Fear Response

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Yuji Ikegaya - One of the best experts on this subject based on the ideXlab platform.

  • ethanol facilitates socially evoked memory recall in mice by recruiting pain sensitive anterior cingulate cortical neurons
    Nature Communications, 2018
    Co-Authors: Tetsuya Sakaguchi, Satoshi Iwasaki, Mami Okada, Kazuki Okamoto, Yuji Ikegaya
    Abstract:

    Alcohol is a traditional social-bonding reinforcer; however, the neural mechanism underlying ethanol-driven social behaviors remains elusive. Here, we report that ethanol facilitates observational Fear Response. Observer mice exhibited stronger defensive immobility while observing cagemates that received repetitive foot shocks if the observer mice had experienced a brief priming foot shock. This enhancement was associated with an observation-induced recruitment of subsets of anterior cingulate cortex (ACC) neurons in the observer mouse that were responsive to its own pain. The vicariously activated ACC neurons projected their axons preferentially to the basolateral amygdala. Ethanol shifted the ACC neuronal balance toward inhibition, facilitated the preferential ACC neuronal recruitment during observation, and enhanced observational Fear Response, independent of an oxytocin signaling pathway. Furthermore, ethanol enhanced socially evoked Fear Response in autism model mice.

  • memory formation and retrieval of neuronal silencing in the auditory cortex
    Proceedings of the National Academy of Sciences of the United States of America, 2015
    Co-Authors: Hiroshi Nomura, Yuji Ikegaya, Kojiro Hara, Reimi Abe, Natsuko Hitoraimamura, Ryota Nakayama, Takuya Sasaki, Norio Matsuki
    Abstract:

    Sensory stimuli not only activate specific populations of cortical neurons but can also silence other populations. However, it remains unclear whether neuronal silencing per se leads to memory formation and behavioral expression. Here we show that mice can report optogenetic inactivation of auditory neuron ensembles by exhibiting Fear Responses or seeking a reward. Mice receiving pairings of footshock and silencing of a neuronal ensemble exhibited a Fear Response selectively to the subsequent silencing of the same ensemble. The valence of the neuronal silencing was preserved for at least 30 d and was susceptible to extinction training. When we silenced an ensemble in one side of auditory cortex for conditioning, silencing of an ensemble in another side induced no Fear Response. We also found that mice can find a reward based on the presence or absence of the silencing. Neuronal silencing was stored as working memory. Taken together, we propose that neuronal silencing without explicit activation in the cerebral cortex is enough to elicit a cognitive behavior.

Pascal Carrive - One of the best experts on this subject based on the ideXlab platform.

  • changes in cutaneous and body temperature during and after conditioned Fear to context in the rat
    European Journal of Neuroscience, 2005
    Co-Authors: D M L Vianna, Pascal Carrive
    Abstract:

    Infrared thermography was used to image changes in cutaneous temperature during a conditioned Fear Response to context. Changes in heart rate, arterial pressure, activity and body (i.p.) temperature were recorded at the same time by radio-telemetry, in addition to freezing immobility. A marked drop in tail and paws temperature (-5.3 and -7.5 degrees C, respectively, down to room temperature), which lasted for the entire duration of the Response (30 min), was observed in Fear-conditioned rats. In sham-conditioned rats, the drop was on average half the magnitude and duration. In contrast, temperature of the eye, head and back increased (between + 0.8 and + 1.5 degrees C), with no difference between the two groups of rats. There was a similar increase in body temperature although it was slightly higher and delayed in the Fear-conditioned animals. Finally, ending of the Fear Response was associated with a gradual decrease in body temperature and a rebound increase in the temperature of the tail (+ 3.3 degrees C above baseline). This study shows that Fear, and to some extent arousal, evokes a strong cutaneous vasoconstriction that is restricted to the tail and paws. This regionally specific reduction in blood flow may be part of a preparatory Response to a possible fight and flight to reduce blood loss in the most exposed parts of the rat's body in case of injury. The data also show that the tail is the main part of the body used for dissipating internal heat accumulated during Fear once the animal has returned to a safe environment.

