Switching from contextual to tone fear conditioning and vice versa: The key role of the glutamatergic hippocampal-lateral septal neurotransmission

Calandreau, Ludovic; Desgranges, Béatrice; Jaffard, Robert; Desmedt, Aline

doi:10.1101/lm.1859810

Cited by 28 publications

(28 citation statements)

References 24 publications

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“…Further experiments involving glutamate agonists and antagonists injected into LS prior to training further support this idea (Calandreau et al 2010). In these experiments, injection of glutamate agonists into LS promoted auditory fear conditioning and disrupted context fear conditioning, whereas the glutamate antagonists had the opposite effect (Calandreau et al 2010). These findings thus suggest that the LS plays a key role in the specificity of fear conditioning, via selection of the relevant stimuli.…”

Section: Lateral Septumsupporting

confidence: 54%

“…These results suggest a specificity of involvement of LS in auditory, or possibly different forms of cued conditioning, over context conditioning. Further experiments involving glutamate agonists and antagonists injected into LS prior to training further support this idea (Calandreau et al 2010). In these experiments, injection of glutamate agonists into LS promoted auditory fear conditioning and disrupted context fear conditioning, whereas the glutamate antagonists had the opposite effect (Calandreau et al 2010).…”

Section: Lateral Septummentioning

confidence: 61%

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Tracking the fear memory engram: discrete populations of neurons within amygdala, hypothalamus, and lateral septum are specifically activated by auditory fear conditioning

et al. 2015

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Memory formation is thought to occur via enhanced synaptic connectivity between populations of neurons in the brain. However, it has been difficult to localize and identify the neurons that are directly involved in the formation of any specific memory. We have previously used fos-tau-lacZ (FTL) transgenic mice to identify discrete populations of neurons in amygdala and hypothalamus, which were specifically activated by fear conditioning to a context. Here we have examined neuronal activation due to fear conditioning to a more specific auditory cue. Discrete populations of learning-specific neurons were identified in only a small number of locations in the brain, including those previously found to be activated in amygdala and hypothalamus by context fear conditioning. These populations, each containing only a relatively small number of neurons, may be directly involved in fear learning and memory.

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Section: Lateral Septumsupporting

confidence: 54%

Section: Lateral Septummentioning

confidence: 61%

Tracking the fear memory engram: discrete populations of neurons within amygdala, hypothalamus, and lateral septum are specifically activated by auditory fear conditioning

et al. 2015

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“…Nevertheless, they also unveiled a more extended role for the hippocampus in fear conditioning. Indeed, our data repeatedly and consistently showed that the hippocampus is differentially engaged in fear conditioning depending on the predictive value of CSs (Calandreau et al, 2005(Calandreau et al, , 2006(Calandreau et al, , 2007(Calandreau et al, , 2010Desmedt et al, 1998Desmedt et al, , 1999. As written above, subjects adaptively select among environmental stimuli those that best predict an aversive event, either a discrete CS when it is paired with, and thus predictive of, the aversive US, or the context when a CS-US unpairing procedure is used.…”

Section: The Classical Role Of the Hippocampus In Fear Memorymentioning

confidence: 69%

“…In accordance with previous electrophysiological data, we showed that pretraining infusion of glutamic acid into the lateral septum, which mimics an increase in the HPC-LS neurotransmission, promotes the selection of a discrete tone CS to the detriment of the context as predictor of a footshock US. In contrast, infusion of glutamatergic antagonist (Kynurenate), which inhibits this neurotransmission, promotes the selection of the context as major predictor of the US, while blocking the identification of the discrete tone CS as predictor (Calandreau et al, 2010). In full accordance with these data, we had previously shown that pre-training infusion of arginine vasopressin or its antagonist into the lateral septum, which are known to indirectly modulate the HPC-LS glutamatergic neurotransmission, could also promote the selection of the discrete tone CS or the context, respectively, as predictor of the US (Desmedt et al, 1999).…”

