Substance abuse, memory, and post-traumatic stress disorder

Tipps, Megan E.; Raybuck, Jonathan D.; Lattal, K. Matthew

doi:10.1016/j.nlm.2013.12.002

Cited by 51 publications

(37 citation statements)

References 203 publications

(279 reference statements)

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“…These data support the further use and development of noradrenergic agents for the treatment of PTSD, and are in strong accordance with the demonstrated efficacy of prazosin in both preclinical models (Olson et al , 2011) and PTSD patient populations (Raskind et al , 2003) (Krystal and Neumeister, 2009). Finally, excessive alcohol exposure and dependence itself may contribute to dysregulated signaling in the PFC (George et al , 2012; Kim et al , 2014), leading to the development or exacerbation of PTSD-associated symptoms in rodents (Holmes et al , 2012), consistent with the human literature (Tipps et al , 2014; Perrin et al , 2014). …”

Section: Recent Neurobiological Insights Gained From Animal Models Ofsupporting

confidence: 75%

Animal models of post-traumatic stress disorder and recent neurobiological insights

Whitaker

Gilpin²,

Edwards

2014

Behavioural Pharmacology

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Section: Recent Neurobiological Insights Gained From Animal Models Ofsupporting

confidence: 75%

Animal models of post-traumatic stress disorder and recent neurobiological insights

Whitaker

Gilpin²,

Edwards

2014

Behavioural Pharmacology

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“…Pavlovian fear conditioning, in which a neutral stimulus (conditioned stimulus; CS) is paired with an aversive stimulus (unconditioned stimulus; US) (Blanchard and Blanchard 1969; Fanselow, 1980), has been used to investigate the effects of alcohol on learning and memory (reviewed in Tipps et al, 2014a). Although much work has been done regarding the effects of alcohol intoxication on fear conditioning (e.g., Gould, 2003; Gulick and Gould, 2007; Lattal, 2007), the potential impact of acute withdrawal on this model is unclear.…”

Section: Introductionmentioning

confidence: 99%

Acute Ethanol Withdrawal Impairs Contextual Learning and Enhances Cued Learning

Tipps

Raybuck

Buck

et al. 2015

Alcoholism Clin & Exp Res

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Background Alcohol affects many of the brain regions and neural processes that support learning and memory, and these effects are thought to underlie, at least in part, the development of addiction. Although much work has been done regarding the effects of alcohol intoxication on learning and memory, little is known about the effects of acute withdrawal from a single alcohol exposure. Methods We assess the effects of acute ethanol withdrawal (6 h post-injection with 4 g/kg ethanol) on two forms of fear conditioning (delay and trace fear conditioning) in C57BL/6J and DBA/2J mice. The influence of a number of experimental parameters (pre- and post-training withdrawal exposure; foreground/background processing; training strength; non-associative effects) is also investigated. Results Acute ethanol withdrawal during training had a bidirectional effect on fear conditioned responses, decreasing contextual responses and increasing cued responses. These effects were apparent for both trace and delay conditioning in DBA/2J mice and for trace conditioning in C57BL/6J mice; however, C57BL/6J mice were selectively resistant to the effects of acute withdrawal on delay cued responses. Conclusions Our results show that acute withdrawal from a single, initial ethanol exposure is sufficient to alter long-term learning in mice. In addition, the differences between the strains and conditioning paradigms used suggest that specific learning processes can be differentially affected by acute withdrawal in a manner that is distinct from the reported effects of both alcohol intoxication and withdrawal following chronic alcohol exposure. Thus, our results suggest a unique effect of acute alcohol withdrawal on learning and memory processes.

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“…In humans, a blood ethanol concentration of 80 mg/dl is considered an intoxicating dose of ethanol, whereas in heavy drinkers and alcoholics blood ethanol concentrations can exceed 300 mg/dl (Perper et al, 1986). These concentrations of ethanol cause cognitive dysfunction including memory impairments in humans and animal models and, in animal models, altered synaptic function in the hippocampus and other brain regions (reviewed in (Tipps et al, 2014; White, 2003; Zorumski et al, 2014)). Brain levels of ethanol have been shown to correspond to blood levels in animal models (Gilpin et al, 2009; Smolen and Smolen, 1989).…”

Section: Methodsmentioning

confidence: 99%

Transgenic mice with increased astrocyte expression of IL-6 show altered effects of acute ethanol on synaptic function

et al. 2016

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A growing body of evidence has revealed that resident cells of the central nervous system (CNS), and particularly the glial cells, comprise a neuroimmune system that serves a number of functions in the normal CNS and during adverse conditions. Cells of the neuroimmune system regulate CNS functions through the production of signaling factors, referred to as neuroimmune factors. Recent studies show that ethanol can activate cells of the neuroimmune system, resulting in the elevated production of neuroimmune factors, including the cytokine interleukin-6 (IL-6). Here we analyzed the consequences of this CNS action of ethanol using transgenic mice that express elevated levels of IL-6 through increased astrocyte expression (IL-6-tg) to model the increased IL-6 expression that occurs with ethanol use. Results show that increased IL-6 expression induces neuroadaptive changes that alter the effects of ethanol. In hippocampal slices from non-transgenic (non-tg) littermate control mice, synaptically evoked dendritic field excitatory postsynaptic potential (fEPSP) and somatic population spike (PS) at the Schaffer collateral to CA1 pyramidal neuron synapse were reduced by acute ethanol (20 or 60 mM). In contrast, acute ethanol enhanced the fEPSP and PS in hippocampal slices from IL-6 tg mice. Long-term synaptic plasticity of the fEPSP (i.e., LTP) showed the expected dose-dependent reduction by acute ethanol in non-tg hippocampal slices, whereas LTP in the IL-6 tg hippocampal slices was resistant to this depressive effect of acute ethanol. Consistent with altered effects of acute ethanol on synaptic function in the IL-6 tg mice, EEG recordings showed a higher level of CNS activity in the IL-6 tg mice than in the non-tg mice during the period of withdrawal from an acute high dose of ethanol. These results suggest a potential role for neuroadaptive effects of ethanol-induced astrocyte production of IL-6 as a mediator or modulator of the actions of ethanol on the CNS, including persistent changes in CNS function that contribute to cognitive dysfunction and the development of alcohol dependence.

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Substance abuse, memory, and post-traumatic stress disorder

Cited by 51 publications

References 203 publications

Animal models of post-traumatic stress disorder and recent neurobiological insights

Animal models of post-traumatic stress disorder and recent neurobiological insights

Acute Ethanol Withdrawal Impairs Contextual Learning and Enhances Cued Learning

Transgenic mice with increased astrocyte expression of IL-6 show altered effects of acute ethanol on synaptic function

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