Stress Enables Synaptic Depression in CA1 Synapses by Acute and Chronic Morphine: Possible Mechanisms for Corticosterone on Opiate Addiction

Yang, Yilin; Zheng, Xiang; Wang, Yongfu; Cao, Jun; Dong, Zhifang; Cai, Jinhua; Song, Nan; Xu, Lin

doi:10.1523/jneurosci.5544-03.2004

Cited by 73 publications

(83 citation statements)

References 85 publications

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“…3 A, B, and E). Although prolonged low-frequency stimulation (LFS; 1 Hz for 15 min) does not induce LTP or LTD in adult rats (26,31,45,46), we found that LFS induced a small LTP in WT mice but not in CKO mice (Fig. 4 A, B, and E).…”

Section: Cko Mice Show Fast Acquisition and Enhanced Fearmentioning

confidence: 68%

Enhanced contextual fear memory in central serotonin-deficient mice

Dai

Han

Tian

et al. 2008

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

123

122

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Central serotonin (5-HT) dysregulation contributes to the susceptibility for mental disorders, including depression, anxiety, and posttraumatic stress disorder, and learning and memory deficits. We report that the formation of hippocampus-dependent spatial memory is compromised, but the acquisition and retrieval of contextual fear memory are enhanced, in central 5-HT-deficient mice. Genetic deletion of serotonin in the brain was achieved by inactivating Lmx1b selectively in the raphe nuclei of the brainstem, resulting in a near-complete loss of 5-HT throughout the brain. These 5-HT-deficient mice exhibited no gross abnormality in brain structures and had normal locomotor activity. Spatial learning in the Morris water maze was unaffected, but the retrieval of spatial memory was impaired. In contrast, contextual fear learning and memory induced by foot-shock conditioning was markedly enhanced, but this enhancement could be prevented by intracerebroventricular administration of 5-HT. Foot shock impaired longterm potentiation and facilitated long-term depression in hippocampal slices in WT mice but had no effect in 5-HT-deficient mice. Furthermore, bath application of 5-HT in 5-HT-deficient mice restored foot shock-induced alterations of hippocampal synaptic plasticity. Thus, central 5-HT regulates hippocampus-dependent contextual fear memory, and 5-HT modulation of hippocampal synaptic plasticity may be the underlying mechanism. The enhanced fear memory in 5-HT-deficient mice supports the notion that 5-HT deficiency confers susceptibility to posttraumatic stress disorder in humans.hippocampus ͉ long-term depression ͉ long-term potentiation ͉ anxiety T he neurotransmitter serotonin (5-HT) exerts a wide spectrum of actions in the nervous system by modulating neural development, synaptic plasticity, pain sensation, rhythm, food intake, and a variety of behaviors (1-4). It has been proposed that perturbation of the 5-HT level in the brain contributes to depression and anxiety, and posttraumatic stress disorder (PTSD) (5-8), which are often accompanied by learning and memory deficits (9-11). The hippocampus is known to be critical for the formation of spatial and contextual fear memories (12-15), and the retrieval of hippocampus-dependent memories was found to be impaired in patients with depression and PTSD (16)(17)(18). Recent studies have also implicated the hippocampus as one of the primary sites for antidepressants (6,(19)(20)(21)(22)(23). Aversive stimuli such as foot shock that led to anxiety, depression, and fear memory in rodents also altered activity-dependent hippocampal synaptic plasticity (24)(25)(26)(27)(28)(29). Because the modulation of 5-HT activity altered hippocampal long-term potentiation (LTP) and long-term depression (LTD) (30-32), it is possible that perturbation of 5-HT level in the brain may affect hippocampusdependent learning and memory, and changes in hippocampal synaptic plasticity may also contribute to mental disorders, including anxiety and fear memory.Inhibitors of 5-HT biosynthesis that...

