Insights into the Neural and Genetic Basis of Vocal Communication

Konopka, Genevieve; Roberts, Todd F.

doi:10.1016/j.cell.2016.02.039

Cited by 77 publications

(76 citation statements)

References 131 publications

(150 reference statements)

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“…Momentary (within a few milliseconds) increases in amplitude of the inappropriate between-words abrupt pauses are consistent with deficits associated with state feedback control theory (Houde & Nagarajan, 2011), with possible control parameters including movement commands for respiratory, laryngeal, and articulatory targets. Phonatory behaviors as biomarkers of apraxia of speech, in particular, have attractive measurement features as they do in research in voice, dysfluency, and other motor speech disorders (e.g., Civier, Bullock, Max, & Guenther, 2013;Cohen, Renshaw, Mitchell, & Kim, 2016;Kim, 2015;Konopka & Roberts, 2016;Kumar, Croxson, & Simonyan, 2016;Ludlow, 2015;Neef, Anwander, & Friederici, 2015;Pouplier, Marin, & Waltl, 2014;Simonyan, 2013;Simonyan & Horwitz, 2011;Vanhoutte et al, 2014). In the present context, the same control mechanism underlying an abrupt inappropriate speech onset could underlie the excessive/equal sentential stress sign of CAS described previously.…”

Section: Abrupt Inappropriate Word Onsets/offsetsmentioning

confidence: 63%

A Diagnostic Marker to Discriminate Childhood Apraxia of Speech From Speech Delay: IV. The Pause Marker Index

Shriberg

Strand

Fourakis

et al. 2017

J Speech Lang Hear Res

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Purpose: Three previous articles provided rationale, methods, and several forms of validity support for a diagnostic marker of childhood apraxia of speech (CAS), termed the pause marker (PM). Goals of the present article were to assess the validity and stability of the PM Index (PMI) to scale CAS severity. Method: PM scores and speech, prosody, and voice precision-stability data were obtained for participants with CAS in idiopathic, neurogenetic, and complex neurodevelopmental disorders; adult-onset apraxia of speech consequent to stroke and primary progressive apraxia; and idiopathic speech delay. Three studies were completed including criterion and concurrent validity studies of the PMI and a temporal stability study of the PMI using retrospective case studies. Results: PM scores were significantly correlated with other signs of CAS precision and stability. The best fit of the distribution of PM scores to index CAS severity was obtained by dividing scores into 4 ordinal severity classifications: mild, mild-moderate, moderate-severe, and severe. Severity findings for the 4 classifications and retrospective longitudinal findings from 8 participants with CAS supported the validity and stability of the PMI. Conclusion: Findings support research and clinical use of the PMI to scale the severity of CAS.A four-article series (Shriberg et al., 2017a(Shriberg et al., , 2017b(Shriberg et al., , 2017c, and the present article) to develop and assess the theoretical and clinical utility of a singlesign, behavioral marker of childhood apraxia of speech (CAS) poses the following three questions: 1.Do findings from construct and criterion validity studies support the diagnostic accuracy of a behavioral marker, the pause marker (PM), to discriminate CAS from speech delay (SD)?2. Do findings from the PM and other measures support the hypothesis of core representational and transcoding deficits in CAS, and is the PM theoretically coherent with those deficits?3. Do findings from cross-sectional and retrospective longitudinal case studies support an ordinal scale of PM scores, the Pause Marker Index (PMI), to quantify the severity of CAS for research and clinical applications?The short-term goal of the PM is to provide a behavioral marker of CAS for research and clinical practice. A longer term goal of the PM is to provide quantitative inclusionary and exclusionary criteria to identify participants who are true positive for CAS in studies to identify and validate a biomarker of CAS. The present article addresses both goals. As proposed in the first article in this series (PM I; Shriberg et al., 2017a, Table 1), a highly valued attribute of diagnostic markers is generality, that is, a marker has research and clinical utility beyond identifying presence or absence of a disorder. In the present context, a behavioral marker of CAS has research and clinical generality when in addition to being diagnostically sensitive to and specific for a prior, active, and/or future disorder, it also quantifies the severity of the disorder. The three...

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Section: Abrupt Inappropriate Word Onsets/offsetsmentioning

confidence: 63%

A Diagnostic Marker to Discriminate Childhood Apraxia of Speech From Speech Delay: IV. The Pause Marker Index

Shriberg

Strand

Fourakis

et al. 2017

J Speech Lang Hear Res

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“…vocalization | expiration | hindbrain | premotor neurons | Olig3 V ocalization is the primary mechanism used by many vertebrate species for communication (1). Whereas adult mice call during courtship, mating, and territorial disputes, newborn mice use vocalization to communicate with their mothers (2,3).…”

mentioning

confidence: 99%

Genetic identification of a hindbrain nucleus essential for innate vocalization

Hernández-Miranda

Ruffault

Bouvier

et al. 2017

Proc. Natl. Acad. Sci. U.S.A.

