The neuroanatomical and neurochemical basis of conditioned fear

Fendt, Markus; Fanselow, Michael S.

doi:10.1016/s0149-7634(99)00016-0

Cited by 982 publications

(712 citation statements)

References 200 publications

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“…A previous study reported that 12 month-old Sprague Dawley rats showed more anxiety-related behavior than young rats, without memory impairment, suggesting that trait anxiety may have determined stronger fear memory in our study (Moyer and Brown, 2006). Based on anatomy, overlapping brain circuitries mediate memory, stress, fear, anxiety and nociception, involving the prefrontal cortex, hippocampus, amygdala and hypothalamus (Fendt and Fanselow, 1999;LeDoux, 2000). Thus, additional modalities, including sensory skills, ability to freeze, reactivity to novelty or sensorimotor functions may explain differences between young adults and middle aged rats (Hodes and Shors, 2007).…”

Section: Middle-aged Modelmentioning

confidence: 57%

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Effects of 900MHz radiofrequency on corticosterone, emotional memory and neuroinflammation in middle-aged rats

Bouji¹,

Lecomte²,

Hode³

et al. 2012

Experimental Gerontology

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. Effects of 900 MHz radiofrequency on corticosterone, emotional memory and neuroinflammation in middle-aged rats. Experimental Gerontology, Elsevier, 2012, 47 (6) ABSTRACTThe widespread use of mobile phones raises the question of the effects of electromagnetic fields (EMF, 900 MHz) on the brain. Previous studies reported increased levels of the glial fibrillary acidic protein (GFAP) in the rat's brain after a single exposure to 900 MHz global system for mobile (GSM) signal, suggesting a potential inflammatory process. While this result was obtained in adult rats, no data is currently available in older animals. Since the transition from middle-age to senescence is highly dependent on environment and lifestyle, we studied the reactivity of middle-aged brains to EMF exposure. We assessed the effects of a single 15 min GSM exposure (900MHz; specific absorption rate (SAR) = 6 W/kg) on GFAP expression in young adults (6 week-old) and middle-aged rats (12 month-old). Brain interleukin (IL)-1β and IL-6, plasmatic levels of corticosterone (CORT), and emotional memory were also assessed.Our data indicated that, in contrast to previously published work, acute GSM exposure did not induce astrocytes activation. Our results showed an IL-1β increase in the olfactory bulb and enhanced contextual emotional memory in GSM-exposed middle-aged rats, and increased plasmatic levels of CORT in GSM-exposed young adults. Altogether, our data showed an age dependency of reactivity to GSM exposure in neuroimmunity, stress and behavioral parameters. Reproducing these effects and studying their mechanisms may allow a better understanding of mobile phone EMF effects on neurobiological parameters.

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Section: Middle-aged Modelmentioning

confidence: 57%

“…Fear is an apprehensive arousal response to an explicit threat and refers to the activation of the defensive behavioral system (Fendt and Fanselow, 1999). Fear conditioning is based on both a Pavlovian conditioning and the induction of fear in response to an aversive unconditioned stimulus.…”

Section: Gsm Exposure Stress and Emotional Memorymentioning

confidence: 99%

Effects of 900MHz radiofrequency on corticosterone, emotional memory and neuroinflammation in middle-aged rats

Bouji¹,

Lecomte²,

Hode³

et al. 2012

Experimental Gerontology

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“…A substantial amount of evidence supports the notion that the amygdala is a key brain structure in the modulation of emotional behavior (Davis, 1992;LeDoux, 2000;Davis, 1997;Fendt and Fanselow, 1999;Maren, 1999) and particularly in pavlovian aversive learning (LeDoux et al, 1990;Gewirtz and Davis, 1997;Miserendino et al, 1990;Fanselow and Kim, 1994). It is known that the basolateral complex (BLA) receives relevant information from the environment via hippocampal, thalamic, and cortical afferents (McDonald, 1998;Davis and Whalen, 2001).…”

Section: Introductionmentioning

confidence: 96%

“…In this aversive learning paradigm, a neutral conditioned stimulus (CS) is repeatedly paired with an unpleasant and unconditioned stimulus (US) such as an electric footshock. As a result of such pairing of events, the previously neutral CS then produces a hypothetical state of fear that is expressed as freezing, one of the most prominent behavioral signs of fear in rats Blanchard, 1971, 1969;Fendt and Fanselow, 1999). In the current study, in order to evaluate the influence of BDZ withdrawal on subsequent emotional learning, BDZ withdrawn animals were tested in a fear-conditioning task.…”

Section: Introductionmentioning

confidence: 99%

Increased Fear Learning Coincides with Neuronal Dysinhibition and Facilitated LTP in the Basolateral Amygdala following Benzodiazepine Withdrawal in Rats