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Section: Cko Mice Show Fast Acquisition and Enhanced Fearmentioning

confidence: 68%

Enhanced contextual fear memory in central serotonin-deficient mice

Dai

Han

Tian

et al. 2008

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

123

122

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“…LTD is an electrical correlate of the weakening of the connection between two neurons, thus leading to long-term reduction in the efficacy of neuronal synapsis as a consequence of a decrease in the density of postsynaptic receptors. Studies have shown that both acute and chronic stress [Yang et al, 2004;Holderbach et al, 2007], including exposure to predators [Kuzmiski et al, 2010;Kim and Diamond, 2002], can lead to LTD. LTD has also been associated with synaptic plasticity and memory formation [Bear, 1999;Malleret et al, 2010;Kim and Diamond, 2002]. Importantly, our study also identified many genes and biological pathways that have not been previously reported.…”

Section: Discussionmentioning

confidence: 99%

Brain Transcriptomic Response of Threespine Sticklebacks to Cues of a Predator

Sanogo

Hankison²,

Band³

et al. 2011

Brain Behav Evol

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Predation pressure represents a strong selective force that influences the development and evolution of living organisms. An increasing number of studies have shown that both environmental and social factors, including exposure to predators, substantially shape the structure and function of the brain. However, our knowledge about the molecular mechanisms underlying the response of the brain to environmental stimuli is limited. In this study, we used whole-genome comparative oligonucleotide microarrays to investigate the brain transcriptomic response to cues of a predator in the threespine stickleback, Gasterosteus aculeatus. We found that repeated exposure to olfactory, visual and tactile cues of a predator (rainbow trout, Oncorrhynchus mykiss) for 6 days resulted in subtle but significant transcriptomic changes in the brain of sticklebacks. Gene functional analysis and gene ontology enrichment revealed that the majority of the transcripts differentially expressed between the fish exposed to cues of a predator and the control group were related to antigen processing and presentation involving the major histocompatibility complex, transmission of synaptic signals, brain metabolic processes, gene regulation and visual perception. The top four identified pathways were synaptic long-term depression, RAN signaling, relaxin signaling and phototransduction. Our study demonstrates that exposure of sticklebacks to cues of a predator results in the activation of a wide range of biological and molecular processes and lays the foundation for future investigations on the molecular factors that modulate the function and evolution of the brain in response to stressors.

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“…Experience with stressful events provokes neuroendocrine responses as well as changes in neurotransmitter systems (Koob, 2006), and drug abuse is related to neurobiological responses to stress, including the release of the glucocorticoid stress hormone corticosterone (Martinelli and Piazza, 2002;Yang, et al, 2004;Le et al, 2005), and changes in monoamine neurotransmitter activity (Heinz et al, 2002;Kalivas and McFarland, 2003;Zhang and Kosten, 2005;Salomon et al, 2006;Sorge and Stewart, 2005). This section reviews evidence that sign-tracking procedures induce changes in corticosterone levels and monoamine neurotransmitters that resemble the stressrelated responses known to accompany alcohol and drug abuse.…”

Section: Stress-related Effectsmentioning

confidence: 99%

Behavioral characteristics and neurobiological substrates shared by Pavlovian sign-tracking and drug abuse

Tomie

Grimes

Pohorecky

2008

Brain Research Reviews

153

134

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Drug abuse researchers have noted striking similarities between behaviors elicited by Pavlovian signtracking procedures and prominent symptoms of drug abuse. In Pavlovian sign-tracking procedures, repeated paired presentations of a small object (conditioned stimulus, CS) with a reward (unconditioned stimulus, US) elicits a conditioned response (CR) that typically consists of approaching the CS, contacting the CS, and expressing consummatory responses at the CS. Signtracking CR performance is poorly controlled and exhibits spontaneous recovery and long-term retention, effects that resemble relapse. Sign-tracking resembles psychomotor activation, a syndrome of behavioral responses evoked by addictive drugs, and the effects of sign-tracking on corticosterone levels and activation of dopamine pathways resemble the neurobiological effects of abused drugs. Finally, the neurobiological profile of individuals susceptible to sign-tracking resembles the pathophysiological profile of vulnerability to drug abuse, and vulnerability to sign-tracking predicts vulnerability to impulsive responding and alcohol self-administration. Implications of sign-tracking for models of drug addiction are considered.

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Stress Enables Synaptic Depression in CA1 Synapses by Acute and Chronic Morphine: Possible Mechanisms for Corticosterone on Opiate Addiction

Cited by 73 publications

References 85 publications

Enhanced contextual fear memory in central serotonin-deficient mice

Enhanced contextual fear memory in central serotonin-deficient mice

Brain Transcriptomic Response of Threespine Sticklebacks to Cues of a Predator

Behavioral characteristics and neurobiological substrates shared by Pavlovian sign-tracking and drug abuse

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