The effects of long-term administration of rubidium or lithium on reactivity to stress and on dopamine output in the nucleus accumbens in rats

Gambarana, Carla; Ghiglieri, O; Masi, Flavio; Scheggi, Simona; Tagliamonte, A.; Montis, Maria Graziella De

doi:10.1016/s0006-8993(99)01286-x

Cited by 37 publications

(24 citation statements)

References 27 publications

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“…Rats exposed to a 3-week unavoidable stress protocol showed a clear-cut escape deficit and a significant decrease in DA output in the NAcS and mPFC, in agreement with previous results (Gambarana et al 1999a;Mangiavacchi et al 2001), but DA output was not modified in the CPu. Moreover, in the NAc of rats exposed to chronic stress, several adaptive modifications occured in the dopaminergic system, both at the pre-and post-synaptic levels.…”

Section: Discussionsupporting

confidence: 92%

Selective modifications in the nucleus accumbens of dopamine synaptic transmission in rats exposed to chronic stress

Scheggi

Leggio

Masi

et al. 2002

Journal of Neurochemistry

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Stressful events are accompanied by modifications in dopaminergic transmission in distinct brain regions. As the activity of the neuronal dopamine (DA) transporter (DAT) is considered to be a critical mechanism for determining the extent of DA receptor activation, we investigated whether a 3-week exposure to unavoidable stress, which produces a reduction in DA output in the nucleus accumbens shell (NAcS) and medial prefrontal cortex (mPFC), would affect DAT density and DA D 1 receptor complex activity in the NAcS, mPFC and caudate-putamen (CPu). Rats exposed to unavoidable stress showed a decreased DA output in the NAcS accompanied by a decrease in the number of DAT binding sites, and an increase in the number of DA D 1 binding sites and Vmax of SKF 38393-stimulated adenylyl cyclase. In the mPFC, stress exposure produced a decrease in DA output with no modification in DAT binding or in DA D 1 receptor complex activity. Moreover, in the CPu stress exposure induced no changes in DA output or in the other neurochemical variables examined. This study shows that exposure to a chronic unavoidable stress that produces a decrease in DA output in frontomesolimbic areas induced several adaptive neurochemical modifications selectively in the nucleus accumbens.

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Section: Discussionsupporting

confidence: 92%

Selective modifications in the nucleus accumbens of dopamine synaptic transmission in rats exposed to chronic stress

Scheggi

Leggio

Masi

et al. 2002

Journal of Neurochemistry

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“…That is, ALCAR treatment enabled stressed rats to learn the appetitive behavior and, in turn, VAB acquisition seemed to strengthen the protective effect of ALCAR in the development of escape deficit. The finding that VAB acquisition coincided with the recovery of avoidance competence was not completely unexpected, as rats chronically treated with lithium show an avoidance deficit similar to that of chronically stressed rats (Gambarana et al, 1999b), which disappears as a consequence of VAB acquisition (Masi et al, 2000). Thus, repeated exposure to a hedonic stimulus, contingently rewarding a specific behavioral pattern, induces the development of a motivated behavior in rats chronically treated with lithium or exposed to stress while treated with ALCAR.…”

Section: Discussionmentioning

confidence: 85%

“…In fact, rats that have acquired VAB and are then exposed to chronic stress develop an avoidance deficit while retaining VAB (Ghiglieri et al, 1997); moreover, they show a DA output in the NAcS similar to that of control rats, and higher than that of chronically stressed rats . Furthermore, long-term treatment with lithium induces an avoidance deficit and a significant decrease in DA output in the NAcS (Gambarana et al, 1999b), but it does not interfere with VAB acquisition (Masi et al, 2000). Thus, no correlation can be demonstrated between basal DA output and VAB acquisition, as both long-term stress exposure and lithium treatment significantly reduce basal DA output in mesolimbic areas (Gambarana et al, 1999a, b;Mangiavacchi et al, 2001), but only lithium-treated rats maintain the competence to acquire VAB (Masi et al, 2000).…”

Section: Introductionmentioning

confidence: 99%

Effects of Long-Term Acetyl-L-Carnitine Administration in Rats—II: Protection Against the Disrupting Effect of Stress on the Acquisition of Appetitive Behavior

