Neuropeptide Y Y1 receptor antagonist BIBP3226 produces conditioned place aversion in rats

Kask, Ants; Kivastik, Toomas; Rägo, Lembit; Harro, Jaanus

doi:10.1016/s0278-5846(99)00029-9

Cited by 25 publications

(11 citation statements)

References 17 publications

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“…While these data underscore the importance of NPY in producing reward, there is some controversy regarding the nature of involved receptors. Intra-amygdala infusion of the NPY Y1 receptor antagonist BIBP3226 attenuated ethanol self-administration in the operant conditioning chamber [16] and produced conditioned place aversion in rats [17]. However, Ault et al [20] reported the involvement of sigma 1 like receptors of Acb in the reward and reinforcement action of NPY.…”

Section: Discussionmentioning

confidence: 99%

“…Intra-Acb injections of NPY produced place preference [15]. Intra-amygdala infusion of the NPY Y1 receptor antagonist BIBP3226 attenuated operant self-administration of ethanol [16] and produced conditioned place aversion in rats [17]. While NPY mediated place preference was blocked by cis-flupenthixol (dopamine antagonist) [18], NPY infusion into the AcbSh increased extracellular levels of dopamine [19] suggesting involvement in reward.…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

NPY mediates reward activity of morphine, via NPY Y1 receptors, in the nucleus accumbens shell

Desai

Upadhya

Subhedar

et al. 2013

Behavioural Brain Research

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

NPY mediates reward activity of morphine, via NPY Y1 receptors, in the nucleus accumbens shell

Desai

Upadhya

Subhedar

et al. 2013

Behavioural Brain Research

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“…I.c.v. administration of BIBP 3226 has been shown to increase anxiety in the elevated plus maze test (Kask et al, 1996) and produce conditioned place aversions (Kask et al, 1999) without altering activity levels. BIBP 3226 injected into the periaquaductal gray also produces anxiogenic effects in the elevated plus maze; however, another study did not see changes in anxiety levels following BIBP 3226 injections into the amygdala, locus coereleus, or the PVN (Kask et al, 1998).…”

Section: Discussionmentioning

confidence: 99%

Effects of Altered Amygdalar Neuropeptide Y Expression on Anxiety-Related Behaviors

Primeaux

Wilson

Cusick

et al. 2005

Neuropsychopharmacol

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Neuropeptide Y (NPY) decreases anxiety-related behaviors in various animal models of anxiety. The purpose of the present study was to examine the role of the amygdalar NPY system in anxiety-related responses in the elevated plus maze. The first experiment determined if herpes virus-mediated alterations in amygdalar NPY levels would alter anxiety-related behaviors in the elevated plus maze. Viral vectors encoding NPY, NPY antisense, or LacZ (control virus) were bilaterally injected into the amygdala, and 4 days postinjection, rats were tested in the elevated plus maze test. NPY-like immunoreactivity (NPY-ir) was measured in the amygdala of these rats. In rats injected with the viral vector encoding NPY, reduced anxiety-related behaviors in the elevated plus maze accompanied by moderate increases in NPY-ir were detected compared to NPY-antisense viral vector-treated subjects. Elevated plus maze behavior did not differ compared to LacZ-treated controls. NPY overexpression at this time point was also suggested by enhanced NPY mRNA expression seen in the amygdala 4 days postinjection using real-time polymerase chain reaction analysis. Experiment 2 was conducted to provide further evidence for a role of amygdalar NPY in regulating anxiety-related behaviors in the elevated plus maze test. The nonpeptide NPY Y1 receptor antagonist, BIBP 3226 (1.5 mg/ml), was bilaterally injected into the amygdala and rats were tested in the elevated plus maze test. Rats receiving BIBP 3226 exhibited increased anxiety-related behaviors in this test. The results of these experiments provide further support for the role of amygdalar NPY in anxiety-related behaviors. Neuropsychopharmacology (2005) 30, 1589-1597.

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“…NPY colocalizes with GABA in local circuit neurons of the basolateral amygdala (BLA) (McDonald and Pearson, 1989) and likely exerts inhibitory control on BLA projection neurons. The anxiolytic effects of NPY generally involve the Y 1 receptor (Heilig, 1995; Wieland et al, 1995; Kask et al, 1999; Sajdyk et al, 1999; Primeaux et al, 2005), although Y 2 and Y 5 receptors have also been implicated (Sajdyk et al, 2002a; Sajdyk et al, 2002b). Most germane to the question of resilience, Sajdyk et al found that injections of NPY into the BLA blocked the anxiogenic effects of a chemical or physical stressor, an effect that persisted for 8 weeks after a series of NPY infusions into the BLA (Sajdyk et al, 2008).…”

Section: Introductionmentioning

confidence: 99%

The Role of Neuropeptide Y in the Expression and Extinction of Fear-Potentiated Startle

Gutman¹,

Yang²,

Ressler³

et al. 2008

J. Neurosci.

121

100

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Neuropeptides are a promising target for novel treatments for anxiety and other psychiatric disorders and neuropeptide Y (NPY) has emerged as a key component of anxiolytic circuits in the brain. For this reason, we have evaluated the role of NPY in the expression and extinction of conditioned fear. We found that intracerebroventricular administration of NPY inhibits both baseline acoustic startle and the expression of fear-potentiated startle. Infusion of NPY (10 pmol/side) into the basolateral, but not the medial, nucleus of the amygdala reproduced the intracerebroventricular effect. Central administration of NPY (10 g) also enhanced within-session extinction of fearpotentiated startle. This finding, coupled with the growing body of literature correlating NPY with resilience in humans, led us to the hypothesis that NPY may enhance the extinction of conditioned fear. When NPY (10 g) is administered intracerebroventricularly before extinction training, extinction retention for both the contextual and cued components of conditioned fear is enhanced when tested 48 h later off drug. Additionally, we found that intra-basolateral amygdala administration of the NPY Y 1 receptor antagonist BIBO 3304 (200 pmol/side) before extinction training led to a profound deficit in extinction retention. This is the first evidence that NPY facilitates and an NPY antagonist blocks the extinction of conditioned fear. We believe that the role of NPY in the extinction of conditioned fear may, at least in part, explain the mechanism underlying the association between NPY and psychobiological resilience in humans.

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Neuropeptide Y Y1 receptor antagonist BIBP3226 produces conditioned place aversion in rats

Cited by 25 publications

References 17 publications

NPY mediates reward activity of morphine, via NPY Y1 receptors, in the nucleus accumbens shell

NPY mediates reward activity of morphine, via NPY Y1 receptors, in the nucleus accumbens shell

Effects of Altered Amygdalar Neuropeptide Y Expression on Anxiety-Related Behaviors

The Role of Neuropeptide Y in the Expression and Extinction of Fear-Potentiated Startle

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