  • role of ventrolateral periaqueductal gray neurons in the behavioral and cardiovascular Responses to contextual conditioned Fear and poststress recovery
    Neuroscience, 2003
    Co-Authors: Peter Walker, Pascal Carrive
    Abstract:

    Abstract We have previously shown that conditioned Fear to context increases Fos expression in the caudal ventrolateral region of the periaqueductal gray in the rat. To understand the reason for this activation and its role in the expression of the contextual Fear Response, the ventrolateral periaqueductal gray was temporarily blocked with bilateral microinjections (0.4 μl) of the GABA agonist muscimol (0.2 mM) or the glutamate antagonist kynurenic acid (0.1 M). Cardiovascular changes and activity were recorded by radio-telemetry and the microinjections were made immediately before testing the conditioned Response in the aversive context. Muscimol and kynurenic acid had the same effects: when compared to saline controls, freezing immobility and ultrasonic vocalizations were reduced and replaced by marked locomotor activity, and the increase in heart rate was enhanced; however, the increase in arterial blood pressure remained the same. Interesting changes were also observed when animals were returned to the safe context of their home box after Fear (recovery). Basically, the recovery Response was either prevented or delayed: instead of returning to resting immobility, the rats remained agitated in their home box with a moderately elevated activity, heart rate and blood pressure. However, the effect of ventrolateral periaqueductal gray blockade on heart rate, arterial pressure and activity did not appear to be specific to the Fear Response or its recovery because they were also observed in animals returned to the safe context of their home box immediately after injection. The later Response was also a recovery Response from the milder stress of handling and the injection procedure. We discuss the results by arguing that the ventrolateral periaqueductal gray is involved in the immobility component of both the Fear Response and poststress recovery Responses. To explain our interpretation we consider the findings in relation to the classic descending defence-arousal system and the hyporeactive-hypotensive immobility pattern that has been attributed to the ventrolateral periaqueductal gray. We propose that there is a dual activation of the defence-arousal system and of the ventrolateral periaqueductal gray during Fear, with the ventrolateral periaqueductal gray acting as a brake on the defence-arousal system. The role of this brake is to impose immobility and hold off active defence Responses such as fight and flight. The result of this combination of arousal and immobility is a hyperreactive freezing immobility associated with ultrasonic vocalizations, and a pressor Response accompanied with a slow rise in heart rate. Basically, the animal is tense and ready for action but temporarily immobilised. The ventrolateral periaqueductal gray also acts to impose immobility during recovery; however, this is without coactivation of the defence-arousal system. The result is a return to resting immobility, associated with a return to baseline blood pressure and heart rate. This is an active process that insures a faster and complete return to rest. We conclude that the ventrolateral periaqueductal gray is an immobility center involved not only in the Fear Response but also in poststress recovery Responses.

Anne-marie Mouly - One of the best experts on this subject based on the ideXlab platform.

  • New insights from 22-kHz ultrasonic vocalizations to characterize Fear Responses: relationship with respiration and brain oscillatory dynamics
    2019
    Co-Authors: Maryne Dupin, Samuel Garcia, Julie Boulanger-bertolus, Nathalie Buonviso, Anne-marie Mouly
    Abstract:

    Fear behavior depends on interactions between the medial prefrontal cortex (mPFC) and the basolateral amygdala (BLA), and the expression of Fear involves synchronized activity in theta and gamma oscillatory activities. In addition, freezing, the most classical measure of Fear Response in rodents, temporally coincides with the development of sustained 4-Hz oscillations in prefrontal-amygdala circuits. Interestingly, these oscillations were recently shown to depend on the animal's respiratory rhythm, supporting the growing body of evidence pinpointing the influence of nasal breathing on brain rhythms. During Fearful states, rats also emit 22-kHz ultrasonic vocalizations (USV) which drastically affect respiratory rhythm. However, the relationship between 22-kHz USV, respiration and brain oscillatory activities is still unknown. Yet such information is crucial for a comprehensive understanding of how the different components of Fear Response collectively modulate rat's brain neural dynamics. Here we trained male rats in an odor Fear conditioning task, while recording simultaneously local field potentials in BLA, mPFC and olfactory piriform cortex, together with USV calls and respiration. We show that USV calls coincide with an increase in delta and gamma power and a decrease in theta power. In addition, during USV emission in contrast to silent freezing, there is no coupling between respiratory rate and delta frequency, and the modulation of fast oscillations amplitude relative to the phase of respiration is modified. We propose that sequences of USV calls could result in a differential gating of information within the network of structures sustaining Fear behavior, thus potentially modulating Fear expression/memory.

