scholarly journals Role of anterior piriform cortex in the acquisition of conditioned flavour preference

2016 ◽  
Vol 6 (1) ◽  
Author(s):  
Cristina Mediavilla ◽  
Mar Martin-Signes ◽  
Severiano Risco
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.


2020 ◽  
Vol 29 (13) ◽  
pp. 2134-2147
Author(s):  
M Laroche ◽  
M Lessard-Beaudoin ◽  
M Garcia-Miralles ◽  
C Kreidy ◽  
E Peachey ◽  
...  

Abstract Olfactory dysfunction and altered neurogenesis are observed in several neurodegenerative disorders including Huntington disease (HD). These deficits occur early and correlate with a decline in global cognitive performance, depression and structural abnormalities of the olfactory system including the olfactory epithelium, bulb and cortices. However, the role of olfactory system dysfunction in the pathogenesis of HD remains poorly understood and the mechanisms underlying this dysfunction are unknown. We show that deficits in odour identification, discrimination and memory occur in HD individuals. Assessment of the olfactory system in an HD murine model demonstrates structural abnormalities in the olfactory bulb (OB) and piriform cortex, the primary cortical recipient of OB projections. Furthermore, a decrease in piriform neuronal counts and altered expression levels of neuronal nuclei and tyrosine hydroxylase in the OB are observed in the YAC128 HD model. Similar to the human HD condition, olfactory dysfunction is an early phenotype in the YAC128 mice and concurrent with caspase activation in the murine HD OB. These data provide a link between the structural olfactory brain region atrophy and olfactory dysfunction in HD and suggest that cell proliferation and cell death pathways are compromised and may contribute to the olfactory deficits in HD.


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.


Perception ◽  
2016 ◽  
Vol 46 (3-4) ◽  
pp. 320-332 ◽  
Author(s):  
Emmanuelle Courtiol ◽  
Donald A. Wilson

Olfactory perception and its underlying neural mechanisms are not fixed, but rather vary over time, dependent on various parameters such as state, task, or learning experience. In olfaction, one of the primary sensory areas beyond the olfactory bulb is the piriform cortex. Due to an increasing number of functions attributed to the piriform cortex, it has been argued to be an associative cortex rather than a simple primary sensory cortex. In fact, the piriform cortex plays a key role in creating olfactory percepts, helping to form configural odor objects from the molecular features extracted in the nose. Moreover, its dynamic interactions with other olfactory and nonolfactory areas are also critical in shaping the olfactory percept and resulting behavioral responses. In this brief review, we will describe the key role of the piriform cortex in the larger olfactory perceptual network, some of the many actors of this network, and the importance of the dynamic interactions among the piriform-trans-thalamic and limbic pathways.


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

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