Acute Ethanol Administration and Acute Allopregnanolone Administration Impair Spatial Memory in the Morris Water Task

Matthews, Douglas B.; Morrow, A. Leslie; Tokunaga, Sayaka; McDaniel, Janelle R.

doi:10.1097/00000374-200211000-00019

Cited by 32 publications

(38 citation statements)

References 45 publications

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“…The results from laboratory animal studies also demonstrate alcohol's impairing effects on cognition. Specifically, acute ethanol administration impaired hippocampus-dependent learning and memory in the Morris Water Maze (Markwiese et al 1998;Shimizu et al 1998;Matthews et al 2002;Berry and Matthews 2004), the radial arm maze (Matthews et al , 1999Vandergriff et al 1995;White et al 1997White et al , 1998, the sandbox maze (Rajendran and Spear 2004), and contextual fear conditioning (see Table 2 for the summary of acute ethanol's effects on hippocampus-dependent learning and memory) (Melia et al 1996;Gould 2003b;Gould and Lommock 2003;Wehner et al 2004;Gould 2007, 2008).…”

Section: Alcoholmentioning

confidence: 99%

Effects of drugs of abuse on hippocampal plasticity and hippocampus-dependent learning and memory: contributions to development and maintenance of addiction

2016

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It has long been hypothesized that conditioning mechanisms play major roles in addiction. Specifically, the associations between rewarding properties of drugs of abuse and the drug context can contribute to future use and facilitate the transition from initial drug use into drug dependency. On the other hand, the self-medication hypothesis of drug abuse suggests that negative consequences of drug withdrawal result in relapse to drug use as an attempt to alleviate the negative symptoms. In this review, we explored these hypotheses and the involvement of the hippocampus in the development and maintenance of addiction to widely abused drugs such as cocaine, amphetamine, nicotine, alcohol, opiates, and cannabis. Studies suggest that initial exposure to stimulants (i.e., cocaine, nicotine, and amphetamine) and alcohol may enhance hippocampal function and, therefore, the formation of augmented drug-context associations that contribute to the development of addiction. In line with the self-medication hypothesis, withdrawal from stimulants, ethanol, and cannabis results in hippocampus-dependent learning and memory deficits, which suggest that an attempt to alleviate these deficits may contribute to relapse to drug use and maintenance of addiction. Interestingly, opiate withdrawal leads to enhancement of hippocampus-dependent learning and memory. Given that a conditioned aversion to drug context develops during opiate withdrawal, the cognitive enhancement in this case may result in the formation of an augmented association between withdrawalinduced aversion and withdrawal context. Therefore, individuals with opiate addiction may return to opiate use to avoid aversive symptoms triggered by the withdrawal context. Overall, the systematic examination of the role of the hippocampus in drug addiction may help to formulate a better understanding of addiction and underlying neural substrates.Addiction is a major worldwide health problem that results in maladaptive behavioral changes, some that can last a lifetime. This behavioral plasticity, often times maladaptive, must be associated changes in neural plasticity. In fact, it has been noted multiple times that there is a high degree of overlap between the neurobiology of learning and memory and the neurobiology of addiction

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Section: Alcoholmentioning

confidence: 99%

Effects of drugs of abuse on hippocampal plasticity and hippocampus-dependent learning and memory: contributions to development and maintenance of addiction

2016

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“…A large body of evidence from multiple laboratories suggests that ethanol-induced elevations of GABAergic neuroactive steroids contribute to many behavioral effects of ethanol in rodents. Neuroactive steroids have been shown to modulate ethanol's anticonvulsant effects (VanDoren et al, 2000), sedation (Khisti et al, 2003), impairment of spatial memory (Morrow et al, 2001;Matthews et al, 2002), anxiolytic-like (Hirani et al, 2005) and antidepressant-like (Hirani et al, 2002) actions. Each of these behavioral responses is prevented by pretreatment with the biosynthesis inhibitor finasteride and/or by prior adrenalectomy.…”

Section: Neuroactive Steroids Mediate Ethanol Actionsmentioning

confidence: 99%

Recent developments in the significance and therapeutic relevance of neuroactive steroids — Introduction to the special issue

Morrow

2007

Pharmacology & Therapeutics

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The special issue heralds an exciting time in the field when the significance of neuroactive steroids in the regulation of inhibitory transmission is being realized and translated to new treatments for intractable neurologic and psychiatric conditions. In the past year, the binding sites for neuroactive steroids on γ-aminobutyric acid type A (GABA A ) receptors have been discovered and clinical trials for epilepsy and traumatic brain injury have been successful. New data in animal models points to the potential value of neuroactive steroids in other central nervous system (CNS) disorders including depression, schizophrenia, alcoholism, multiple sclerosis and other neurodegenerative conditions. How can one class of compounds have so many potential applications? The answer may lie in the ability of neuroactive steroids to regulate synaptic and extrasynaptic inhibitory transmission across brain, hypothalamic-pituitary-adrenal (HPA) axis function, inflammatory processes and myelin formation. The manuscripts in this issue of Pharmacology and Therapeutics will bring you up to date on the sites of neurosteroid actions, the systemic and molecular consequences of these actions and the potential therapeutic relevance of neuroactive steroid effects for CNS disease. These studies point to the opportunity for more translational research into potential therapeutic applications and evaluation of potential untoward side effects following long-term treatment.

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“…Numerous studies have investigated the effects of ETOH administration on animal models of learning and memory. In general, ETOH impairs spatial learning (Givens 1995;Matthews et al 2002;Boulouard et al 2002;Wright et al 2003;Gonenc et al 2005;Rajendran and Spear 2004), working memory (Gibson 1985;Melchior et al 1993;Givens and McMahon 1997;White et al 1997;Escher and Mittleman 2004), and avoidance (Bammer and Chesher 1982;Markel et al 1986;File and Mabbutt 1990;Melis et al 1996;Singh et al 2003) …”

Section: Introductionmentioning

confidence: 99%

Dissociation of the effects of ethanol on memory, anxiety, and motor behavior in mice tested in the plus-maze discriminative avoidance task

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Acute Ethanol Administration and Acute Allopregnanolone Administration Impair Spatial Memory in the Morris Water Task

Cited by 32 publications

References 45 publications

Effects of drugs of abuse on hippocampal plasticity and hippocampus-dependent learning and memory: contributions to development and maintenance of addiction

Effects of drugs of abuse on hippocampal plasticity and hippocampus-dependent learning and memory: contributions to development and maintenance of addiction

Recent developments in the significance and therapeutic relevance of neuroactive steroids — Introduction to the special issue

Dissociation of the effects of ethanol on memory, anxiety, and motor behavior in mice tested in the plus-maze discriminative avoidance task

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