regions. Western blot analysis was performed to detect expressions of Nestin, Bcl-2 and SYN proteins in the entorhinal cortex. After tMCAO, NOR memory impairment was found in SHR. Rats subjected to PE post-tMCAO showed increased discrimination ratio, as well as significant decreases in infarct volumes and modified neurological severity scores (mNSS), when compared with tMCAO rats without PE. After stroke, NeuN-positive cell number was drastically reduced in the entorhinal cortex, rather than in the prefrontal cortex. Ischemic stroke had no impact on myelin and phospholipids, and the ratio of SMI-32/MBP in the corpus callosum. PE increased NeuN, Nestin, Ki67, MBP, SYN, PSD-95 and Bcl-2 expressions in the entorhinal cortex, while TUNEL and SMI-32 expressions were decreased. In conclusion, the NOR memory-improving capacity promoted by PE was closely related to neuronal cell proliferation and synaptic plasticity of the entorhinal cortex.

| S-EPMC5682296 | biostudies-literature

A realistic neural mass model of the cortex with laminar-specific connections and synaptic plasticity - evaluation with auditory habituation.

Project description:In this work we propose a biologically realistic local cortical circuit model (LCCM), based on neural masses, that incorporates important aspects of the functional organization of the brain that have not been covered by previous models: (1) activity dependent plasticity of excitatory synaptic couplings via depleting and recycling of neurotransmitters and (2) realistic inter-laminar dynamics via laminar-specific distribution of and connections between neural populations. The potential of the LCCM was demonstrated by accounting for the process of auditory habituation. The model parameters were specified using Bayesian inference. It was found that: (1) besides the major serial excitatory information pathway (layer 4 to layer 2/3 to layer 5/6), there exists a parallel "short-cut" pathway (layer 4 to layer 5/6), (2) the excitatory signal flow from the pyramidal cells to the inhibitory interneurons seems to be more intra-laminar while, in contrast, the inhibitory signal flow from inhibitory interneurons to the pyramidal cells seems to be both intra- and inter-laminar, and (3) the habituation rates of the connections are unsymmetrical: forward connections (from layer 4 to layer 2/3) are more strongly habituated than backward connections (from Layer 5/6 to layer 4). Our evaluation demonstrates that the novel features of the LCCM are of crucial importance for mechanistic explanations of brain function. The incorporation of these features into a mass model makes them applicable to modeling based on macroscopic data (like EEG or MEG), which are usually available in human experiments. Our LCCM is therefore a valuable building block for future realistic models of human cognitive function.

| S-EPMC3813749 | biostudies-literature

Early Blindness Results in Developmental Plasticity for Auditory Motion Processing within Auditory and Occipital Cortex.

Project description:Early blind subjects exhibit superior abilities for processing auditory motion, which are accompanied by enhanced BOLD responses to auditory motion within hMT+ and reduced responses within right planum temporale (rPT). Here, by comparing BOLD responses to auditory motion in hMT+ and rPT within sighted controls, early blind, late blind, and sight-recovery individuals, we were able to separately examine the effects of developmental and adult visual deprivation on cortical plasticity within these two areas. We find that both the enhanced auditory motion responses in hMT+ and the reduced functionality in rPT are driven by the absence of visual experience early in life; neither loss nor recovery of vision later in life had a discernable influence on plasticity within these areas. Cortical plasticity as a result of blindness has generally be presumed to be mediated by competition across modalities within a given cortical region. The reduced functionality within rPT as a result of early visual loss implicates an additional mechanism for cross modal plasticity as a result of early blindness-competition across different cortical areas for functional role.

| S-EPMC4932114 | biostudies-literature

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data