Inhibitory neurons in the anterior piriform cortex of the mouse: Classification using molecular markers

2010 ◽  
Vol 518 (10) ◽  
pp. 1670-1687 ◽  
Author(s):  
Norimitsu Suzuki ◽  
John M. Bekkers
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.


2021 ◽  
Vol 11 (1) ◽  
pp. 191
Author(s):  
Dorothy W. Gietzen

Our health requires continual protein synthesis for maintaining and repairing tissues. For protein synthesis to function, all the essential (indispensable) amino acids (IAAs) 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, which makes is 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.


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.


2018 ◽  
Author(s):  
Xiaoxing Zhang ◽  
Wenjun Yan ◽  
Wenliang Wang ◽  
Hongmei Fan ◽  
Ruiqing Hou ◽  
...  

SummaryWorking memory is a critical function of the brain to maintain and manipulate information over delay periods of seconds. Sensory areas have been implicated in working memory; however, it is debated whether the delay-period activity of sensory regions is actively maintaining information or passively reflecting top-down inputs. We hereby examined the anterior piriform cortex, an olfactory cortex, in head-fixed mice performing a series of olfactory working memory tasks. Information maintenance is necessary in these tasks, especially in a dual-task paradigm in which mice are required to perform another distracting task while actively maintaining information during the delay period. Optogenetic suppression of the piriform cortex activity during the delay period impaired performance in all the tasks.Furthermore, electrophysiological recordings revealed that the delay-period activity of the anterior piriform cortex encoded odor information with or without the distracting task.Thus, this sensory cortex is critical for active information maintenance in working memory.


1999 ◽  
Vol 81 (3) ◽  
pp. 1147-1149 ◽  
Author(s):  
Linda J. Magrum ◽  
M. Anne Hickman ◽  
Dorothy W. Gietzen

Increased intracellular calcium in rat anterior piriform cortex in response to threonine after threonine deprivation The anterior piriform cortex (APC) may serve as the chemosensor for amino acid (AA) deficiency in rats. To investigate the mechanism by which the APC recognizes a limiting indispensable AA (IAA), we examined changes in intracellular calcium ([Ca2+]i) in APC slices after culture in medium with or without threonine (Thr) or lysine (Lys). The addition of 1 or 10 mM Thr to slices previously incubated in Thr-devoid medium resulted in a significant and sustained increase in [Ca2+]i compared to control slices; an effect not seen when isoleucine, another IAA, was added. Similar results were seen when lysine, but not threonine, was added to slices incubated in lysine-devoid medium. The rise in [Ca2+]iresulting from the addition of the limiting IAA to deficient slices may be linked to enhanced activity of the appropriate AA transporter. This is suggested by preliminary findings that serine, a small neutral AA that uses the same transporter as threonine, gave rise to an enhanced response in the Thr-deficient slice.


2013 ◽  
Vol 110 (1) ◽  
pp. 141-152 ◽  
Author(s):  
Gillian L. Morrison ◽  
Christine J. Fontaine ◽  
Carolyn W. Harley ◽  
Qi Yuan

cFos activation in the anterior piriform cortex (aPC) occurs in early odor preference learning in rat pups ( Roth and Sullivan 2005 ). Here we provide evidence that the pairing of odor as a conditioned stimulus and β-adrenergic activation in the aPC as an unconditioned stimulus generates early odor preference learning. β-Adrenergic blockade in the aPC prevents normal preference learning. Enhancement of aPC cAMP response element-binding protein (CREB) phosphorylation in trained hemispheres is consistent with a role for this cascade in early odor preference learning in the aPC. In vitro experiments suggested theta-burst-mediated long-term potentiation (LTP) at the lateral olfactory tract (LOT) to aPC synapse depends on N-methyl-d-aspartate (NMDA) receptors and can be significantly enhanced by β-adrenoceptor activation, which causes increased glutamate release from LOT synapses during LTP induction. NMDA receptors in aPC are also shown to be critical for the acquisition, but not expression, of odor preference learning, as would be predicted if they mediate initial β-adrenoceptor-promoted aPC plasticity. Ex vivo experiments 3 and 24 h after odor preference training reveal an enhanced LOT-aPC field excitatory postsynaptic potential (EPSP). At 3 h both presynaptic and postsynaptic potentiations support EPSP enhancement while at 24 h only postsynaptic potentiation is seen. LOT-LTP in aPC is excluded by odor preference training. Taken together with earlier work on the role of the olfactory bulb in early odor preference learning, these outcomes suggest early odor preference learning is normally supported by and requires multiple plastic changes at least at two levels of olfactory circuitry.


2011 ◽  
Vol 71 ◽  
pp. e155
Author(s):  
Akira Shimizu ◽  
Jiani Wang ◽  
Shinya Ohara ◽  
Ken-Ichiro Tsutsui ◽  
Toshio Iijima

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