Disinhibitory circuitry gates associative synaptic plasticity in olfactory cortex

AbstractInhibitory microcircuits play an essential role in regulating cortical responses to sensory stimuli. Interneurons that inhibit dendritic or somatic integration in pyramidal neurons act as gatekeepers for neural activity, synaptic plasticity and the formation of sensory representations. Conversely, interneurons that specifically inhibit other interneurons can open gates through disinhibition. In the rodent piriform cortex, relief of dendritic inhibition permits long-term potentiation (LTP) of the recurrent synapses between pyramidal neurons (PNs) thought to underlie ensemble odor representations. We used an optogenetic approach to identify the inhibitory interneurons and disinhibitory circuits that regulate LTP. We focused on three prominent inhibitory neuron classes-somatostatin (SST), parvalbumin (PV), and vasoactive intestinal polypeptide (VIP) interneurons. We find that VIP interneurons inhibit SST interneurons and promote LTP through subthreshold dendritic disinhibition. Alternatively, suppression of PV-interneuron inhibition promotes LTP but requires suprathreshold spike activity. Thus, we have identified two disinhibitory mechanisms to regulate synaptic plasticity during olfactory processing.

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IGF-1 facilitates extinction of conditioned fear

eLife ◽

10.7554/elife.67267 ◽

2021 ◽

Vol 10 ◽

Author(s):

Laura E Maglio ◽

José A Noriega-Prieto ◽

Irene B Maroto ◽

Jesús Martin-Cortecero ◽

Antonio Muñoz-Callejas ◽

...

Keyword(s):

Synaptic Plasticity ◽

Synaptic Transmission ◽

Pyramidal Neurons ◽

Conditioned Fear ◽

Long Term Potentiation ◽

Fear Extinction ◽

Neuronal Firing ◽

Term Potentiation ◽

Extinction Memory

Insulin-like growth factor-1 (IGF-1) plays a key role in synaptic plasticity, spatial learning and anxiety-like behavioral processes. While IGF-1 regulates neuronal firing and synaptic transmission in many areas of the central nervous system, its signaling and consequences on excitability, synaptic plasticity, and animal behavior dependent on the prefrontal cortex remain unexplored. Here, we show that IGF-1 induces a long-lasting depression of the medium and slow post-spike afterhyperpolarization (mAHP and sAHP), increasing the excitability of layer 5 pyramidal neurons of the rat infralimbic cortex. Besides, IGF-1 mediates a presynaptic long-term depression of both inhibitory and excitatory synaptic transmission in these neurons. The net effect of this IGF-1 mediated synaptic plasticity is a long-term potentiation of the postsynaptic potentials. Moreover, we demonstrate that IGF-1 favors the fear extinction memory. These results show novel functional consequences of IGF-1 signaling, revealing IGF-1 as a key element in the control of the fear extinction memory.

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Faculty Opinions recommendation of Dendritic sodium spikes are required for long-term potentiation at distal synapses on hippocampal pyramidal neurons.

Faculty Opinions – Post-Publication Peer Review of the Biomedical Literature ◽

10.3410/f.725702799.793521723 ◽

2016 ◽

Author(s):

Johannes Hell

Keyword(s):

Pyramidal Neurons ◽

Long Term Potentiation ◽

Hippocampal Pyramidal Neurons ◽

Term Potentiation

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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

Current Neurovascular Research ◽

10.2174/1567202617666200514114917 ◽

2020 ◽

Vol 17 (4) ◽

pp. 354-360 ◽

Cited By ~ 1

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.

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Relationship between Long-Term Potentiation and the Initial Properties of CA3–CA1 Synapses: Importance of the Effects of External Factors on Hippocampal Synaptic Plasticity for Studies

Neuroscience and Behavioral Physiology ◽

10.1007/s11055-019-00776-2 ◽

2019 ◽

Vol 49 (5) ◽

pp. 603-614

Author(s):

I. V. Kudryashova

Keyword(s):

Synaptic Plasticity ◽

Long Term Potentiation ◽

External Factors ◽

Hippocampal Synaptic Plasticity ◽

Term Potentiation

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Prenatal stress in rats attenuates hippocampal long-term potentiation and induces deficits in synaptic plasticity

European Neuropsychopharmacology ◽

10.1016/s0924-977x(06)80063-5 ◽

2006 ◽

Vol 16 ◽

pp. S52

Author(s):

S. Salomon ◽

Y. Nachum-Biala ◽

Y. Bogush ◽

M. Lineal ◽

H. Matzner ◽

...

