Structure of Rat Ultrasonic Vocalizations and Its Relevance to Behavior

Takahashi, Nobuaki; Kashino, Makio; Hironaka, Naoyuki

doi:10.1371/journal.pone.0014115

Cited by 100 publications

(92 citation statements)

References 33 publications

(35 reference statements)

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“…These results add to evidence that call rate and profile can be manipulated independently by drugs or lesions (Ciucci et al, 2009(Ciucci et al, , 2007. Moreover, although several groups currently distinguish between FM and flat 50-kHz calls Burgdorf et al, 2007Burgdorf et al, , 2008aBurgdorf and Panksepp, 2006;Simola et al, 2009;Wohr et al, 2008), only a few investigators have extended their analysis beyond those two classes (Ciucci et al, 2009;Kaltwasser, 1990;Takahashi et al, 2010;Vivian and Miczek, 1993;White et al, 1990;Wright et al, 2010). Importantly, our detailed analysis reveals that the prevalent trill call subtype (Wright et al, 2010) is not representative of all FM calls.…”

Section: Information Gained From 50-khz Call Subtype Analysis Vs Callmentioning

confidence: 57%

α- and β-Adrenergic Receptors Differentially Modulate the Emission of Spontaneous and Amphetamine-Induced 50-kHz Ultrasonic Vocalizations in Adult Rats

Wright

Dobosiewicz

Clarke

2011

Neuropsychopharmacol

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Amphetamine (AMPH) increases adult rat 50-kHz ultrasonic vocalizations, preferentially promoting frequency-modulated (FM) calls that have been proposed to reflect positive affect. The main objective of this study was to investigate a possible noradrenergic contribution to AMPH-induced calling. Adult male Long-Evans rats were tested with AMPH (1 mg/kg intraperitoneal) or saline combined with various systemic pretreatments: clonidine (α2 adrenergic agonist), prazosin (α1 antagonist), atipamezole (α2 antagonist), propranolol, betaxolol, and/or ICI 118,551 (β1/β2, β1, and β2 antagonists, respectively), nadolol (β1/β2 antagonist, peripheral only), or NAD-299 (5HT(1A) antagonist). In addition, effects of cirazoline (α1 adrenergic agonist) and cocaine (0.25-1.5 mg/kg intravenous) were studied alone. AMPH-induced calling was suppressed by low-dose clonidine and prazosin. Cirazoline and atipamezole did not significantly affect calling rate. Propranolol, without affecting the call rate, dose dependently promoted 'flat' calls under AMPH while suppressing 'trills,' thus reversing the effects of AMPH on the 'call subtype profile.' This effect of propranolol seemed to be mediated by simultaneous inhibition of CNS β1 and β2 rather than by 5HT(1A) receptors. Finally, cocaine elicited fewer calls than did AMPH, but produced the same shift in the call subtype profile. Taken together, these results reveal differential drug effects on flat vs trill vs other FM 50-kHz calls. These findings highlight the value of detailed call subtype analyses, and show that 50-kHz calls are associated with adrenergic α1- and β-receptor mechanisms. These preclinical findings suggest that noradrenergic contributions to psychostimulant subjective effects may warrant further investigation.

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Section: Information Gained From 50-khz Call Subtype Analysis Vs Callmentioning

confidence: 57%

α- and β-Adrenergic Receptors Differentially Modulate the Emission of Spontaneous and Amphetamine-Induced 50-kHz Ultrasonic Vocalizations in Adult Rats

Wright

Dobosiewicz

Clarke

2011

Neuropsychopharmacol

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“…Although rodents do not produce speech per se, male mice vocalize at ultrasonic frequencies (40–120kHz) when presented with a female mouse (17, 18, 19, 20). These courtship songs have been analyzed for spectrogram patterns and quantity in normal mice, but analysis of chronic changes in vocalization patterns and quantity in males after stroke has not been investigated (19, 20, 21, 22, 23). USVs have also been well characterized in neonatal mice, which vocalize robustly when removed from the dam (24).…”

Section: Introductionmentioning

confidence: 99%

Ultrasonic vocalization changes and FOXP2 expression after experimental stroke

Doran

Trammel

Benashaski

et al. 2015

Behavioural Brain Research

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Speech impairments affect one in four stroke survivors. However, animal models of post-ischemic vocalization deficits are limited. Male mice vocalize at ultrasonic frequencies when exposed to an estrous female mouse. In this study we assessed vocalization patterns and quantity in male mice after cerebral ischemia. FOXP2, a gene associated with verbal dyspraxia in humans, with known roles in neurogenesis and synaptic plasticity, was also examined after injury. Using a transient middle cerebral artery occlusion (MCAO) model, we assessed correlates of vocal impairment at several time-points after stroke. Further, to identify possible lateralization of vocalization deficits induced by left and right hemispheric strokes were compared. Significant differences in vocalization quantity were observed between stroke and sham animals that persisted for a month after injury. Injury to the left hemisphere reduced early vocalizations more profoundly than those to the right hemisphere. Nuclear expression of Foxp2 was elevated early after stroke (at 6 hours), but significantly decreased 24 hours after injury in both the nucleus and the cytoplasm. Neuronal Foxp2 expression increased in stroke mice compared to sham animals 4 weeks after injury. This study demonstrates that quantifiable deficits in ultrasonic vocalizations (USVs) are seen after stroke. USV may be a useful tool to assess chronic behavioral recovery in murine models of stroke.

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“…Rats use ultrasonic vocalizations (USVs) for communication (Knutson et al 2002;Portfors 2007;Sewell 1970;Takahashi et al 2010). Like mouse USVs (Galindo-Leon et al 2009;Liu and Schreiner 2007;Marlin et al 2015;Portfors 2007), male USVs evoke temporally precise and predictable patterns of activity across A1 (Carruthers et al 2013), thereby providing us an ideal set of stimuli with which to probe invariance to acoustic transformations in the auditory cortex.…”

mentioning

confidence: 99%