Decreased experimental anxiety and voluntary ethanol consumption in rats following central but not basolateral amygdala lesions

Möller, Christian; Wiklund, Lisa; Sommer, Wolfgang; Thorsell, Annika; Heilig, Markus

doi:10.1016/s0006-8993(97)00308-9

Cited by 212 publications

(167 citation statements)

References 41 publications

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“…In the absence of a challenge, cell body-selective ibotenic acid lesions of central, but not basolateral, amygdala produce anti-conflict effects in the punished drinking procedure, while leaving plus-maze behavior unaffected. However, when plus-maze testing was preceded by a 1-hr restraint stress, an anxiolytic-like effect of central amygdala lesions became apparent in the plus-maze (Möller et al 1997). In the present study, we therefore examined the role of 5,7-DHT amygdala lesions on plus-maze behavior under both unstressed and stressed conditions.…”

Section: Discussionmentioning

confidence: 99%

“…Thus, modulatory effect of central serotonin on ethanol intake are likely to be mediated by brain structures other than the amygdala. Furthermore, basal levels of experimental anxiety, as approached by the elevated plus-maze, have been reported to predict alcohol preference (Spanagel et al 1995), and decreased voluntary ethanol consumption was observed in central amygdala lesioned rats, a treatment which produces anxiolyticlike effects (Möller et al 1997). Since both plus-maze behavior and ethanol preference were unchanged by our 5,7-DHT lesions, while direct lesions of the central nucleus have been shown to affect both these behaviors, we find here further support for a conclusion that central nucleus function is not a major regulatory target for the serotonergic input to the amygdala.…”

Section: Discussionmentioning

confidence: 99%

“…A modified Vogel's drinking test (Vogel et al 1971) was used as recently described (Möller et al 1997). Training and testing of animals was performed in sound-attenuated operant chambers (Med Associates, St Albans, VT) equipped with a grid floor of stainless steel bars and a drinking bottle containing 5% (w/v) glucose solution.…”

Section: Punished Drinking Testmentioning

confidence: 99%

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Local 5,7-Dihydroxytryptamine Lesions of Rat Amygdala Release of Punished Drinking, Unaffected Plus-Maze Behavior and Ethanol Consumption

Sommer

2001

Neuropsychopharmacology

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Accumulating data indicate that serotonin uptake inhibitors are clinically effective for most if not all anxiety disorders (Perse et al. 1987;Den Boer and Westenberg 1988;Katzelnick et al. 1995;Rocca et al. 1997;Ballenger et al. 1998). While this provides renewed evidence for an involvement of 5-HT transmission in mechanisms of fear and anxiety, the role of serotonergic transmission in this context is not well understood. Experimental findings in animal studies aimed at elucidating serotonergic mechanisms in fear and anxiety have been inconsistent, possibly due to the diversity of central 5-HT systems.Thus, a 'classical hypothesis' states that increased 5-HT transmission is anxiogenic and reduction is anxiolytic. This is supported by data from animal models based on fear-induced response inhibition, such as conflict tests, for example. However, in animal models which rely on suppression of exploratory behavior by an innate fear stimulus, such as the elevated plus-maze,

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Local 5,7-Dihydroxytryptamine Lesions of Rat Amygdala Release of Punished Drinking, Unaffected Plus-Maze Behavior and Ethanol Consumption

Sommer

2001

Neuropsychopharmacology

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“…This is an important consideration since specific nuclei in the amygdala and in other nearby brain regions appear to play differing roles in various models of anxiety and effects of anxiolytics (Pesold and Treit 1995;Gonzalez et al 1996;Davis et al 1997;Moller et al 1997).…”

Section: Discussionmentioning

confidence: 99%

Overexpression of Proenkephalin in the Amygdala Potentiates the Anxiolytic Effects of Benzodiazepines

