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Segmental disinhibition suppresses C-fiber inputs to the rat superficial medullary dorsal horn via the activation of GABAB receptors.

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Title: Segmental disinhibition suppresses C-fiber inputs to the rat superficial medullary dorsal horn via the activation of GABAB receptors.
Authors: Melin, Céline, Jacquot, Florian, Dallel, Radhouane, Artola, Alain
Source: European Journal of Neuroscience. Feb2013, Vol. 37 Issue 3, p417-428. 12p.
Subjects: GABA receptors, Allergies, Neural transmission, Chronic pain, Laboratory rats, Electric stimulation
Abstract: Specialized primary afferents, although they terminate in different laminae within the dorsal horn ( DH), are known to interact through local circuit excitatory and inhibitory neurons. That a loss of segmental inhibition probably contributes to persistent pain hypersensitivity during chronic pain raises the question as to how disinhibition-induced changes in cross-modal interactions account for chronic pain symptoms. We sought to characterize how pharmacological blockade of glycine and gamma-aminobutyric acid ( GABA) receptors modifies synaptic transmission between primary afferent fibers and second-order neurons by recording field potentials in the superficial medullary dorsal horn ( MDH) of anesthetized rats. Transcutaneous electrical stimulation evokes three negative field potentials elicited by, from earliest to latest, Aβ-, Aδ- and C-fiber primary afferents. Blocking segmental glycine and/or GABAA receptors, with strychnine and bicuculline, respectively, strongly facilitates Aβ- and Aδ-fiber-evoked polysynaptic field potentials but, conversely, inhibits, or even abolishes, the whole C-fiber field potential. Blocking segmental GABAB receptors, with phaclofen, reverses such suppression of C-fiber field potentials. Interestingly, it also potentiates C-fiber field potentials under control conditions. Finally, activation of segmental GABAB receptors, with baclofen, preferentially inhibits C-fiber field potentials. Our results suggest that activation of A-fiber primary afferents inhibits C-fiber inputs to the MDH by the way of polysynaptic excitatory pathways, last-order GABAergic interneurons and presynaptic GABAB receptors on C-fiber primary afferents. Under physiological conditions, activation of such local DH circuits is closely controlled by segmental inhibition but it might contribute to paradoxically reduced pain hypersensitivity under pathological disinhibition. [ABSTRACT FROM AUTHOR]
Copyright of European Journal of Neuroscience is the property of Wiley-Blackwell and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)
Database: Psychology and Behavioral Sciences Collection
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  Data: Segmental disinhibition suppresses C-fiber inputs to the rat superficial medullary dorsal horn via the activation of GABA<subscript>B</subscript> receptors.
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  Data: <searchLink fieldCode="AR" term="%22Melin%2C+Céline%22">Melin, Céline</searchLink><br /><searchLink fieldCode="AR" term="%22Jacquot%2C+Florian%22">Jacquot, Florian</searchLink><br /><searchLink fieldCode="AR" term="%22Dallel%2C+Radhouane%22">Dallel, Radhouane</searchLink><br /><searchLink fieldCode="AR" term="%22Artola%2C+Alain%22">Artola, Alain</searchLink>
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  Data: <searchLink fieldCode="JN" term="%22European+Journal+of+Neuroscience%22">European Journal of Neuroscience</searchLink>. Feb2013, Vol. 37 Issue 3, p417-428. 12p.
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  Data: <searchLink fieldCode="DE" term="%22GABA+receptors%22">GABA receptors</searchLink><br /><searchLink fieldCode="DE" term="%22Allergies%22">Allergies</searchLink><br /><searchLink fieldCode="DE" term="%22Neural+transmission%22">Neural transmission</searchLink><br /><searchLink fieldCode="DE" term="%22Chronic+pain%22">Chronic pain</searchLink><br /><searchLink fieldCode="DE" term="%22Laboratory+rats%22">Laboratory rats</searchLink><br /><searchLink fieldCode="DE" term="%22Electric+stimulation%22">Electric stimulation</searchLink>
– Name: Abstract
  Label: Abstract
  Group: Ab
  Data: Specialized primary afferents, although they terminate in different laminae within the dorsal horn ( DH), are known to interact through local circuit excitatory and inhibitory neurons. That a loss of segmental inhibition probably contributes to persistent pain hypersensitivity during chronic pain raises the question as to how disinhibition-induced changes in cross-modal interactions account for chronic pain symptoms. We sought to characterize how pharmacological blockade of glycine and gamma-aminobutyric acid ( GABA) receptors modifies synaptic transmission between primary afferent fibers and second-order neurons by recording field potentials in the superficial medullary dorsal horn ( MDH) of anesthetized rats. Transcutaneous electrical stimulation evokes three negative field potentials elicited by, from earliest to latest, Aβ-, Aδ- and C-fiber primary afferents. Blocking segmental glycine and/or GABAA receptors, with strychnine and bicuculline, respectively, strongly facilitates Aβ- and Aδ-fiber-evoked polysynaptic field potentials but, conversely, inhibits, or even abolishes, the whole C-fiber field potential. Blocking segmental GABAB receptors, with phaclofen, reverses such suppression of C-fiber field potentials. Interestingly, it also potentiates C-fiber field potentials under control conditions. Finally, activation of segmental GABAB receptors, with baclofen, preferentially inhibits C-fiber field potentials. Our results suggest that activation of A-fiber primary afferents inhibits C-fiber inputs to the MDH by the way of polysynaptic excitatory pathways, last-order GABAergic interneurons and presynaptic GABAB receptors on C-fiber primary afferents. Under physiological conditions, activation of such local DH circuits is closely controlled by segmental inhibition but it might contribute to paradoxically reduced pain hypersensitivity under pathological disinhibition. [ABSTRACT FROM AUTHOR]
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  Data: <i>Copyright of European Journal of Neuroscience is the property of Wiley-Blackwell and its content may not be copied or emailed to multiple sites without the copyright holder's express written permission. Additionally, content may not be used with any artificial intelligence tools or machine learning technologies. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract.</i> (Copyright applies to all Abstracts.)
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        Value: 10.1111/ejn.12048
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      – SubjectFull: Neural transmission
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              Text: Feb2013
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              Y: 2013
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