Limits...
Environmental and Pharmacological Modulation of Amphetamine- Induced 50-kHz Ultrasonic Vocalizations in Rats.

Rippberger H, van Gaalen MM, Schwarting RK, Wohr M - Curr Neuropharmacol (2015)

Bottom Line: NA neurotransmission also regulates AMPH-induced 50-kHz USV emission given that α 1 receptor antagonists and α 2 receptor agonists exert attenuating effects.Supporting the involvement of the 5-HT system, AMPH-induced 50-kHz USV are attenuated by 5-HT2C receptor activation, whereas 5-HT2C receptor antagonism leads to the opposite effect.Finally, treatment with lithium, tamoxifen, and myricitrin was all found to result in a complete abolishment of the AMPH-induced increase in 50-kHz USV, suggesting the involvement of PKC signaling.

View Article: PubMed Central - PubMed

Affiliation: Behavioral Neuroscience, Experimental and Biological Psychology, Philipps-University of Marburg, Gutenbergstr. 18, 35032 Marburg, Germany. markus.woehr@staff.uni-marburg.de.

ABSTRACT
Rats emit high-frequency 50-kHz ultrasonic vocalizations (USV) in appetitive situations like social interactions. Drugs of abuse are probably the most potent non-social elicitors of 50-kHz USV, possibly reflecting their euphorigenic properties. Psychostimulants induce the strongest elevation in 50-kHz USV emission, particularly amphetamine (AMPH), either when applied systemically or locally into the nucleus accumbens (Nacc). Emission of AMPH-induced 50-kHz USV depends on test context, such as the presence of conspecifics, and can be manipulated pharmacologically by targeting major neurotransmitter systems, including dopamine (DA), noradrenaline (NA), and serotonin (5-HT), but also protein kinase C (PKC) signaling. Several D1 and D2 receptor antagonists, as well as typical and atypical antipsychotics block the AMPH-induced elevation in 50-kHz USV. Inhibiting D1 and D2 receptors in the Nacc abolishes AMPH-induced 50-kHz USV, indicating a key role for this brain area. NA neurotransmission also regulates AMPH-induced 50-kHz USV emission given that α 1 receptor antagonists and α 2 receptor agonists exert attenuating effects. Supporting the involvement of the 5-HT system, AMPH-induced 50-kHz USV are attenuated by 5-HT2C receptor activation, whereas 5-HT2C receptor antagonism leads to the opposite effect. Finally, treatment with lithium, tamoxifen, and myricitrin was all found to result in a complete abolishment of the AMPH-induced increase in 50-kHz USV, suggesting the involvement of PKC signaling. Neurotransmitter systems involved in AMPH-induced 50-kHz USV emission only partially overlap with other AMPH-induced behaviors like hyperlocomotion. The validity of AMPHinduced 50-kHz USV as a preclinical model for neuropsychiatric disorders is discussed, particularly with relevance to altered drive and mood seen in bipolar disorder.

No MeSH data available.


Related in: MedlinePlus

Mosaic overview on the pharmacological modulation of 50-kHz ultrasonic vocalizations (USV) induced by amphetamine (AMPH):call rate and call profile (microinjection studies). Color coding reflects direction and strength of observed effects: yellow = no change; orange= attenuation of AMPH-induced changes; red = complete abolishment of AMPH-induced changes; green = enhancement of AMPH-inducedchanges (or in absence of AMPH: induction of changes similar to AMPH).
© Copyright Policy - open-access
Related In: Results  -  Collection

License
getmorefigures.php?uid=PMC4598433&req=5

Figure 3: Mosaic overview on the pharmacological modulation of 50-kHz ultrasonic vocalizations (USV) induced by amphetamine (AMPH):call rate and call profile (microinjection studies). Color coding reflects direction and strength of observed effects: yellow = no change; orange= attenuation of AMPH-induced changes; red = complete abolishment of AMPH-induced changes; green = enhancement of AMPH-inducedchanges (or in absence of AMPH: induction of changes similar to AMPH).

Mentions: The number of studies investigating the pharmacological modulation of AMPH-induced 50-kHz calling is limited. Most of them use systemic application of test substances [11,16,19,20], and so far only two microinjection studies are available, in which the substances were injected locally into specific brain areas [29,30,32]. Targeted neurotransmitter systems include DA, NA, and 5-HT, but also glutamate and others (Figs. 2 & 3). Typically, numbers of 50-kHz USV were assessed, with most studies determining changes in the proportions of 50-kHz USV subtypes as well.


