Modulation of synaptic plasticity in the hippocampus and piriform cortex by physiologically meaningful olfactory cues in an olfactory association task

When an animal is facing unfamiliar food, its odor, together with semiochemicals emanating from a conspecific, can constitute a safety message and authorize intake. The piriform cortex (PiC) codes olfactory information, and the inactivation of neurons in the nucleus accumbens (NAc) can acutely trigger consumption. However, the neural circuit and cellular substrate of transition of olfactory perception into value-based actions remain elusive. We detected enhanced activity after social transmission between two mice in neurons of the medial prefrontal cortex (mPFC) that target the NAc and receive projections from the PiC. Exposure to a conspecific potentiated the excitatory postsynaptic currents in NAc projectors, whereas blocking transmission from PiC to mPFC prevented social transmission. Thus, synaptic plasticity in the mPFC is a cellular substrate of social transmission of food safety.

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Disinhibitory circuitry gates associative synaptic plasticity in olfactory cortex

10.1101/2020.09.24.312686 ◽

2020 ◽

Author(s):

Martha Canto-Bustos ◽

F. Kathryn Friason ◽

Constanza Bassi ◽

Anne-Marie M. Oswald

Keyword(s):

Synaptic Plasticity ◽

Pyramidal Neurons ◽

Piriform Cortex ◽

Inhibitory Neuron ◽

Long Term Potentiation ◽

Inhibitory Interneurons ◽

Sensory Stimuli ◽

Term Potentiation ◽

Cortical Responses

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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LRP4 mediated synaptic plasticity in the piriform cortex

10.21203/rs.3.rs-539406/v1 ◽

2021 ◽

Author(s):

Min Yan ◽

Hongyang Jing ◽

Mingtao Xiong ◽

Dong Lin ◽

Peng Chen ◽

...

Keyword(s):

Synaptic Plasticity ◽

Transmembrane Domain ◽

Low Density Lipoprotein ◽

Critical Role ◽

Piriform Cortex ◽

Density Lipoprotein ◽

Spine Density ◽

Excitatory Postsynaptic Current ◽

Density Lipoprotein Receptor ◽

The Central Nervous System

Abstract Background Low-density lipoprotein receptor-related protein 4(LRP4) plays a critical role in the central nervous system (CNS), including hippocampal synaptic plasticity, maintenance of excitatory synaptic transmission, fear regulation, as well as long-term enhancement. Results In this study, we found that Lrp4 was highly expressed in the piriform cortex and located in the second layer of the piriform cortex. When the transmembrane domain (TMD) and the intracellular domain (ICD) were missing, the Lrp4ECD/ECD mice appeared to be smaller, and the brain’s weight decreased, compared with the control mice. Simultaneously, finding food was prolonged for Lrp4ECD/ECD mice in the buried food-seeking test. In the piriform cortex of Lrp4ECD/ECD mice, the spine density of layer Ⅱ increased, and the frequency of both miniature excitatory postsynaptic current (mEPSC) and spontaneous excitatory postsynaptic current (sEPSC) enhanced. Conclusions This study indicated that LRP4 mediated synaptic plasticity in the piriform cortex. Moreover, it also suggested that TMD and ICD of LRP4 are nonnegligible for the LRP4 function in the piriform cortex.

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Reconciling contrast invariance and non-linear computation in cortical circuits

10.1101/2021.04.23.441165 ◽

2021 ◽

Author(s):

L. Bernáez Timón ◽

P. Ekelmans ◽

S. Konrad ◽

A. Nold ◽

T. Tchumatchenko

Keyword(s):

Synaptic Plasticity ◽

Piriform Cortex ◽

Mean Field ◽

Dependent Manner ◽

Cortical Circuits ◽

Stimulus Contrast ◽

Spiking Network ◽

Network Simulations ◽

Contrast Invariance ◽

Balanced Networks

AbstractNetwork selectivity for orientation is invariant to changes in the stimulus contrast in the primary visual cortex. Similarly, the selectivity for odor identity is invariant to changes in odorant concentration in the piriform cortex. Interestingly, invariant network selectivity appears robust to local changes in synaptic strength induced by synaptic plasticity, even though: i) synaptic plasticity can potentiate or depress connections between neurons in a feature-dependent manner, and ii) in networks with balanced excitation and inhibition, synaptic plasticity is a determinant for the network non-linearity. In this study, we investigate whether network contrast invariance is consistent with a variety of synaptic states and connectivities in balanced networks. By using mean-field models and spiking network simulations, we show how the synaptic state controls the non-linearity in the network response to contrast and how it can lead to the emergence of contrast-invariant or contrast-dependent selectivity. Different forms of synaptic plasticity sharpen or broaden the network selectivity, while others do not affect it. Our results explain how the physiology of individual synapses is linked to contrast-invariant selectivity at the network level.

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Age-Dependent Contributions of NMDA Receptors and L-Type Calcium Channels to Long-Term Depression in the Piriform Cortex

International Journal of Molecular Sciences ◽

10.3390/ijms222413551 ◽

2021 ◽

Vol 22 (24) ◽

pp. 13551

Author(s):

Vishaal Rajani ◽

Aida Maziar ◽

Kwun Nok Mimi Man ◽

Johannes W. Hell ◽

Qi Yuan

Keyword(s):

Synaptic Plasticity ◽

Calcium Channels ◽

Piriform Cortex ◽

Confocal Imaging ◽

Receptor Expression ◽

Sprague Dawley ◽

Long Term Depression ◽

Age Dependent ◽

Fluorescent Immunohistochemistry

In the hippocampus, the contributions of N-methyl-D-aspartate receptors (NMDARs) and L-type calcium channels (LTCCs) to neuronal transmission and synaptic plasticity change with aging, underlying calcium dysregulation and cognitive dysfunction. However, the relative contributions of NMDARs and LTCCs in other learning encoding structures during aging are not known. The piriform cortex (PC) plays a significant role in odor associative memories, and like the hippocampus, exhibits forms of long-term synaptic plasticity. Here, we investigated the expression and contribution of NMDARs and LTCCs in long-term depression (LTD) of the PC associational fiber pathway in three cohorts of Sprague Dawley rats: neonatal (1–2 weeks), young adult (2–3 months) and aged (20–25 months). Using a combination of slice electrophysiology, Western blotting, fluorescent immunohistochemistry and confocal imaging, we observed a shift from an NMDAR to LTCC mediation of LTD in aged rats, despite no difference in the amount of LTD expression. These changes in plasticity are related to age-dependent differential receptor expression in the PC. LTCC Cav1.2 expression relative to postsynaptic density protein 95 is increased in the associational pathway of the aged PC layer Ib. Enhanced LTCC contribution in synaptic depression in the PC may contribute to altered olfactory function and learning with aging.

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