Section: The Classical Role Of the Hippocampus In Fear Memorymentioning

confidence: 92%

“…Dysfunction in hippocampal-amygdalar interactions might underlie PTSD-related memory Experimental studies just described above indicate that direct (Calandreau et al, 2006) or indirect manipulation (Calandreau et al, 2010;Desmedt et al, 1999) of the hippocampal cholinergic neurotransmission can result in maladaptive fear memories. The identification of the discrete CS instead of the context in a predicting-context situation, or conversely, the selection of the context instead of the discrete CS in a predicting-tone CS situation reflects the formation of false memory that leads to the expression of inappropriate fear responses to the wrong predictor of a threat.…”

Section: Hippocampal-amygdalar Interaction Qualify Emotional Memory Rmentioning

confidence: 97%

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Adaptive emotional memory: the key hippocampal–amygdalar interaction

Desmedt

Marighetto

Richter‐Levin

et al. 2015

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For centuries philosophical and clinical studies have emphasized a fundamental dichotomy between emotion and cognition, as, for instance, between behavioral/emotional memory and explicit/representative memory. However, the last few decades cognitive neuroscience have highlighted data indicating that emotion and cognition, as well as their underlying neural networks, are in fact in close interaction. First, it turns out that emotion can serve cognition, as exemplified by its critical contribution to decision-making or to the enhancement of episodic memory. Second, it is also observed that reciprocally cognitive processes as reasoning, conscious appraisal or explicit representation of events can modulate emotional responses, like promoting or reducing fear. Third, neurobiological data indicate that reciprocal amygdalar-hippocampal influences underlie such mutual regulation of emotion and cognition. While supporting this view, the present review discusses experimental data, obtained in rodents, indicating that the hippocampal and amygdalar systems not only regulate each other and their functional outcomes, but also qualify specific emotional memory representations through specific activations and interactions. Specifically, we review consistent behavioral, electrophysiological, pharmacological, biochemical and imaging data unveiling a direct contribution of both the amygdala and hippocampal-septal system to the identification of the predictor of a threat in different situations of fear conditioning. Our suggestion is that these two brain systems and their interplay determine the selection of relevant emotional stimuli, thereby contributing to the adaptive value of emotional memory. Hence, beyond the mutual quantitative regulation of these two brain systems described so far, we develop the idea that different activations of the hippocampus and amygdala, leading to specific configurations of neural activity, qualitatively impact the formation of emotional memory representations, thereby producing either adaptive or maladaptive fear memories.

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Genetic deletion of the 67‐kDa isoform of glutamate decarboxylase alters conditioned fear behavior in rats

et al. 2020

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The GABAergic system is thought to play an important role in the control of cognition and emotion, such as fear, and is related to the pathophysiology of psychiatric disorders. For example, the expression of the 67-kDa isoform of glutamate decarboxylase (GAD67), a GABA-producing enzyme, is downregulated in the postmortem brains of patients with major depressive disorder and schizophrenia. However, knocking out the Gad1 gene, which encodes GAD67, is lethal in mice, and thus, the association between Gad1 and cognitive/emotional functions is unclear. We recently developed Gad1 knockout rats and found that some of them can grow into adulthood. Here, we performed fear-conditioning tests in adult Gad1 knockout rats to assess the impact of the loss of Gad1 on fear-related behaviors and the formation of fear memory. In a protocol assessing both cued and contextual memory, Gad1 knockout rats showed a partial antiphase pattern of freezing during training and significantly excessive freezing during the contextual test compared with wild-type rats. However, Gad1 knockout rats did not show any synchronous increase in freezing with auditory tones in the cued test. On the other hand, in a contextual memory specialized protocol, Gad1 knockout rats exhibited comparable freezing behavior to wildtype rats, while their fear extinction was markedly impaired. These results suggest that GABA synthesis by GAD67 has differential roles in cued and contextual fear memory.

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Switching from contextual to tone fear conditioning and vice versa: The key role of the glutamatergic hippocampal-lateral septal neurotransmission

Cited by 28 publications

References 24 publications

Tracking the fear memory engram: discrete populations of neurons within amygdala, hypothalamus, and lateral septum are specifically activated by auditory fear conditioning

Tracking the fear memory engram: discrete populations of neurons within amygdala, hypothalamus, and lateral septum are specifically activated by auditory fear conditioning

Adaptive emotional memory: the key hippocampal–amygdalar interaction

Genetic deletion of the 67‐kDa isoform of glutamate decarboxylase alters conditioned fear behavior in rats

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