Novelty seeking behavior in the rat is dependent upon the integrity of the noradrenergic system

Sara, Susan J.; Dyon-Laurent, Carole; Hervé, Anne

doi:10.1016/0926-6410(95)90007-1

Cited by 109 publications

(65 citation statements)

References 27 publications

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“…However, we cannot rule out the possibility that some memory consolidation occurs during the CS presentation sessions and the adrenergic system modulates this fast consolidation. Interestingly, some have suggested that adrenergic activity promotes memory formation by signaling novelty (Sara et al 1994(Sara et al , 1995, not necessarily emotionality, a notion that is also consistent with our observed drug effects, assuming that, after learning of the CS-US association, nondelivery of the expected US is more novel than reactivating the contingent CS-US association with brief exposures.…”

Section: Learning and Memory 183supporting

confidence: 74%

Adrenergic Transmission Facilitates Extinction of Conditional Fear in Mice

Cain¹,

Blouin²,

Barad³

2004

Learn. Mem.

191

178

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Extinction of classically conditioned fear, like its acquisition, is active learning, but little is known about its molecular mechanisms. We recently reported that temporal massing of conditional stimulus (CS) presentations improves extinction memory acquisition, and suggested that temporal spacing was less effective because individual CS exposures trigger two opposing processes: (1) fear extinction, which is favored by CS massing, and (2) fear incubation (increase), which is favored by spacing. We here report the effects of manipulating the adrenergic system during massed or spaced CS presentations in fear-conditioned mice. We administered yohimbine (5 mg/kg), an ␣ 2 -receptor antagonist, or propranolol (10 mg/kg), a ␤-receptor antagonist, systemically prior to CS presentation sessions and recorded both short-and long-term changes in conditional freezing. Yohimbine treatment facilitated extinction of both cue and context fear with massed protocols. When given before spaced CS presentations, propranolol led to a persistent incubation of cue fear, whereas yohimbine led to persistent extinction, compared with vehicle-treated animals, which showed no change in fear. These results suggest that norepinephrine positively modulates the formation of fear extinction memories in mice. They also provide clear evidence that spaced CS presentations trigger both fear-reducing (extinction) and fear-increasing (incubation) mechanisms.

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Section: Learning and Memory 183supporting

confidence: 74%

Adrenergic Transmission Facilitates Extinction of Conditional Fear in Mice

Cain¹,

Blouin²,

Barad³

2004

Learn. Mem.

191

178

View full text Add to dashboard Cite

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“…We will first consider results from the hole-board test, which is typically used as an index of exploratory behavior (Makanjuola et al, 1977), particularly with respect to entries into holes not previously sampled. Behavior in the hole-board test was reported previously to be altered by several compounds acting on the dopaminergic and noradrenergic systems (Makanjuola et al, 1977;Sara et al, 1995). Serotonin has also been implicated in exploratory behavior, as shown by reduced head dipping behavior in rats treated chronically with the 5-HT reuptake inhibitor clomipramine (García-Marquez et al, 1987) as well as impaired habituation of this response in animals given prior administration of the serotonergic neurotoxin 5,7-DHT (Mogensen et al, 2003).…”

Section: Discussionmentioning

confidence: 96%

Dissociation of the Neurochemical and Behavioral Toxicology of MDMA (‘Ecstasy’) by Citalopram

Piper

Fraiman

Owens

et al. 2007

Neuropsychopharmacol

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High or repeated doses of the recreational drug 3,4-methylenedioxymethamphetamine (MDMA, or 'Ecstasy') produce long-lasting deficits in several markers of serotonin (5-HT) system integrity and also alter behavioral function. However, it is not yet clear whether MDMA-induced serotonergic neurotoxicity is responsible for these behavioral changes or whether other mechanisms are involved. The present experiment tested the hypothesis that blocking serotonergic neurotoxicity by pretreatment with the selective 5-HT reuptake inhibitor citalopram will also prevent the behavioral and physiological consequences of an MDMA binge administration. Male, SpragueDawley rats (N ¼ 67) received MDMA (4 Â 10 mg/kg) with or without citalopram (10 mg/kg) pretreatment. Core temperature, ejaculatory response, and body weight were monitored during and immediately following drug treatments. A battery of tests assessing motor, cognitive, exploratory, anxiety, and social behaviors was completed during a 10-week period following MDMA administration. Brain tissue was collected at 1 and 10 weeks after drug treatments for measurement of regional 5-HT transporter binding and (for the 1-week samples) 5-HT and 5-HIAA concentrations. Citalopram pretreatment blocked MDMA-related reductions in aggressive and exploratory behavior measured in the social interaction and hole-board tests respectively. Such pretreatment also had the expected protective effect against MDMA-induced 5-HT neurotoxicity at 1 week following the binge. In contrast, citalopram did not prevent most of the acute effects of MDMA (eg hyperthermia and weight loss), nor did it block the decreased motor activity seen in the binge-treated animals 1 day after dosing. These results suggest that some of the behavioral and physiological consequences of a high-dose MDMA regimen in rats are mediated by mechanisms other than the drug's effects on the serotonergic system. Elucidation of these mechanisms requires further study of the influence of MDMA on other neurotransmitter systems.

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“…Mice carrying a maternally derived targeted allele of the gene Nesp showed a reduced propensity to explore a novel environment. Nesp is expressed only maternally, and is found in discrete locations in the brain including the noradrenergic locus coeruleus (Plagge et al 2005), a key brain area in the control of reactivity to novel stimuli (Sara et al 1995;Cole et al 1988). In mice at least, it appears that the paternal interest may be to limit risk-taking (by silencing the paternal copy of Nesp), while it is in the maternal interest to promote these behaviours.…”

Section: Sex-biased Dispersal Intragenomic Conflict and Social Behavmentioning

confidence: 99%

Genomic imprinting and the social brain

Isles

Davies

Wilkinson

2006

Phil. Trans. R. Soc. B

109

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Genomic imprinting refers to the parent-of-origin-specific epigenetic marking of a number of genes. This epigenetic mark leads to a bias in expression between maternally and paternally inherited imprinted genes, that in some cases results in monoallelic expression from one parental allele. Genomic imprinting is often thought to have evolved as a consequence of the intragenomic conflict between the parental alleles that occurs whenever there is an asymmetry of relatedness. The two main examples of asymmetry of relatedness are when there is partiality of parental investment in offspring (as is the case for placental mammals, where there is also the possibility of extended postnatal care by one parent), and in social groups where there is a sex-biased dispersal. From this evolutionary starting point, it is predicted that, at the behavioural level, imprinted genes will influence what can broadly be termed bonding and social behaviour. We examine the animal and human literature for examples of imprinted genes mediating these behaviours, and divide them into two general classes. Firstly, mother-offspring interactions (suckling, attachment and maternal behaviours) that are predicted to occur when partiality in parental investment in early postnatal offspring occurs; and secondly, adult social interactions, when there is an asymmetry of relatedness in social groups. Finally, we return to the evolutionary theory and examine whether there is a pattern of behavioural functions mediated by imprinted genes emerging from the limited data, and also whether any tangible predictions can be made with regards to the direction of action of genes of maternal or paternal origin.

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Novelty seeking behavior in the rat is dependent upon the integrity of the noradrenergic system

Cited by 109 publications

References 27 publications

Adrenergic Transmission Facilitates Extinction of Conditional Fear in Mice

Adrenergic Transmission Facilitates Extinction of Conditional Fear in Mice

Dissociation of the Neurochemical and Behavioral Toxicology of MDMA (‘Ecstasy’) by Citalopram

Genomic imprinting and the social brain

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