Speech prosody can be conceptually intended as the affective dimension of verbal communication. The recognition of speech prosody during social interactions has an adaptive function since it provides information about the speaker's intention and its emotional states, allowing an appropriate response in different situations (Frith Reference Frith2009).

Current models of brain organization for prosody propose lateralized representation based on featural (timing vs. pitch) or functional (affective vs. linguistic) characteristics of prosodic material (see Sidtis et al. Reference Sidtis and Van Lancker Sidtis2003). However, the role of subcortical structures in prosody is being increasingly described.

From the arguments provided by Ackermann et al. in the target article, one could argue that the corticobulbar tract is a key structure linking both the affective related dimensions of verbal communication and the reward system. For example, the authors discuss the pivotal role of dopamine in speech prosody. Surprisingly, no mention was made about the role of serotonin, another key monoamine of the reward system (Vicario Reference Vicario2013b), whose involvement at corticobulbar level has been reported in several articles (e.g., Raul Reference Raul2003).

Here, I expand upon these issues by providing arguments in support of the suggestion that, in humans, speech prosody might have evolved from the basic mechanisms implied in reward/affective-related functions. In particular, I propose an integrative overview which argues that speech prosody is subserved, at least in part, by the same anatomical and neurochemical mechanisms involved in the processing of reward/affective outcomes.

Evidence is provided by the case of patients with Parkinson's disease (PD), a clinical condition characterized by a dysfunctional neurotransmission of dopaminergic and serotoninergic neural circuits (Bédard et al. Reference Bédard, Wallman, Pourcher, Gould, Parent and Parent2011). PD patients are affected by a disruption of the prosodic aspect of verbal utterance (Van Lancker Sidtis et al. Reference Van Lancker Sidtis, Pachana, Cummings and Sidtis2006), but these patients are known also for their swallowing disorder (Potulska et al. Reference Potulska, Friedman, Królicki and Spychala2003). Interestingly, De Letter et al. (Reference De Letter, Santens, Estercam, Van Maele, De Bodt, Boon and Van Borsel2007) have shown that Levodopa induces modifications of prosody in advanced PD. Moreover, it was recently reported that the deep brain stimulation of the subthalamic nucleus (STN), which modulates the activity of both dopaminergic (Lhommée et al. Reference Lhommée, Klinger, Thobois, Schmitt, Ardouin, Bichon, Kistner, Fraix, Xie, Aya, Chabardès, Seigneuret, Benabid, Mertens, Polo, Carnicella, Quesada, Bosson, Broussolle, Pollak and Krack2012) and serotoninergic (Creed et al. Reference Creed, Hamani, Bridgman, Fletcher and Nobrega2012) neurons, improves tongue force (Skodda Reference Skodda2012) and emotional speech (Brück et al. Reference Brück, Wildgruber, Kreifelts, Krüger and Wächter2011) in PD.

Studies on animal models provide further support to this link between reward, prosody, and the corticobulbar tract. For example, Nuckolls et al. (Reference Nuckolls, Worley, Leto, Zhang, Morris and Stanford2012) have shown that nigrostriatal dopaminergic depletion affects tongue force output. This phenomenon is probably mediated by the effect of dopamine depletion on several structures of the neural pathway connecting the tongue muscle with midbrain, for example, the nucleus tractus solitarius (NTS) (Granata & Woodruff Reference Granata and Woodruff1982), a key area of the corticobulbar system involved in the regulation of reward-related behaviors such as food intake and swallowing. Interestingly, studies have shown that agonists and antagonists of dopamine spontaneously activate neurons in the NTS (Granata & Woodruff Reference Granata and Woodruff1982).

Tongue muscle control might also involve serotoninergic mechanisms. For example, there is evidence that clozapine, a serotoninergic antagonist, affects lick frequency in rats (Das & Fowler Reference Das and Fowler1995). Moreover, it has been documented that NTS is an important site of action for serotonin (Lam et al. Reference Lam, Zhou, Vegge, Xiu, Christensen, Osundiji, Yueh, Evans and Heisler2009).

The study of animal models has also shown an involvement of both these two monoamines in reward-oriented communication. For example, the research by Huang and Hessler (Reference Huang and Hessler2008) on male songbirds reports a relationship between direct rewarding communications (such as singing used for courtship) and dopaminergic mechanisms. These authors speculate that the ventral tegmentum (VT), a dopaminergic area which mediates rewarding and motivated behaviors (Ghanbarian & Motamedi Reference Ghanbarian and Motamedi2013), might modulate songbirds output to the higher stereotypy typical of courtship. Interestingly, a direct connectivity between VT and NTS has recently been shown (Alhadeff et al. Reference Alhadeff, Rupprecht and Hayes2012), which suggests some influence of VT at corticobulbar level. Salvante et al. (Reference Salvante, Racke, Campbell and Sockman2010) have also reported that serotonin may modulate communication in birds since it influences the effect of extrinsic social factors on their singing effort.

Finally, the work by Alipour et al. (Reference Alipour, Chen and Jürgens2002) on new world monkeys, Saguinus fuscicollis, provides the anatomical rationale to the link between corticobulbar pathway, reward, and prosody. In fact, this study documents the existence of a direct connectivity between the motor cortical tongue area and several subcortical regions – such as the anterior cingulate cortex, the insula, the ventral putamen, the caudate nucleus, and the amygdale – involved in the processing of affective and rewarding outcomes.

A further support to the current discussion is provided by neurogenetic investigation. Ackermann et al. discuss the role of the FOXP2 gene on verbal communication. For example, a mutation in this gene has been associated with apraxia of speech (Laffin et al. Reference Laffin, Raca, Jackson, Strand, Jakielski and Shriberg2012; see also Vicario Reference Vicario2013a). Moreover, Shriberg et al. (Reference Shriberg, Ballard, Tomblin, Duffy, Odell and Williams2006) have shown that these alterations may extend to prosody. The impact of FOXP2 on the activity of striatum (French et al. Reference French, Jin, Campbell, Gerfen, Groszer, Fisher and Costa2012) suggests the dopaminergic nature (Gale et al. Reference Gale, Lee, Amirnovin, Roberts, Williams, Blaha and Eskandar2013) of the effect played by this gene on verbal communication. However, it is known that FOXP2 may modulate the serotoninergic activity of corticobulbar structures involved in the regulation of rewarding signals. For example, the neurons of the parabrachial nucleus (PB) of rats constitutively express the FOXP2 transcription factor (Miller et al. Reference Miller, Stein and Loewy2011). PB is another key structure of the reward system; consisting of taste-responsive neurons (Simon et al. Reference Simon, de Araujo, Gutierrez and Nicolelis2006), it receives an obligatory relay from the NTS, in rodents (Tokita et al. Reference Tokita, Karadi, Shimura and Yamamoto2004).

The research described above offers an overview about the relationship between prosody, reward, and the corticobulbar system. In particular, it shows that speech prosody and reward processing may share similar neuroanatomical and neurochemical mechanisms. However, the evidence that both serotoninergic and dopaminergic mechanisms are involved in prosody, though corroborating the initial hypothesis of this commentary, poses the problem of understanding how these monoamines work. A possible insight is provided by two recent articles suggesting a distinct role for dopamine (Fiorillo Reference Fiorillo2013) and serotonin (Vicario Reference Vicario2013c), respectively, in the processing of reward and aversiveness. By extending this argument to speech prosody, one could speculate that dopamine subserves reward-oriented (e.g., approach) communication, while serotonin subserves punishment-oriented (e.g., threat) communication.