Facilitation of conditioned odor aversion by entorhinal cortex lesions in the rat.

Ferry, Barbara; Oberling, Philippe; Jarrard, Leonard E.; Scala, Georges Di

doi:10.1037/0735-7044.110.3.443

Cited by 52 publications

(53 citation statements)

References 53 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In the present study, we sought to investigate odor processing in higher order structures in response to AβPP pathology at the single-unit level by performing acute electrophysiological recordings in LEC in the Tg2576 mouse. The LEC is an area that has been demonstrated to play an important role in odor processing and associative memory (Chapuis, et al, 2013, Ferry, et al, 1996, Frasnelli, et al, 2010, Mouly and Di Scala, 2006, Staubli, et al, 1984, Wirth, et al, 1998, Xu and Wilson, 2012). Our results show that odor processing at the single unit level in LEC remains surprisingly robust in the face of accumulating AβPP metabolites, including Aβ.…”

Section: Discussionmentioning

confidence: 99%

“…In addition, the LEC projects back to both the olfactory bulb and piriform cortex (Chapuis, et al, 2013). This top-down pathway is critical for fine odor discrimination (Chapuis, et al, 2013), as well as modulating piriform cortical odor responses (Chapuis, et al, 2013, Mouly and Di Scala, 2006), and non-hippocampal dependent odor memory (Boisselier, et al, 2014, Ferry, et al, 1996, Wirth, et al, 1998). …”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Early hyperactivity in lateral entorhinal cortex is associated with elevated levels of AβPP metabolites in the Tg2576 mouse model of Alzheimer's disease

Fitzgerald

Nixon

et al. 2015

Experimental Neurology

View full text Add to dashboard Cite

Alzheimer’s disease (AD) is a neurodegenerative disorder that is the most common cause of dementia in the elderly today. One of the earliest symptoms of AD is olfactory dysfunction. The present study investigated the effects of amyloid β precursor protein (AβPP) metabolites, including amyloid-β (Aβ) and AβPP C-terminal fragments (CTF), on olfactory processing in the lateral entorhinal cortex (LEC) using the Tg2576 mouse model of human AβPP over-expression. The entorhinal cortex is an early target of AD related neuropathology, and the LEC plays an important role in fine odor discrimination and memory. Cohorts of transgenic and age-matched wild-type (WT) mice at 3, 6, and 16 months of age (MO) were anesthetized and acute, single-unit electrophysiology was performed in the LEC. Results showed that Tg2576 exhibited early LEC hyperactivity at 3 and 6 MO compared to WT mice in both local field potential and single-unit spontaneous activity. However, LEC single-unit odor responses and odor receptive fields showed no detectable difference compared to WT at any age. Finally, the very early emergence of olfactory system hyper-excitability corresponded not to detectable Aβ deposition in the olfactory system, but rather to high levels of intracellular AβPP-CTF and soluble Aβ in the anterior piriform cortex (aPCX), a major afferent input to the LEC, by 3 MO. The present results add to the growing evidence of AβPP-related hyper-excitability, and further implicate both soluble Aβ and non-Aβ AβPP metabolites in its early emergence.

show abstract

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Early hyperactivity in lateral entorhinal cortex is associated with elevated levels of AβPP metabolites in the Tg2576 mouse model of Alzheimer's disease

Fitzgerald

Nixon

et al. 2015

Experimental Neurology

View full text Add to dashboard Cite

show abstract

“…Furthermore, inhibitory interneurons are a target of some descending inputs to the piriform cortex (Luna 2011;Mouly and Di Scala 2006), which help contribute to experiencedependent shaping of cortical odor responses. Thus a contribution from either changes in local inhibitory circuitry (Poo and Isaacson 2009;Suzuki and Bekkers 2007;Zhang et al 2006) or higher order centers such as the amygdala (Luna 2011), orbitofrontal cortex (Cohen et al 2008), or entorhinal cortex (Ferry et al 1996) may contribute to the constellation of learning induced changes observed here. Manipulation of the described learned changes in aPCX sensory physiology will be required to determine their necessary and/or sufficient contribution to the behavioral changes.…”

Section: Discussionmentioning

confidence: 99%

Generalized vs. stimulus-specific learned fear differentially modifies stimulus encoding in primary sensory cortex of awake rats