Isoardi

Martijena

Carrer

et al. 2004

Neuropsychopharmacol

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Animals chronically administered with diazepam (DZM -2 mg/kg/day i.p.) or vehicle (VEH) for 21 days were tested in a fear-conditioning paradigm 4 days after the last administration. Increased freezing was observed in DZM withdrawn rats as compared to VEH injected control rats in both associative and nonassociative context and this increase was greatest for the DZM withdrawal group in the paired context. In animals anesthetized with urethane, single pulses in the medial prefrontal cortex evoked a field potential including a population spike (PS) in the basolateral complex of the amygdala (BLA) of control animals, whereas in DZM withdrawn animals multiple PSs were evoked. In brain slices from control rats, stimulation of the external capsule evoked a field potential including a PS in the BLA, whereas in DZM withdrawn rats multiple PSs were evoked. The amplitude of the PS was smaller in slices obtained from DZM withdrawn rats than from control rats, and paired pulse inhibition was significantly less in the former. Perfusion with DZM 2 mM of slices obtained from DZM withdrawn rats eliminated repetitive spiking. GABAergic blockade with 50 mM picrotoxin in control rats resulted in the appearance of multiple secondary PSs. In slices from DZM withdrawn rats high-frequency stimulation induced a highly significant potentiation that lasted at least 2 h (LTP), whereas in control rats the same stimulation did not induce LTP. Neuronal hyperexcitability leading to facilitated LTP observed in BLA of DZM withdrawn rats could be due to depressed GABAergic activity (dysinhibition). The increased synaptic plasticity may be at the root of the increased fear learning observed in withdrawn animals.

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“…The association formed between the CS and US can elicit a conditioned fear response (CR) when the CS is presented alone. In rodents the most readily observable CRs include freezing, response suppression (Quirk et al, 1995;Killcross et al, 1997;Fendt and Fanselow, 1999;Gewirtz and Davis, 2000;LeDoux, 2000), and autonomic changes such as tachycardia (Young and Leaton, 1994;Nijsen et al, 1998) and increased body temperature (Noble and Delini-Stula, 1976). Although the neural and molecular mechanisms underlying the formation of CS-US associations are well established (for reviews, see Davis, 2000;Rodrigues et al, 2004), those mechanisms that mediate the suppression of an established fear response in extinction are less clear.…”

Section: Introductionmentioning

confidence: 99%

Disruption of AMPA Receptor Endocytosis Impairs the Extinction, but not Acquisition of Learned Fear

Dalton

Wang

Floresco

et al. 2007

Neuropsychopharmacol

144

135

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Synaptic plasticity in the form of long-term potentiation (LTP) plays a critical role in the formation of a Pavlovian fear association. However, the role that synaptic plasticity plays in the suppression of a learned fear response remains to be clarified. Here, we assessed the role that long-term depression (LTD) plays in the acquisition, expression, and extinction of a conditioned fear response. We report that blockade of LTD with a GluR2-derived peptide (Tat-GluR2 3Y ; 1.5 mmol/kg, i.v.) that blocks regulated a-amino-3-hydroxy-5-methyl-isoxazole-4-propionic acid (AMPA) receptor endocytosis during an initial extinction training session disrupted both the expression and recall of extinction learning. A similar impairment of extinction during training, but not recall, was observed when NMDA receptor-dependent LTD was inhibited through the selective blockade of NMDA NR2B receptors with Ro 25-6981. In contrast, blockade of LTD with Tat-GluR2 3Y during fear conditioning or during a fear recall test did not effect the expression or recall of either contextual or cue-induced conditioned fear. Similarly, administration of Tat-GluR2 3Y prior to an extinction recall test did not affect spontaneous recovery or rate of re-extinction in previously extinguished rats. These data demonstrate that AMPA receptor endocytosis does not mediate acquisition or expression of conditioned fear, but may play a role in the extinction of fear memories. Furthermore, these findings suggest that LTD may be a molecular mechanism that facilitates the selective modification of a learned association while leaving intact the ability to form a new memory.

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The neuroanatomical and neurochemical basis of conditioned fear

Cited by 982 publications

References 200 publications

Effects of 900MHz radiofrequency on corticosterone, emotional memory and neuroinflammation in middle-aged rats

Effects of 900MHz radiofrequency on corticosterone, emotional memory and neuroinflammation in middle-aged rats

Increased Fear Learning Coincides with Neuronal Dysinhibition and Facilitated LTP in the Basolateral Amygdala following Benzodiazepine Withdrawal in Rats

Disruption of AMPA Receptor Endocytosis Impairs the Extinction, but not Acquisition of Learned Fear

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