Inferior frontal oscillations reveal visuo-motor matching for actions and speech: evidence from human intracranial recordings.

The neural correspondence between the systems responsible for the execution and recognition of actions has been suggested both in humans and non-human primates. Apart from being a key region of this visuo-motor observation-execution matching (OEM) system, the human inferior frontal gyrus (IFG) is also important for speech production. The functional overlap of visuo-motor OEM and speech, together with the phylogenetic history of the IFG as a motor area, has led to the idea that speech function has evolved from pre-existing motor systems and to the hypothesis that an OEM system may exist also for speech. However, visuo-motor OEM and speech OEM have never been compared directly. We used electrocorticography to analyze oscillations recorded from intracranial electrodes in human fronto-parieto-temporal cortex during visuo-motor (executing or visually observing an action) and speech OEM tasks (verbally describing an action using the first or third person pronoun). The results show that neural activity related to visuo-motor OEM is widespread in the frontal, parietal, and temporal regions. Speech OEM also elicited widespread responses partly overlapping with visuo-motor OEM sites (bilaterally), including frontal, parietal, and temporal regions. Interestingly a more focal region, the inferior frontal gyrus (bilaterally), showed both visuo-motor OEM and speech OEM properties independent of orolingual speech-unrelated movements. Building on the methodological advantages in human invasive electrocorticography, the present findings provide highly precise spatial and temporal information to support the existence of a modality-independent action representation system in the human brain that is shared between systems for performing, interpreting and describing actions

Body ownership and embodiment: vestibular and multisensory mechanisms

Body ownership and embodiment are two fundamental mechanisms of self-consciousness. The present article reviews neurological data about paroxysmal illusions during which body ownership and embodiment are affected differentially: autoscopic phenomena (out-of-body experience, heautoscopy, autoscopic hallucination, feeling-of-a-presence) and the room tilt illusion. We suggest that autoscopic phenomena and room tilt illusion are related to different types of failures to integrate body-related information (vestibular, proprioceptive and tactile cues) in addition to a mismatch between vestibular and visual references. In these patients, altered body ownership and embodiment has been shown to occur due to pathological activity at the temporoparietal junction and other vestibular-related areas arguing for a key importance of vestibular processing. We also review the possibilities of manipulating body ownership and embodiment in healthy subjects through exposition to weightlessness as well as caloric and galvanic stimulation of the peripheral vestibular apparatus. In healthy subjects, disturbed self-processing might be related to interference of vestibular stimulation with vestibular cortex leading to disintegration of bodily information and altered body ownership and embodiment. We finally propose a differential contribution of the vestibular cortical areas to the different forms of altered body ownership and embodiment

Cell phone-supported cognitive behavioural therapy for anxiety disorders: a protocol for effectiveness studies in frontline settings

The resulting protocol (NCT01205191 at clinicaltrials.gov) for use in frontline clinical practice in which effectiveness, adherence, and the role of the therapists are analyzed, provides evidence for what are truly valuable cell phone-supported CBT treatments and guidance for the broader introduction of CBT in health services.Original Publication:Joakim Ekberg, Toomas Timpka, Magnus Bång, Anders Fröberg, Karin Halje and Henrik Eriksson, Cell phone-supported cognitive behavioural therapy for anxiety disorders: a protocol for effectiveness studies in frontline settings., 2011, BMC medical research methodology, (11), 3.http://dx.doi.org/10.1186/1471-2288-11-3Copyright: BioMed Centralhttp://www.biomedcentral.com

Optostimulation of striatonigral terminals in substantia nigra induces dyskinesia that increases after L‐DOPA in a mouse model of Parkinson's disease