Chen

Barnes

Wilson

2011

Journal of Neurophysiology

View full text Add to dashboard Cite

Chen CF, Barnes DC, Wilson DA. Generalized vs. stimulus-specific learned fear differentially modifies stimulus encoding in primary sensory cortex of awake rats. J Neurophysiol 106: 3136 -3144, 2011. First published September 14, 2011 doi:10.1152/jn.00721.2011.-Experience shapes both central olfactory system function and odor perception. In piriform cortex, odor experience appears critical for synthetic processing of odor mixtures, which contributes to perceptual learning and perceptual acuity, as well as contributing to memory for events and/or rewards associated with odors. Here, we examined the effect of odor fear conditioning on piriform cortical single-unit responses to the learned aversive odor, as well as its effects on similar (overlapping mixtures) in freely moving rats. We found that odor-evoked fear responses were training paradigm dependent. Simple association of a condition stimulus positive (CSϩ) odor with foot shock (unconditioned stimulus) led to generalized fear (cue-evoked freezing) to similar odors. However, after differential conditioning, which included trials where a CSϪ odor (a mixture overlapping with the CSϩ) was not paired with shock, freezing responses were CSϩ odor specific and less generalized. Pseudoconditioning led to no odor-evoked freezing. These differential levels of stimulus control over freezing were associated with different training-induced changes in single-unit odor responses in anterior piriform cortex (aPCX). Both simple and differential conditioning induced a significant decrease in aPCX single-unit spontaneous activity compared with pretraining levels while pseudoconditioning did not. Simple conditioning enhanced mean receptive field size (breadth of tuning) of the aPCX units, while differential conditioning reduced mean receptive field size. These results suggest that generalized fear is associated with an impairment of olfactory cortical discrimination. Furthermore, changes in sensory processing are dependent on the nature of training and can predict the stimuluscontrolled behavioral outcome of the training. piriform cortex; fear conditioning; learning-induced plasticity THE OLFACTORY SYSTEM INVOLVES a memory-based odor processing function that allows its acuity to be constantly shaped by experience (Wilson and Stevenson 2006). This function enables animals to not only identify myriad novel odors and odor combinations in the environment but also to associate odors with their ecological significance, which is critical for adaptive behavior. Experience-dependent perceptual changes (perceptual learning) and their underlying neural plasticity have been reported across phylogeny from the first to third order neurons in the olfactory system (Davis 2004).

show abstract

“…Its role in olfactory learning seems to be complex (Kaut et al 2003), and the internal nutritional state could differentially modulate odor processing in this cortical area (Chabaud et al 2000). Lesion of the EC facilitates COA learning by prolonging the olfactory trace duration and renders it tolerant to extended interstimulus interval (Ferry et al 1996). Our present data suggest a role of the EC in TPOA expression.…”

Section: Discussionmentioning

confidence: 47%

“…In contrast, the lesion of central amygdaloid nucleus (Ce) does not interfere with TPOA learning (Hatfield et al 1992). As it is one of the main outputs of the BLA, the involvement of the entorhinal cortex (EC) was also studied (Ferry et al 1996). Its lesion facilitates the acquisition of conditioned odor aversion (COA).…”

mentioning

confidence: 99%

Fos and Egr1 expression in the rat brain in response to olfactory cue after taste-potentiated odor aversion retrieval

Dardou¹,

Datiche²,

Cattarelli³

2006

Learn. Mem.

View full text Add to dashboard Cite

When an odor is paired with a delayed illness, rats acquire a relatively weak odor aversion. In contrast, rats develop a strong aversion to an olfactory cue paired with delayed illness if it is presented simultaneously with a gustatory cue. Such a conditioning effect has been referred to as taste-potentiated odor aversion learning (TPOA). TPOA is an interesting model for studying neural mechanisms of plasticity because of its robustness and rapid acquisition. However, the neural substrate involved in TPOA retrieval has not been well characterized. To address this question, we used immunocytochemical detection of inducible transcription factors encoded by the immediate-early genes Fos and Egr1. Thirsty male rats were conditioned to TPOA learning, and they were submitted to retrieval in the presence of the learned odor 3 d later. Significant increases in both Fos and Egr1 expressions were observed in basolateral amygdala, insular cortex, and hippocampus in aversive rats in comparison with the all the control groups. The pattern of neuronal activity seemed unlikely to be related to the sole LiCl injection. Lastly, opposite patterns of Fos and Egr1 were noted in the entorhinal cortex and the central nucleus of amygdala, suggesting a differential involvement of these markers in retrieval of TPOA.Odors are critical cues for rodents since odors give the rodents information about their environment. Odors allow the rodents to escape from predators, to find food, or to avoid consumption of toxic products. Memorization of such information is crucial for animal survival. Moreover, olfactory learning permits a previously neutral cue to acquire significance after having been paired with a biologically relevant reinforcement. Rats can acquire weak aversion when an odor is paired with delayed-illness (Bernstein 1991). In contrast, when an odor is simultaneously presented with a taste cue, rats can develop strong aversion to the odor cue. Such a conditioning has been referred to as tastepotentiated odor aversion (TPOA) learning (Palmerino et al. 1980). Thus, taste-mediated potentiation allows odor to gain associative strength and the animals to avoid consumption of poisonous substance on the basis of its odor only (Bernstein 1991). TPOA learning is an attractive model for studying odor memory because of its robustness, rapid acquisition, and adaptive feature (Welzl et al. 2001).Most of the data regarding the brain areas that could mediate TPOA learning are provided by either lesion or pharmalogical experiments. Various brains areas involved in olfactory, gustatory, and visceral pain processing could play a role in TPOA learning. Several studies (Bermùdez-Rattoni et al. 1986;Hatfield et al. 1992;Ferry et al. 1995) indicate that the basolateral nucleus of amygdala (BLA) could play a major role in the acquisition but not in the retrieval of TPOA. In addition, the BLA is known for its involvement in learning the biological significance of events and could modulate memory storage of emotional events (McGaugh 2002). In contrast, the l...

show abstract

Facilitation of conditioned odor aversion by entorhinal cortex lesions in the rat.

Cited by 52 publications

References 53 publications

Early hyperactivity in lateral entorhinal cortex is associated with elevated levels of AβPP metabolites in the Tg2576 mouse model of Alzheimer's disease

Early hyperactivity in lateral entorhinal cortex is associated with elevated levels of AβPP metabolites in the Tg2576 mouse model of Alzheimer's disease

Generalized vs. stimulus-specific learned fear differentially modifies stimulus encoding in primary sensory cortex of awake rats

Fos and Egr1 expression in the rat brain in response to olfactory cue after taste-potentiated odor aversion retrieval

Contact Info

Product

Resources

About