  • the rub cage respiration ultrasonic vocalizations behavior acquisition setup for assessing emotional memory in rats
    Frontiers in Behavioral Neuroscience, 2011
    Co-Authors: Chloe Hegoburu, Samuel Garcia, Kiseko Shionoya, Belkacem Messaoudi, Marc Thevenet, Anne-marie Mouly
    Abstract:

    In animals, emotional memory is classically assessed through pavlovian Fear conditioning in which a neutral novel stimulus (conditioned stimulus) is paired with an aversive unconditioned stimulus. After conditioning, the conditioned stimulus elicits a Fear Response characterized by a wide range of behavioral and physiological Responses. Despite the existence of this large repertoire of Responses, freezing behavior is often the sole parameter used for quantifying Fear Response, thus limiting emotional memory appraisal to this unique index. Interestingly, respiratory changes and ultrasonic vocalizations (USV) can occur during Fear Response, yet very few studies investigated the link between these different parameters and freezing. The aim of the present study was to design an experimental setup allowing the simultaneous recording of respiration, USV, and behavior (RUB cage), and the offline synchronization of the collected data for fine-grain second by second analysis. The setup consisted of a customized plethysmograph for respiration monitoring, equipped with a microphone capturing USV, and with four video cameras for behavior recording. In addition, the bottom of the plethysmograph was equipped with a shock-floor allowing foot-shock delivery, and the top received tubing for odor presentations. Using this experimental setup we first described the characteristics of respiration and USV in different behaviors and emotional states. Then we monitored these parameters during contextual Fear conditioning and showed that they bring complementary information about the animal's anxiety state and the strength of aversive memory. The present setup may be valuable in providing a clearer appraisal of the physiological and behavioral changes that occur during acquisition as well as retrieval of emotional memory.

Naoki Matsuo - One of the best experts on this subject based on the ideXlab platform.

  • pharmacogenetic reactivation of the original engram evokes an extinguished Fear memory
    Neuropharmacology, 2017
    Co-Authors: Takahiro Yoshii, Hiroshi Hosokawa, Naoki Matsuo
    Abstract:

    Fear memory extinction has several characteristic behavioral features, such as spontaneous recovery, renewal, and reinstatement, suggesting that extinction training does not erase the original association between the conditioned stimulus (CS) and the unconditioned stimulus (US). However, it is unclear whether reactivation of the original physical record of memory (i.e., memory trace) is sufficient to produce conditioned Fear Response after extinction. Here, we performed pharmacogenetic neuronal activation using transgenic mice expressing hM3Dq DREADD (designer receptor exclusively activated by designer drug) under the control of the activity-dependent c-fos gene promoter. Neuronal ensembles activated during Fear-conditioned learning were tagged with hM3Dq and subsequently reactivated after extinction training. The mice exhibited significant freezing, even when the Fear memory was no longer triggered by external CS, indicating that the artificial reactivation of a specific neuronal ensemble was sufficient to evoke the extinguished Fear Response. This freezing was not observed in non-Fear-conditioned mice expressing hM3dq in the same brain areas. These results directly demonstrated that at least part of the original Fear memory trace remains after extinction, and such residual plasticity might reflect the persistent memory.

Jun Jiang - One of the best experts on this subject based on the ideXlab platform.

  • switching from Fear to no Fear by different neural ensembles in mouse retrosplenial cortex
    Cerebral Cortex, 2019
    Co-Authors: Guangyu Wang, Hong Xie, Lun Wang, Wenhan Luo, Yixiang Wang, Jun Jiang
    Abstract:

    Fear extinction is generally considered a form of new learning that inhibits previously acquired Fear memories. Here, by tracking immediate early gene expression in vivo, we found that contextual Fear extinction training evoked distinct neural ensembles in mouse retrosplenial cortex (RSC). The optogenetic reactivation of these extinction-activated neurons in the RSC was sufficient to suppress a Fear Response, while the reactivation of conditioning-activated neurons in the same area promoted a Fear Response. The generation of such an extinction-memory-related neural ensemble was associated with adult neurogenesis, as abolishing newborn neurons in the adult hippocampus via X-ray irradiation eliminated both the extinction-activated neurons in the RSC and the optogenetic-reactivation-induced suppression of contextual Fear memory. Therefore, switching from Fear to no Fear in Response to the same context is modulated by the RSC through an extinction-activated neural ensemble, the generation of which might require adult neurogenesis in the hippocampus.