GABAergic activity in autism spectrum disorders: an investigation of cortical inhibition via transcranial magnetic stimulation

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Abstract

Mounting evidence suggests a possible role for ?-aminobutyric acid (GABA) in the neuropathophysiology of autism spectrum disorders (ASD), but the extent of this impairment is unclear. A non-invasive, in vivo measure of GABA involves transcranial magnetic stimulation (TMS) of the primary motor cortex to probe cortical inhibition. Individuals diagnosed with ASD (high-functioning autism or Asperger s disorder) (n = 36 [28 male]; mean age: 26.00 years) and a group of healthy individuals (n = 34 [23 male]; mean age: 26.21 years) (matched for age, gender, and cognitive function) were administered motor cortical TMS paradigms putatively measuring activity at GABAA and GABAB receptors (i.e., short and long interval paired pulse TMS, cortical silent period). All cortical inhibition paradigms yielded no difference between ASD and control groups. There was, however, evidence for short interval cortical inhibition (SICI) deficits among those ASD participants who had experienced early language delay, suggesting that GABA may be implicated in an ASD subtype. The current findings do not support a broad role for GABA in the neuropathophysiology of ASD, but provide further indication that GABAA could be involved in ASD where there is a delay in language acquisition.
Original languageEnglish
Pages (from-to)202 - 209
Number of pages8
JournalNeuropharmacology
Volume68
DOIs
Publication statusPublished - 2013

Cite this

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title = "GABAergic activity in autism spectrum disorders: an investigation of cortical inhibition via transcranial magnetic stimulation",
abstract = "Mounting evidence suggests a possible role for ?-aminobutyric acid (GABA) in the neuropathophysiology of autism spectrum disorders (ASD), but the extent of this impairment is unclear. A non-invasive, in vivo measure of GABA involves transcranial magnetic stimulation (TMS) of the primary motor cortex to probe cortical inhibition. Individuals diagnosed with ASD (high-functioning autism or Asperger s disorder) (n = 36 [28 male]; mean age: 26.00 years) and a group of healthy individuals (n = 34 [23 male]; mean age: 26.21 years) (matched for age, gender, and cognitive function) were administered motor cortical TMS paradigms putatively measuring activity at GABAA and GABAB receptors (i.e., short and long interval paired pulse TMS, cortical silent period). All cortical inhibition paradigms yielded no difference between ASD and control groups. There was, however, evidence for short interval cortical inhibition (SICI) deficits among those ASD participants who had experienced early language delay, suggesting that GABA may be implicated in an ASD subtype. The current findings do not support a broad role for GABA in the neuropathophysiology of ASD, but provide further indication that GABAA could be involved in ASD where there is a delay in language acquisition.",
author = "Enticott, {Peter Gregory} and Kennedy, {Hayley Ann} and Rinehart, {Nicole Joan} and Tonge, {Bruce John} and Bradshaw, {John Lockyer} and Fitzgerald, {Paul Bernard}",
year = "2013",
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language = "English",
volume = "68",
pages = "202 -- 209",
journal = "Neuropharmacology",
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GABAergic activity in autism spectrum disorders: an investigation of cortical inhibition via transcranial magnetic stimulation. / Enticott, Peter Gregory; Kennedy, Hayley Ann; Rinehart, Nicole Joan; Tonge, Bruce John; Bradshaw, John Lockyer; Fitzgerald, Paul Bernard.

In: Neuropharmacology, Vol. 68, 2013, p. 202 - 209.

Research output: Contribution to journalArticleResearchpeer-review

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AU - Fitzgerald, Paul Bernard

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AB - Mounting evidence suggests a possible role for ?-aminobutyric acid (GABA) in the neuropathophysiology of autism spectrum disorders (ASD), but the extent of this impairment is unclear. A non-invasive, in vivo measure of GABA involves transcranial magnetic stimulation (TMS) of the primary motor cortex to probe cortical inhibition. Individuals diagnosed with ASD (high-functioning autism or Asperger s disorder) (n = 36 [28 male]; mean age: 26.00 years) and a group of healthy individuals (n = 34 [23 male]; mean age: 26.21 years) (matched for age, gender, and cognitive function) were administered motor cortical TMS paradigms putatively measuring activity at GABAA and GABAB receptors (i.e., short and long interval paired pulse TMS, cortical silent period). All cortical inhibition paradigms yielded no difference between ASD and control groups. There was, however, evidence for short interval cortical inhibition (SICI) deficits among those ASD participants who had experienced early language delay, suggesting that GABA may be implicated in an ASD subtype. The current findings do not support a broad role for GABA in the neuropathophysiology of ASD, but provide further indication that GABAA could be involved in ASD where there is a delay in language acquisition.

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