Mesolimbic dopaminergic pathways in fear conditioning

Pezze, Marie A.; Feldon, Joram

doi:10.1016/j.pneurobio.2004.09.004

Cited by 455 publications

(309 citation statements)

References 260 publications

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“…The findings that DA is also involved in aversive conditioning by LiCl (Di Chiara, 2002) and fear conditioning (Nader and LeDoux, 1999;Pezze and Feldon, 2004) support its role in associative learning and memory consolidation. Blockade of D1-like and D2-like DA receptors interferes with consolidation of Pavlovian conditioned behavior (Greba et al, 2001;Koch et al, 2000;LaLumiere et al, 2005;Nader and LeDoux, 1999).…”

Section: Introductionmentioning

confidence: 66%

Impairment in Consolidation of Learned Place Preference Following Dopaminergic Neurotoxicity in Mice is Ameliorated by N-acetylcysteine but not D1 and D2 Dopamine Receptor Agonists

Achat-Mendes

Anderson

Itzhak

2006

Neuropsychopharmacol

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Some of the major concerns related to methamphetamine (METH) abuse are the neuronal damage inflicted at dopamine (DA) nerve terminals and the cognitive deficits observed in human METH abusers. We have shown that a high dose of METH selectively depleted dopaminergic markers in striatum, frontal cortex and amygdala of Swiss Webster mice, and impaired learned place preference. In this study, we investigated whether deficits in consolidation of place learning, as a consequence of METH neurotoxicity, underlie the underperformance of cocaine conditioned place preference (CPP). Administration of METH (5 mg/kg Â 3) to Swiss Webster mice decreased striatal tyrosine hydroxylase (TH) immunoreactive neurons and significantly increased glial fibrillary acidic protein (GFAP) expression, confirming the neurotoxic potential of METH in mice. This treatment significantly attenuated the establishment of cocaine (15 mg/kg) CPP compared to control. To investigate whether manipulation of the consolidation phase improves learned place preference, mice were trained by cocaine and received daily post-training injections of DA receptor agonists or N-acetylcysteine (NAC). As memory consolidation occurs shortly after training, drugs were administered either immediately or 2 h post-training. Immediate posttraining administration of the D1 DA receptor agonist SKF38393 (5, 10, and 20 mg/kg) or the D2 DA receptor agonist quinpirole (0.25, 0.5, and 1.0 mg/kg) did not improve the establishment of CPP following METH neurotoxicity. However, immediate but not delayed NAC administration (50 and 100 mg/kg) enhanced cocaine CPP following METH neurotoxicity and had no effect on control CPP. The levels of the reduced form of glutathione (GSH) in striatum, amygdala, hippocampus and frontal cortex were significantly lower in METH-treated mice compared to control during the period of CPP training. Acute and repeated administration of NAC to METH-treated mice restored the decreased brain GSH but had no effect on controls. Results suggest that METH-induced dopaminergic neurotoxicity is associated with impairment of consolidation of learned place preference, and that this impairment is improved by immediate posttraining administration of the glutathione precursor NAC and not by D1 or D2 DA receptor agonists. Restoration of brain glutathione levels immediately post-training may facilitate the consolidation process.

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Section: Introductionmentioning

confidence: 66%

Impairment in Consolidation of Learned Place Preference Following Dopaminergic Neurotoxicity in Mice is Ameliorated by N-acetylcysteine but not D1 and D2 Dopamine Receptor Agonists

Achat-Mendes

Anderson

Itzhak

2006

Neuropsychopharmacol

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“…Furthermore, reduced dopaminergic signaling in the NAc is associated with emotional signs of nicotine withdrawal (Cryan et al, 2003;Paterson et al, 2007). Further confirmation that the mesolimbic dopaminergic system contributes to withdrawal from other addictive drugs would cohere with a growing body of literature demonstrating that it is also involved in a wide variety of aversive behaviors, including conditioned place aversion (Acquas et al, 1989;Calcagnetti and Schechter, 1991;Schechter and Meechan, 1994;Liu et al, 2008), fear conditioning (Borowski and Kokkinidis, 1996;Nader and LeDoux, 1999;Pezze and Feldon, 2004;Fadok et al, 2009;Muschamp et al, 2011), anxiety (Fride and Weinstock, 1988;Barrot et al, 2002;Barrot et al, 2005;Meloni et al, 2006;Rezayof et al, 2009;Richard and Berridge, 2011;Zweifel et al, 2011), intrinsic aversion to gustatory cues (Roitman et al, 2008), conditioned taste aversion Fenu et al, 2001), responses to stress (Geyer and Segal, 1974;Herman et al, 1982;Inglis and Moghaddam, 1999;Belda and Armario, 2009), and responses to nociceptive stimulation (Gear et al, 1999;Becerra et al, 2001;Barrot et al, 2002).…”