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Vocalization in young mice is an innate response to isolation or mechanical stimulation. Neuronal circuits that control vocalization and breathing overlap and rely on motor neurons that innervate laryngeal and expiratory muscles, but the brain center that coordinates these motor neurons has not been identified. Here, we show that the hindbrain nucleus tractus solitarius (NTS) is essential for vocalization in mice. By generating genetically modified newborn mice that specifically lack excitatory NTS neurons, we show that they are both mute and unable to produce the expiratory drive required for vocalization. Furthermore, the muteness of these newborns results in maternal neglect. We also show that neurons of the NTS directly connect to and entrain the activity of spinal (L1) and nucleus ambiguus motor pools located at positions where expiratory and laryngeal motor neurons reside. These motor neurons control expiratory pressure and laryngeal tension, respectively, thereby establishing the essential biomechanical parameters used for vocalization. In summary, our work demonstrates that the NTS is an obligatory component of the neuronal circuitry that transforms breaths into calls.V ocalization is the primary mechanism used by many vertebrate species for communication (1). Whereas adult mice call during courtship, mating, and territorial disputes, newborn mice use vocalization to communicate with their mothers (2, 3). Newborn mice, when isolated, produce ultrasonic calls (USCs) that elicit search and retrieval behavior by their mothers. Thus, vocalizations of newborn mice represent an innate behavior that is thought to rely on a genetically determined circuit. Such innate vocalizations are reminiscent of nonverbal utterances of humans like laughing, crying, sighing, and moaning.The central circuits that control vocalization have been widely studied in adult vertebrates, where they overlap in their executive components with respiratory circuits (4). Forebrain pathways that control the frequency and sequence of ultrasounds in mice are not essential for innate vocalization (5, 6); rather, it is the periaqueductal gray in the midbrain that modulates the activity of motor neurons in the hindbrain and spinal cord to implement calls and modulate breathing (7,8). Calls are shaped through a biomechanical process that involves variations in subglottal air pressure and laryngeal muscle tension (9, 10). Expiration is an important determinant of subglottal air pressure (11), suggesting that expiratory muscle activity and laryngeal tension are highly coordinated during vocalization. However, because expiratory and laryngeal motor neurons are located at markedly different axial levels of the nervous system, in the spinal cord (T11-L1 levels, expiratory) and hindbrain (nucleus ambiguus, laryngeal), how the activities of these motor pools are coordinated is unclear (12, 13). More importantly, the identity and location of functionally important premotor neurons for vocalization are little known.Using mouse genetics to investigate the ...

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“…Three reference points were suggested to specify the network, responsible for 1 of the behaviour characteristics selected by Pankseep: (1) similar neuronal circuits maintain coherent functions; (2) artificial stimulation of the particular network (with a pharmacological, electrophysiological, and opto-/chemo-genetic means) generates predicted responses; and (3) changes in the carriers of the network activity (neurotransmitters and other substances with messenger activity) predict the behavioural changes (Panksepp, 1998). A lot of research aims to decipher the circuitries that predominantly control (1) arousal and sleep (Herrera et al., 2016, Kim et al., 2012, Landgraf et al., 2016), (2) fear, (3) anxiety, (4) aversive memories (Bravo-Rivera et al., 2014, Kim et al., 2013, McCullough et al., 2016, Tovote et al., 2015), (5) reward (Kelley, 2004, Kelley and Berridge, 2002, Smith et al., 2011), (6) attention and motivation (Berthet et al., 2016, Carli and Invernizzi, 2014, Kim, 2013), (7) goal-oriented behaviour and habits (Burguière et al., 2015, Chersi et al., 2013, Frank, 2011, Gremel and Costa, 2013, Medendorp et al., 2011) and (8) social functions (Konopka and Roberts, 2016, Kragel et al., 2015, Sladky et al., 2015, Zikopoulos and Barbas, 2013). …”

Section: Evolutional and Neurobiological Understanding Of Psychopathomentioning

confidence: 99%

Animal models in psychiatric research: The RDoC system as a new framework for endophenotype-oriented translational neuroscience

Anderzhanova

Kirmeier

Wotjak

2017

Neurobiology of Stress

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The recently proposed Research Domain Criteria (RDoC) system defines psychopathologies as phenomena of multilevel neurobiological existence and assigns them to 5 behavioural domains characterizing a brain in action. We performed an analysis on this contemporary concept of psychopathologies in respect to a brain phylogeny and biological substrates of psychiatric diseases. We found that the RDoC system uses biological determinism to explain the pathogenesis of distinct psychiatric symptoms and emphasises exploration of endophenotypes but not of complex diseases. Therefore, as a possible framework for experimental studies it allows one to evade a major challenge of translational studies of strict disease-to-model correspondence. The system conforms with the concept of a normality and pathology continuum, therefore, supports basic studies. The units of analysis of the RDoC system appear as a novel matrix for model validation. The general regulation and arousal, positive valence, negative valence, and social interactions behavioural domains of the RDoC system show basic construct, network, and phenomenological homologies between human and experimental animals. The nature and complexity of the cognitive behavioural domain of the RDoC system deserve further clarification. These homologies in the 4 domains justifies the validity, reliably and translatability of animal models appearing as endophenotypes of the negative and positive affect, social interaction and general regulation and arousal systems’ dysfunction.

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Insights into the Neural and Genetic Basis of Vocal Communication

Cited by 77 publications

References 131 publications

A Diagnostic Marker to Discriminate Childhood Apraxia of Speech From Speech Delay: IV. The Pause Marker Index

A Diagnostic Marker to Discriminate Childhood Apraxia of Speech From Speech Delay: IV. The Pause Marker Index

Genetic identification of a hindbrain nucleus essential for innate vocalization

Animal models in psychiatric research: The RDoC system as a new framework for endophenotype-oriented translational neuroscience

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