Wen

Wilson

2000

Neuropsychopharmacology

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To elucidate the role of opioid peptides in control of the anxiety-like behavior and anxiety-reducing actions of benzodiazepines, a recombinant, replication-defective herpes virus (SHPE) carrying human preproenkephalin cDNA was delivered to rat amygdala. Viral infection resulted in a strong, localized transgene expression after 2-4 days which diminished after one week. Anxiety-like behavior and the anxiolytic effect of diazepam were assessed three days afterIn addition to its well known role in mediating fear and anxiety responses (Davis et al. 1994), the amygdala may also be a key neural substrate for the anxiolytic actions of benzodiazepines. Benzodiazepines (BZs) are believed to induce their anxiolytic properties by binding to GABA/benzodiazepine receptors in the brain (Haefely 1990). In addition, the amygdala has a high density of GABA/benzodiazepine receptors (Young and Kuhar 1980;Richards and Mohler 1984). Local infusion of benzodiazepine agonists into the amygdala produces anxiolytic effects which can be blocked by co-administration of GABA A or benzodiazepine antagonists (Scheel-Kruger and Petersen 1982;Petersen et al. 1985; Treit 1994, 1995). Furthermore, the anxietyreducing actions of systemic benzodiazepines can be blocked by intra-amygdala injection of GABA/benzodiazepine antagonists (Sanders and Shekhar 1995).The amygdala also has high levels of endogenous opioid peptides and opioid receptors (Loughlin et al. 1995), and opioid mechanisms have been implicated in many biological functions, including nociception, memory, and fear conditioning (Good and Westbrook 1995;McGaugh et al. 1996;Valverde et al. 1996). A partial anxiolytic action has been reported following microinjection of morphine into amygdala (File and Rodgers 1979).Although opioid agonists are not used as anxiolytics in general, recent evidence strongly indicates a role for endogenous opioid peptides in the control of stress and anxiety (Olson et al. 1996). Preproenkephalin knockout (Konig et al. 1996), and some novel -opioid agonists show anxiolytic properties (Privette and Terrian 1995). Several lines of evidence also indicate the involvement of endogenous opioid peptides in various aspects of benzodiazepine action, including their influences on food intake, locomotor activity, conflict, and anxiety-like behaviors (Millan and Duka 1981;Cooper 1983;Nowakowska and Chodera 1990). Interestingly, clinical studies suggest interactions between responses to benzodiazepines and opioids in humans (Darke et al. 1993). The anxiolytic effects of benzodiazepines can be blocked by opioid antagonists in both humans and laboratory animals (Billingsley and Kubena 1978;Koob et al. 1980;Duka et al. 1981Duka et al. , 1982Agmo et al 1995;Tsuda et al. 1996).Prior studies using herpes virus-mediated gene transfer demonstrated that overexpression of proenkephalin in amygdala produced antinociceptive effects, and illustrated the usefulness of this methodology for examining the role of neuropeptides in behavioral responses (Kang et al. 1998). To investigate if mo...

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“…Opioid antagonists also block the anxiolytic effects of diazepam in humans (Duka et al, 1982). Although the role of opioid receptor systems in regulating the anxiolytic properties of ethanol has received less attention, there is evidence that this system mediates some of the motivational responses associated with ethanol administration (Wilson et al, 2003;Moller et al, 1997). Both high doses of morphine (Volpicelli et al, 1991) and intraventricular infusion of met-enkephalin (Ho and Rossi, 1982) decrease ethanol consumption in rats.…”

Section: Introductionmentioning

confidence: 99%

Microinjection of Naltrexone into the Central, but not the Basolateral, Amygdala Blocks the Anxiolytic Effects of Diazepam in the Plus Maze

Burghardt

Wilson

2005

Neuropsychopharmacol

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The amygdala is involved in behavioral and physiological responses to fear, and the anxiolytic properties of several drugs are localized to this region. Activation of endogenous opioid systems is known to occur in response to stress and a growing body of literature suggests that opioid systems regulate the properties of anxiolytic drugs. These experiments sought to elucidate the role of opioid receptors in the central (CeA) and basolateral (BLA) nuclei of the amygdala in regulating the anxiolytic properties of ethanol and diazepam. Male rats fitted with cannula received bilateral microinjections of the nonselective opioid receptor antagonist naltrexone (NAL) immediately followed by systemic delivery of either ethanol (1 g/kg) or diazepam (2 mg/kg) in the elevated plus maze. Both diazepam and ethanol decreased anxiety-like behavior. Delivery of NAL into the CeA blocked the anxiolytic properties of diazepam. Delivery of NAL into the BLA slightly increased open arm avoidance, but had no effect on the anxiolytic properties of diazepam. Microinjection of NAL into either nucleus failed to block the effects of ethanol. These results were specific to the anxiolytic properties of diazepam, since baseline behaviors were unaffected by microinjection of NAL. Microinjection of lidocaine produced results distinct from NAL and failed to block the anxiolytic actions of diazepam. These studies indicate distinct roles for opioid receptor systems in the CeA and BLA in regulating the anxiolytic properties of diazepam in the elevated plus maze. Further, opioid receptor systems in the CeA and BLA do not regulate the anxiolytic properties of ethanol in this test.

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Decreased experimental anxiety and voluntary ethanol consumption in rats following central but not basolateral amygdala lesions

Cited by 212 publications

References 41 publications

Local 5,7-Dihydroxytryptamine Lesions of Rat Amygdala Release of Punished Drinking, Unaffected Plus-Maze Behavior and Ethanol Consumption

Local 5,7-Dihydroxytryptamine Lesions of Rat Amygdala Release of Punished Drinking, Unaffected Plus-Maze Behavior and Ethanol Consumption

Overexpression of Proenkephalin in the Amygdala Potentiates the Anxiolytic Effects of Benzodiazepines

Microinjection of Naltrexone into the Central, but not the Basolateral, Amygdala Blocks the Anxiolytic Effects of Diazepam in the Plus Maze

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