Environmental and Pharmacological Modulation of Amphetamine- Induced 50-kHz Ultrasonic Vocalizations in Rats.

Rippberger H, van Gaalen MM, Schwarting RK, Wohr M - Curr Neuropharmacol (2015)

Mosaic overview on the pharmacological modulation of 50-kHz ultrasonic vocalizations (USV) induced by amphetamine (AMPH):call rate and call profile (microinjection studies). Color coding reflects direction and strength of observed effects: yellow = no change; orange= attenuation of AMPH-induced changes; red = complete abolishment of AMPH-induced changes; green = enhancement of AMPH-inducedchanges (or in absence of AMPH: induction of changes similar to AMPH).
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4598433&req=5

Figure 3: Mosaic overview on the pharmacological modulation of 50-kHz ultrasonic vocalizations (USV) induced by amphetamine (AMPH):call rate and call profile (microinjection studies). Color coding reflects direction and strength of observed effects: yellow = no change; orange= attenuation of AMPH-induced changes; red = complete abolishment of AMPH-induced changes; green = enhancement of AMPH-inducedchanges (or in absence of AMPH: induction of changes similar to AMPH).
Mentions: The number of studies investigating the pharmacological modulation of AMPH-induced 50-kHz calling is limited. Most of them use systemic application of test substances [11,16,19,20], and so far only two microinjection studies are available, in which the substances were injected locally into specific brain areas [29,30,32]. Targeted neurotransmitter systems include DA, NA, and 5-HT, but also glutamate and others (Figs. 2 & 3). Typically, numbers of 50-kHz USV were assessed, with most studies determining changes in the proportions of 50-kHz USV subtypes as well.

Bottom Line: NA neurotransmission also regulates AMPH-induced 50-kHz USV emission given that α 1 receptor antagonists and α 2 receptor agonists exert attenuating effects.Supporting the involvement of the 5-HT system, AMPH-induced 50-kHz USV are attenuated by 5-HT2C receptor activation, whereas 5-HT2C receptor antagonism leads to the opposite effect.Finally, treatment with lithium, tamoxifen, and myricitrin was all found to result in a complete abolishment of the AMPH-induced increase in 50-kHz USV, suggesting the involvement of PKC signaling.

View Article: PubMed Central - PubMed

Affiliation: Behavioral Neuroscience, Experimental and Biological Psychology, Philipps-University of Marburg, Gutenbergstr. 18, 35032 Marburg, Germany. markus.woehr@staff.uni-marburg.de.

ABSTRACT
Rats emit high-frequency 50-kHz ultrasonic vocalizations (USV) in appetitive situations like social interactions. Drugs of abuse are probably the most potent non-social elicitors of 50-kHz USV, possibly reflecting their euphorigenic properties. Psychostimulants induce the strongest elevation in 50-kHz USV emission, particularly amphetamine (AMPH), either when applied systemically or locally into the nucleus accumbens (Nacc). Emission of AMPH-induced 50-kHz USV depends on test context, such as the presence of conspecifics, and can be manipulated pharmacologically by targeting major neurotransmitter systems, including dopamine (DA), noradrenaline (NA), and serotonin (5-HT), but also protein kinase C (PKC) signaling. Several D1 and D2 receptor antagonists, as well as typical and atypical antipsychotics block the AMPH-induced elevation in 50-kHz USV. Inhibiting D1 and D2 receptors in the Nacc abolishes AMPH-induced 50-kHz USV, indicating a key role for this brain area. NA neurotransmission also regulates AMPH-induced 50-kHz USV emission given that α 1 receptor antagonists and α 2 receptor agonists exert attenuating effects. Supporting the involvement of the 5-HT system, AMPH-induced 50-kHz USV are attenuated by 5-HT2C receptor activation, whereas 5-HT2C receptor antagonism leads to the opposite effect. Finally, treatment with lithium, tamoxifen, and myricitrin was all found to result in a complete abolishment of the AMPH-induced increase in 50-kHz USV, suggesting the involvement of PKC signaling. Neurotransmitter systems involved in AMPH-induced 50-kHz USV emission only partially overlap with other AMPH-induced behaviors like hyperlocomotion. The validity of AMPHinduced 50-kHz USV as a preclinical model for neuropsychiatric disorders is discussed, particularly with relevance to altered drive and mood seen in bipolar disorder.

No MeSH data available.


Related in: MedlinePlus