Keyword(s):

Synaptic Plasticity ◽

Prenatal Stress ◽

Long Term Potentiation ◽

Term Potentiation

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Synaptic plasticity-dependent competition rule influences memory formation

Nature Communications ◽

10.1038/s41467-021-24269-4 ◽

2021 ◽

Vol 12 (1) ◽

Author(s):

Yire Jeong ◽

Hye-Yeon Cho ◽

Mujun Kim ◽

Jung-Pyo Oh ◽

Min Soo Kang ◽

...

Keyword(s):

Synaptic Plasticity ◽

Fear Conditioning ◽

Long Term Potentiation ◽

Memory Formation ◽

Specific Pattern ◽

Memory Encoding ◽

Competition Rule ◽

Term Potentiation ◽

Input Activity

AbstractMemory is supported by a specific collection of neurons distributed in broad brain areas, an engram. Despite recent advances in identifying an engram, how the engram is created during memory formation remains elusive. To explore the relation between a specific pattern of input activity and memory allocation, here we target a sparse subset of neurons in the auditory cortex and thalamus. The synaptic inputs from these neurons to the lateral amygdala (LA) are not potentiated by fear conditioning. Using an optogenetic priming stimulus, we manipulate these synapses to be potentiated by the learning. In this condition, fear memory is preferentially encoded in the manipulated cell ensembles. This change, however, is abolished with optical long-term depression (LTD) delivered shortly after training. Conversely, delivering optical long-term potentiation (LTP) alone shortly after fear conditioning is sufficient to induce the preferential memory encoding. These results suggest a synaptic plasticity-dependent competition rule underlying memory formation.

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Altered Short-Term Synaptic Plasticity in Mice Lacking the Metabotropic Glutamate Receptor mGlu7

The Scientific World JOURNAL ◽

10.1100/tsw.2002.146 ◽

2002 ◽

Vol 2 ◽

pp. 730-737 ◽

Cited By ~ 35

Author(s):

Trevor J. Bushell ◽

Gilles Sansig ◽

Valerie J. Collett ◽

Herman van der Putten ◽

Graham L. Collingridge

Keyword(s):

Synaptic Plasticity ◽

Molecular Mechanisms ◽

Pyramidal Neurons ◽

Metabotropic Glutamate Receptor ◽

Long Term Potentiation ◽

Short Term ◽

Metabotropic Glutamate ◽

Term Potentiation ◽

Commissural Pathway ◽

Frequency Facilitation

Eight subtypes of metabotropic glutamate (mGlu) receptors have been identified of which two, mGlu5 and mGlu7, are highly expressed at synapses made between CA3 and CA1 pyramidal neurons in the hippocampus. This input, the Schaffer collateral-commissural pathway, displays robust long-term potentiation (LTP), a process believed to utilise molecular mechanisms that are key processes involved in the synaptic basis of learning and memory. To investigate the possible function in LTP of mGlu7 receptors, a subtype for which no specific antagonists exist, we generated a mouse lacking this receptor, by homologous recombination. We found that LTP could be induced in mGlu7-/- mice and that once the potentiation had reached a stable level there was no difference in the magnitude of LTP between mGlu7-/- mice and their littermate controls. However, the initial decremental phase of LTP, known as short-term potentiation (STP), was greatly attenuated in the mGlu7-/- mouse. In addition, there was less frequency facilitation during, and less post-tetanic potentiation following, a high frequency train in the mGlu7-/- mouse. These results show that the absence of mGlu7 receptors results in alterations in short-term synaptic plasticity in the hippocampus.

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