Section: Discussionmentioning

confidence: 91%

Increased Dopamine Receptor Activity in the Nucleus Accumbens Shell Ameliorates Anxiety during Drug Withdrawal

Radke¹,

Gewirtz

2012

Neuropsychopharmacol

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A number of lines of evidence suggest that negative emotional symptoms of withdrawal involve reduced activity in the mesolimbic dopamine system. This study examined the contribution of dopaminergic signaling in structures downstream of the ventral tegmental area to withdrawal from acute morphine exposure, measured as potentiation of the acoustic startle reflex. Systemic administration of the general dopamine receptor agonist apomorphine or a cocktail of the D1-like receptor agonist SKF82958 and the D2-like receptor agonist quinpirole attenuated potentiated startle during morphine withdrawal. This effect was replicated by apomorphine infusion into the nucleus accumbens shell. Finally, apomorphine injection was shown to relieve startle potentiation during nicotine withdrawal and conditioned place aversion to morphine withdrawal. These results suggest that transient activation of the ventral tegmental area mesolimbic dopamine system triggers the expression of anxiety and aversion during withdrawal from multiple classes of abused drugs.

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“…We focused on the consolidation of classically conditioned fear responses to auditory cues because this form of learning was shown to cause synaptic plasticity in a widely distributed network of structures, including different amygdala nuclei (BLA and central amygdala) (28)(29)(30)(31), multiple stages of the auditory pathways (32,33), Hi (34), and mPFC (35). Thus, auditory fear conditioning constitutes an ideal model to study the role of sleep activity in system-level memory consolidation.…”

Section: Resultsmentioning

confidence: 99%

Coherent amygdalocortical theta promotes fear memory consolidation during paradoxical sleep

Popa

Duvarci

Popescu

et al. 2010

Proc. Natl. Acad. Sci. U.S.A.

297

237

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Brain activity in sleep plays a crucial role in memory consolidation, an offline process that determines the long-term strength of memory traces. Consolidation efficacy differs across individuals, but the brain activity dynamics underlying these differences remain unknown. Here, we studied how interindividual variability in fear memory consolidation relates to neural activity in brain structures that participate in Pavlovian fear learning. From the end of training to testing 24 h later, some rats showed increased and others decreased conditioned fear responses. We found that overnight bidirectional changes in fear memory were selectively correlated with modifications in theta coherence between the amygdala, medial prefrontal cortex, and hippocampus during paradoxical sleep. Thus, our results suggest that theta coordination in the limbic system may influence interindividual differences in memory consolidation of aversive experiences.amygdala | fear conditioning | prefrontal cortex | hippocampus | Granger causality R ecently formed memories undergo a period of consolidation (1, 2), and neuronal activity taking place during sleep is thought to play a critical role in this process (3-7). Consolidation of emotional memories determines their long-term retention, and interindividual variations in memory performance have been related to various factors affecting consolidation, including neuromodulatory transmission (8), levels of circulating stress hormones (9), or genetic factors (10). Several strongly interconnected brain structures are involved in the formation and maintenance of emotional memories, including the hippocampus (Hi), medial prefrontal cortex (mPFC), and basolateral amygdala (BLA) (11-13). The latter structure in particular was shown to mediate the facilitating effects of emotions on memory consolidation (14). Indeed, we form more vivid and enduring memories for emotionally arousing experiences (15). Via the release of peripheral stress hormones (16), emotional arousal causes long-lasting increases in the firing rate of BLA neurons (17), and pharmacologic manipulations that prevent this increased activity interfere with memory for events that took place shortly before, in many learning tasks (18). Importantly, in most learning paradigms, the same interventions performed shortly before testing long-term memory recall have no effect, indicating that the BLA can facilitate the consolidation of memories in other brain structures (14,18).Potentially related to the facilitation of emotional memories by BLA activity, various lines of evidence implicate posttraining paradoxical sleep (PS) in memory consolidation (6,19). These include PS reactivation of brain areas implicated in prior learning (20) and spontaneous replay of waking activity patterns during PS (21). In fact, it was suggested that the distinct pattern of neuronal activity occurring during PS favors memory consolidation (4,22) and that emotional memories are particularly susceptible to this effect (5, 23). Indeed, after fear conditioning, the respons...

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Mesolimbic dopaminergic pathways in fear conditioning

Cited by 455 publications

References 260 publications

Impairment in Consolidation of Learned Place Preference Following Dopaminergic Neurotoxicity in Mice is Ameliorated by N-acetylcysteine but not D1 and D2 Dopamine Receptor Agonists

Impairment in Consolidation of Learned Place Preference Following Dopaminergic Neurotoxicity in Mice is Ameliorated by N-acetylcysteine but not D1 and D2 Dopamine Receptor Agonists

Increased Dopamine Receptor Activity in the Nucleus Accumbens Shell Ameliorates Anxiety during Drug Withdrawal

Coherent amygdalocortical theta promotes fear memory consolidation during paradoxical sleep

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