GABAB receptors involvement in the effects induced by nicotine on anxiety-related behaviour in mice

Varani, Andrés Pablo; Balerio, Graciela N.

doi:10.1016/j.phrs.2012.03.001

Cited by 26 publications

(21 citation statements)

References 36 publications

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“…Alternatively, an anxiogenic‐like response was observed in HINT1 −/− mice at the highest nicotine dose tested in this paradigm. Nicotine has been reported to produce both anxiolytic and anxiogenic effects in the plus maze, depending on the dose (Biala & Budzynska ; O'Neill & Brioni ; Varani & Balerio ); thus, our results may suggest that HINT1 −/− are more sensitive to the anxiogenic effects of nicotine. Previous studies report that male HINT1 −/− mice are more anxious under basal conditions than HINT1 +/+ mice (Varadarajulu et al .…”

Section: Discussionmentioning

confidence: 59%

Acute behavioral effects of nicotine in male and female HINT1 knockout mice

Jackson

Wang

Barbier

et al. 2012

Genes Brain and Behavior

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Human genetic association and brain expression studies, and mouse behavioral and molecular studies implicate a role for the histidine triad nucleotide-binding protein 1 (HINT1) in schizophrenia, bipolar disorder, depression and anxiety. The high comorbidity between smoking and psychiatric disorders, schizophrenia in particular, is well established. Associations with schizophrenia and HINT1 are also sex specific, with effects more predominant in males; however, it is unknown if sex differences associated with the gene extend to other phenotypes. Thus, in this study, using a battery of behavioral tests, we elucidated the role of HINT1 in acute nicotine-mediated behaviors using male and female HINT1 wild-type (+/+) and knockout (−/−) mice. The results show that male HINT1 −/− mice were less sensitive to acute nicotineinduced antinociception in the tail-flick, but not hot-plate test. At low nicotine doses, male and female HINT1 −/− mice were less sensitive to nicotine-induced hypomotility, although the effect was more pronounced in females. Baseline differences in locomotor activity observed in male HINT1 +/+ and −/− mice were absent in females. Nicotine did not produce an anxiolytic effect in male HINT1 −/− mice, but rather an anxiogenic response. Diazepam also failed to induce an anxiolytic response in these mice, suggesting a general anxiety phenotype not specific to nicotine. Differences in anxiety-like behavior were not observed in female mice. These results further support a role for HINT1 in nicotine-mediated behaviors and suggest that alterations in the gene may have differential effects on phenotype in males and females.

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Section: Discussionmentioning

confidence: 59%

Acute behavioral effects of nicotine in male and female HINT1 knockout mice

Jackson

Wang

Barbier

et al. 2012

Genes Brain and Behavior

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“…As mentioned before, we showed that NIC anxiolytic-like effect was selectively abolished in KO mice. Accordingly, the administration of the GABA B receptor antagonist 2-OH-saclofen was able to block the anxiolytic-like effects of NIC in mice (Varani and Balerio, 2012). Therefore, the abolishment of NIC-induced anxiolytic-like response in KO mice appears to be due to the absence of GABA effects on GABA B receptors.…”

Section: Discussionmentioning

confidence: 89%

“…The total number of visits to the closed and open arms and the cumulative time spent in the open and closed arms were then observed on a monitor through a video camera system (Vision Robot, Buenos Aires, Argentina). Entries into the open and closed arms were recorded when the mouse moved both forepaws and the head into the arm, as we previously described (Balerio et al, 2005(Balerio et al, , 2006Varani and Balerio, 2012). All observation sessions started 5 min after the acute injection of NIC or SAL.…”

Section: Anxiety-related Behaviourmentioning

confidence: 99%

“…It has been demonstrated that GABA B receptors can modulate NIC acute effects, as well as different addictive properties of NIC. In this sense, we have recently shown that the GABA B antagonist, 2-OH-saclofen, is able to block the anxiolytic and anxiogenic effects induced by NIC (Varani and Balerio, 2012). In addition, the administration of baclofen, a GABA B receptor agonist, attenuates the antinociceptive, hypolocomotive (Aso et al, 2007) and rewarding effects induced by NIC (Le Foll et al, 2008).…”

Section: Introductionmentioning

confidence: 96%

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Acute behavioural responses to nicotine and nicotine withdrawal syndrome are modified in GABAB1 knockout mice

et al. 2012

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“…The dose of BAC (2 mg/kg) was selected based on our previous reports (Diaz et al, 2001(Diaz et al, , 2003(Diaz et al, , 2004(Diaz et al, , 2006 and did not induce changes in SAL chronically treated mice in the EPM according with previous results from our laboratory (Varani and Balerio, 2012;Varani et al, 2014b). NAL administration alone did not produce changes on EPM behavioral responses in mice chronically treated with SAL (SAL-SAL-NAL group) as well as the combination with BAC and NAL (SAL-BAC-NAL group) in agreement with our previous report (Varani et al, 2014a).…”

Section: Discussionmentioning

confidence: 99%

Baclofen prevents the elevated plus maze behavior and BDNF expression during naloxone precipitated morphine withdrawal in male and female mice

Pedrón

Varani

Balerio

2016

Synapse

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In previous studies we have shown that baclofen, a selective GABAB receptor agonist, prevents the somatic expression and reestablishes the dopamine and μ-opioid receptors levels, modified during naloxone-precipitated morphine withdrawal syndrome in male and female mice. There are no previous reports regarding sex differences in the elevated plus maze (EPM) and the expression of BDNF in morphine-withdrawn mice. The present study analyses the behavioral and biochemical variations during morphine withdrawal in mice of both sexes, and whether these variations are prevented with baclofen. Swiss-Webster albino prepubertal mice received morphine (2 mg/kg, i.p.) twice daily, for 9 consecutive days. On the 10th day, one group of morphine-treated mice received naloxone (opioid receptor antagonist; 6 mg/kg, i.p.) 1 h after the last dose of morphine to precipitate withdrawal. A second group received baclofen (2 mg/kg, i.p.) before naloxone administration. The EPM behavior was measured during 15 min after naloxone injection. The expression of BDNF-positive cells was determined by immunohistochemistry. Withdrawn male mice showed a higher percentage of time spent and number of entries to the open arms compared to withdrawn female mice. Baclofen prevented this behavior in both sexes. BDNF expression decreased in the AcbC, BNST, CeC, and CA3 of the hippocampus while increased in the BLA of morphine withdrawn male. Baclofen pretreatment prevented the BDNF expression observed in morphine withdrawn male mice in all the brain areas studied except in the CeC. Baclofen prevention of the EPM behavior associated to morphine withdrawal could be partially related to changes in BDNF expression.

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GABAB receptors involvement in the effects induced by nicotine on anxiety-related behaviour in mice

Cited by 26 publications

References 36 publications

Acute behavioral effects of nicotine in male and female HINT1 knockout mice

Acute behavioral effects of nicotine in male and female HINT1 knockout mice

Acute behavioural responses to nicotine and nicotine withdrawal syndrome are modified in GABAB1 knockout mice

Baclofen prevents the elevated plus maze behavior and BDNF expression during naloxone precipitated morphine withdrawal in male and female mice

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