Masi

Leggio

Nanni

et al. 2002

Neuropsychopharmacol

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Long-term acetyl-L-carnitine (ALCAR) administration prevents the development of escape deficit produced by acute exposure to unavoidable stress. However, it does not revert the escape deficit sustained by chronic stress exposure. Rats exposed to chronic stress show a low dopamine (DA) output in the nucleus accumbens shell (NAcS) and do not acquire an appetitive behavior sustained by the earning of vanilla sugar (VS) made contingent on the choice of one of the two divergent arms of a Y-maze (VS-sustained appetitive behavior, VAB), while control rats consistently do. The present study shows that ALCAR treatment in rats exposed to a 7-day stress protocol prevented a decrease in DA output in the NAcS and medial prefrontal cortex (mPFC) of rats, and that it strengthened the DA response to VS consummation in the same two areas. Moreover, rats treated with long-term ALCAR or exposed to chronic stress while treated with ALCAR acquired VAB as efficiently as control rats. Moreover, VAB acquisition in stressed rats treated with ALCAR coincided with the reversal of the deficits in escape and in dopaminergic transmission in the NAcS. Thus, repeated ALCAR treatment preserved the DA response to VS in chronically stressed rats and this effect appeared to be predictive of the rat's competence to acquire VAB.

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“…Therefore, this model is relevant to the study of antipsychotic medications, and dopamine itself, in the treatment of bipolar disorder. Lithium has been reported to affect the levels of synaptic dopamine in animal models; specifically, long-term administration of lithium alters dopamine levels or release, an effect that is not generally observed following short-term administration (Baptista et al, 1993;Beaulieu et al, 2004;Berggren, 1985;Corrodi et al, 1967;Dziedzicka-Wasylewska et al, 1996;Ferrie et al, 2005a, b;Friedman and Gershon, 1973;Gambarana et al, 1999). Most recently, Ferrie et al (2005a) have reported that 4 weeks of lithium administration decreases potassium-evoked dopamine release in the shell of the nucleus accumbens.…”

Section: Discussionmentioning

confidence: 99%

Strain Differences in Lithium Attenuation of d-Amphetamine-Induced Hyperlocomotion: A Mouse Model for the Genetics of Clinical Response to Lithium

Gould

O’Donnell

Picchini

et al. 2006

Neuropsychopharmacol

109

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Lithium attenuation of stimulant-induced hyperlocomotion is a rodent model that may be useful both to understand the mechanism of the therapeutic action of lithium and to develop novel lithium-mimetic compounds. To lay the foundation for future investigations into the neurobiology and genetics of lithium as a therapeutic agent, we studied the effect of lithium on d-amphetamine-induced hyperlocomotion in 12 (3 outbred) mouse strains. In our initial screening, mice received either (1) no drugs, (2) LiCl only, (3) damphetamine only, or (4) d-amphetamine and LiCl. Whereas there was no significant effect of LiCl alone on locomotion in any strain, there was a large degree of strain variation in the effects of LiCl combined with d-amphetamine. LiCl attenuated d-amphetamine-induced hyperlocomotion in C57BL/6J, C57BL/6Tac, Black Swiss, and CBA/J mice, whereas CD-1, FVB/NJ, SWR/J, and NIH Swiss mice, which were responsive to d-amphetamine, showed no significant effect of LiCl. d-Amphetamine-induced hyperlocomotion in the C3H/HeJ strain was increased by pretreatment with lithium. A subset of strains were treated for 4 weeks with lithium carbonate before the damphetamine challenge, and in each of these strains, lithium produced effects identical to those seen following acute administration. Strain responsiveness to lithium was not dependent upon the dose of either d-amphetamine or LiCl. Further, the results are not explained by brain lithium levels, which suggests that these behavioral responses to lithium are under the control of inherent genetic or other biological mechanisms specific to the effects of lithium on brain function.

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The effects of long-term administration of rubidium or lithium on reactivity to stress and on dopamine output in the nucleus accumbens in rats

Cited by 37 publications

References 27 publications

Selective modifications in the nucleus accumbens of dopamine synaptic transmission in rats exposed to chronic stress

Selective modifications in the nucleus accumbens of dopamine synaptic transmission in rats exposed to chronic stress

Effects of Long-Term Acetyl-L-Carnitine Administration in Rats—II: Protection Against the Disrupting Effect of Stress on the Acquisition of Appetitive Behavior

Strain Differences in Lithium Attenuation of d-Amphetamine-Induced Hyperlocomotion: A Mouse Model for the Genetics of Clinical Response to Lithium

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