Background and Purpose: L-DOPA-induced dyskinesia (LID) remains a major complication of L-DOPA therapy in Parkinson's disease. LID is believed to result from inhibition of substantia nigra reticulata (SNr) neurons by GABAergic striatal projection neurons that become supersensitive to dopamine receptor stimulation after severe nigrostriatal degeneration. Here, we asked if stimulation of direct medium spiny neuron (dMSN) GABAergic terminals at the SNr can produce a full dyskinetic state similar to that induced by L-DOPA. Experimental Approach: Adult C57BL6 mice were lesioned with 6-hydroxydopamine in the medial forebrain bundle. Channel rhodopsin was expressed in striatonigral terminals by ipsilateral striatal injection of adeno-associated viral particles under the CaMKII promoter. Optic fibres were implanted on the ipsilateral SNr. Optical stimulation was performed before and 24 hr after three daily doses of L-DOPA at subthreshold and suprathreshold dyskinetic doses. We also examined the combined effect of light stimulation and an acute L-DOPA challenge. Key Results: Optostimulation of striatonigral terminals inhibited SNr neurons and induced all dyskinesia subtypes (optostimulation-induced dyskinesia [OID]) in 6-hydroxydopamine animals, but not in sham-lesioned animals. Additionally, chronic L-DOPA administration sensitised dyskinetic responses to striatonigral terminal optostimulation, as OIDs were more severe 24 hr after L-DOPA administration. Furthermore, L-DOPA combined with light stimulation did not result in higher dyskinesia scores than OID alone, suggesting that optostimulation has a masking effect on LID. Conclusion and Implications: This work suggests that striatonigral inhibition of basal ganglia output (SNr) is a decisive mechanism mediating LID and identifies the SNr as a target for managing LID.Fil: Keifman, Ettel. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Fisiología y Biofísica Bernardo Houssay. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Fisiología y Biofísica Bernardo Houssay; Argentina. Consejo Superior de Investigaciones Científicas; EspañaFil: Ruiz De Diego, Irene. Consejo Superior de Investigaciones Científicas; EspañaFil: Pafundo, Diego Esteban. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Fisiología y Biofísica Bernardo Houssay. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Fisiología y Biofísica Bernardo Houssay; ArgentinaFil: Paz, Rodrigo Manuel. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Fisiología y Biofísica Bernardo Houssay. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Fisiología y Biofísica Bernardo Houssay; ArgentinaFil: Solís, Oscar. Consejo Superior de Investigaciones Científicas; EspañaFil: Murer, Mario Gustavo. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Fisiología y Biofísica Bernardo Houssay. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Fisiología y Biofísica Bernardo Houssay; ArgentinaFil: Moratalla, Rosario. Consejo Superior de Investigaciones Científicas; Españ

Body ownership and embodiment: Vestibular and multisensory mechanisms

International audienceBody ownership and embodiment are two fundamental mechanisms of self-consciousness. The present article reviews neurological data about paroxysmal illusions during which body ownership and embodiment are affected differentially: autoscopic phenomena (out-of-body experience, heautoscopy, autoscopic hallucination, feeling-of-a-presence) and the room tilt illusion. We suggest that autoscopic phenomena and room tilt illusion are related to different types of failures to integrate body-related information (vestibular, proprioceptive and tactile cues) in addition to a mismatch between vestibular and visual references. In these patients, altered body ownership and embodiment has been shown to occur due to pathological activity at the temporoparietal junction and other vestibular-related areas arguing for a key importance of vestibular processing. We also review the possibilities of manipulating body ownership and embodiment in healthy subjects through exposition to weightlessness as welt as caloric and galvanic stimulation of the peripheral, vestibular apparatus. In healthy subjects, disturbed self-processing might be related to interference of vestibular stimulation with vestibular cortex leading to disintegration of bodily information and altered body ownership and embodiment. We finally propose a differential contribution of the vestibular cortical areas to the different forms of altered body ownership and embodiment. (C) 2008 Elsevier Masson SAS. All rights reserved

The translationally relevant mouse model of the 15q13.3 microdeletion syndrome reveals deficits in neuronal spike firing matching clinical neurophysiological biomarkers seen in schizophrenia

AIM: To date, the understanding and development of novel treatments for mental illness is hampered by inadequate animal models. For instance, it is unclear to what extent commonly used behavioural tests in animals can inform us on the mental and affective aspects of schizophrenia.METHODS: To link pathophysiological processes in an animal model to clinical findings, we have here utilized the recently developed Df(h15q13)/+ mouse model for detailed investigations of cortical neuronal engagement during pre-attentive processing of auditory information from two back-translational auditory paradigms. We also investigate if compromised putative fast-spiking interneurone (FSI) function can be restored through pharmacological intervention using the Kv3.1 channel opener RE1. Chronic multi-array electrodes in primary auditory cortex were used to record single cell firing from putative pyramidal and FSI in awake animals during processing of auditory sensory information.RESULTS: We find a decreased amplitude in the response to auditory stimuli and reduced recruitment of neurones to fast steady-state gamma oscillatory activity. These results resemble encephalography recordings in patients with schizophrenia. Furthermore, the probability of interneurones to fire with low interspike intervals during 80 Hz auditory stimulation was reduced in Df(h15q13)/+ mice, an effect that was partially reversed by the Kv3.1 channel modulator, RE1.CONCLUSIONS: This study offers insight into the consequences on a neuronal level of carrying the 15q13.3 microdeletion. Furthermore, it points to deficient functioning of interneurones as a potential pathophysiological mechanism in schizophrenia and suggests a therapeutic potential of Kv3.1 channel openers