scholarly journals Differential inhibition of pyramidal cells and inhibitory interneurons along the rostrocaudal axis of anterior piriform cortex

2018 ◽  
Vol 115 (34) ◽  
pp. E8067-E8076 ◽  
Author(s):  
Adam M. Large ◽  
Nathan W. Vogler ◽  
Martha Canto-Bustos ◽  
F. Kathryn Friason ◽  
Paul Schick ◽  
...  

The spatial representation of stimuli in sensory neocortices provides a scaffold for elucidating circuit mechanisms underlying sensory processing. However, the anterior piriform cortex (APC) lacks topology for odor identity as well as afferent and intracortical excitation. Consequently, olfactory processing is considered homogenous along the APC rostral–caudal (RC) axis. We recorded excitatory and inhibitory neurons in APC while optogenetically activating GABAergic interneurons along the RC axis. In contrast to excitation, we find opposing, spatially asymmetric inhibition onto pyramidal cells (PCs) and interneurons. PCs are strongly inhibited by caudal stimulation sites, whereas interneurons are strongly inhibited by rostral sites. At least two mechanisms underlie spatial asymmetries. Enhanced caudal inhibition of PCs is due to increased synaptic strength, whereas rostrally biased inhibition of interneurons is mediated by increased somatostatin–interneuron density. Altogether, we show differences in rostral and caudal inhibitory circuits in APC that may underlie spatial variation in odor processing along the RC axis.

2017 ◽  
Author(s):  
Adam M. Large ◽  
Nathan W. Vogler ◽  
Martha Canto-Bustos ◽  
Paul Schick ◽  
Anne-Marie M. Oswald

AbstractThe spatial representation of stimuli in primary sensory cortices is a convenient scaffold for elucidating the circuit mechanisms underlying sensory processing. In contrast, the anterior piriform cortex (APC) lacks topology for odor identity and appears homogenous in terms of afferent and intracortical excitatory circuitry. Here, we show that an increasing rostral-caudal (RC) gradient of inhibition onto pyramidal cells is commensurate with a decrease in active neurons along the RC axis following exploration of a novel odor environment. This inhibitory gradient is supported by somatostatin interneurons that provide an opposing, rostrally-biased, gradient of inhibition to interneurons. Optogenetic or chemogenetic modulation of somatostatin cells neutralizes the inhibitory gradient onto pyramidal cells. This suggests a novel circuit mechanism whereby opposing spatial gradients of inhibition and disinhibition regulate neural activity along the RC-axis. These findings challenge our current understanding of the spatial profiles of neural circuits and odor processing within APC.


2021 ◽  
Author(s):  
Norimitsu Suzuki ◽  
Malinda L. S. Tantirigama ◽  
Helena H.-Y. Huang ◽  
John M. Bekkers

Feedforward inhibitory circuits are key contributors to the complex interplay between excitation and inhibition in the brain. Little is known about the function of feedforward inhibition in the primary olfactory (piriform) cortex. Using in vivo two-photon targeted patch clamping and calcium imaging in mice, we find that odors evoke strong excitation in two classes of interneurons – neurogliaform (NG) cells and horizontal (HZ) cells – that provide feedforward inhibition in layer 1 of the piriform cortex. NG cells fire much earlier than HZ cells following odor onset, a difference that can be attributed to the faster odor-driven excitatory synaptic drive that NG cells receive from the olfactory bulb. As a consequence, NG cells strongly but transiently inhibit odor-evoked excitation in layer 2 principal cells, whereas HZ cells provide more diffuse and prolonged feedforward inhibition. Our findings reveal unexpected complexity in the operation of inhibition in the piriform cortex.


2019 ◽  
Vol 27 (1) ◽  
pp. 20-32 ◽  
Author(s):  
Enver Miguel Oruro ◽  
Grace V.E. Pardo ◽  
Aldo B. Lucion ◽  
Maria Elisa Calcagnotto ◽  
Marco A. P. Idiart

2019 ◽  
pp. 185-188 ◽  
Author(s):  
Denis Zakharov ◽  
Martin Krupa ◽  
Victor Tyutin ◽  
Boris Gutkin

Gamma rhythm plays a key role in a number of cognitive tasks: working memory, sensory processing and routing of information across neural circuits. In comparison with other (lower frequency) oscillations it is sparser and heterogeneous in space. One way to model such properties of gamma rhythm is to describe it through a neural network consisting of interacting populations of pyramidal cells (excitatory neurons) and interneurons (inhibitory neurons), demonstrating cluster synchronization. The structure of such clusters can be modulated by endogenous neuromodulators: dopamine, acetylcholine, adrenaline, etc. In this article we consider the reconfiguring of synchronous clusters of pyramidal interneuron gamma rhythm (pyramidal interneuron gamma, PING) due to the variation of the frequency adaptation parameter of pyramidal cells and the strength of excitatory synaptic connections. We have shown that the variation of the frequency adaptation parameter has the strongest impact on the strongest influence on the cluster structure and can lead to either an increase or a decrease of the number of synchronous clusters.


Author(s):  
Dorothy Winter Gietzen

Our health requires continual protein synthesis for maintaining and repairing tissues. For protein synthesis to function, all the essential (indispensable) amino acids (IAA) that must be available in the diet, along with those AAs that the cells can synthesize, the dispensable amino acids. Here we review studies that have shown the location of the detector for IAA deficiency in the brain, specifically for recognition of IAA deficient diets (IAAD diets) in the anterior piriform cortex (APC), with subsequent responses in downstream brain areas. The APC is highly excitable, uniquely suited to serve as an alarm for reductions in IAAs. With a balanced diet, these neurons are kept from over-excitation by GABAergic inhibitory neurons. Because several transporters and receptors on the GABAergic neurons have rapid turnover times, they rely on intact protein synthesis to function. When an IAA is missing, its unique tRNA cannot be charged. This activates the enzyme General Control Nonderepressible 2 (GCN2) that is important in the initiation phase of protein synthesis. Without the inhibitory control supplied by GABAergic neurons, excitation in the circuitry is free to signal an urgent alarm. Studies in rodents have shown rapid recognition of IAA deficiency by quick rejection of the IAAD diet.


2017 ◽  
Vol 18 (1) ◽  
Author(s):  
Junli Yang ◽  
Gerhard Litscher ◽  
Zhongren Sun ◽  
Qiang Tang ◽  
Kiyoshi Kishi ◽  
...  

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