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Pharmacological Mechanisms of Cortical Enhancement Induced by the Repetitive Pairing of Visual/Cholinergic Stimulation.

Kang JI, Huppé-Gourgues F, Vaucher E - PLoS ONE (2015)

Bottom Line: The post-training VEP amplitude was significantly increased compared to the pre-training values for the trained spatial frequency and to adjacent spatial frequencies up to 0.3 CPD, suggesting a long-term increase of V1 sensitivity.However, the M1 mAChR antagonist blocked the increase of the VEP amplitude only for the high spatial frequency (0.3 CPD), suggesting that M1 role was limited to the spread of the enhancement effect to a higher spatial frequency.These findings demonstrate that visual training coupled with cholinergic stimulation improved perceptual sensitivity by enhancing cortical responsiveness in V1.

View Article: PubMed Central - PubMed

Affiliation: École d'optométrie, Université de Montréal, CP 6128 succursale centre-ville, Montréal, Qc, H3C 3J7, Canada; Département de Neuroscience, Université de Montréal, CP 6128 succursale centre-ville, Montréal, Qc, H3C 3J7, Canada.

ABSTRACT
Repetitive visual training paired with electrical activation of cholinergic projections to the primary visual cortex (V1) induces long-term enhancement of cortical processing in response to the visual training stimulus. To better determine the receptor subtypes mediating this effect the selective pharmacological blockade of V1 nicotinic (nAChR), M1 and M2 muscarinic (mAChR) or GABAergic A (GABAAR) receptors was performed during the training session and visual evoked potentials (VEPs) were recorded before and after training. The training session consisted of the exposure of awake, adult rats to an orientation-specific 0.12 CPD grating paired with an electrical stimulation of the basal forebrain for a duration of 1 week for 10 minutes per day. Pharmacological agents were infused intracortically during this period. The post-training VEP amplitude was significantly increased compared to the pre-training values for the trained spatial frequency and to adjacent spatial frequencies up to 0.3 CPD, suggesting a long-term increase of V1 sensitivity. This increase was totally blocked by the nAChR antagonist as well as by an M2 mAChR subtype and GABAAR antagonist. Moreover, administration of the M2 mAChR antagonist also significantly decreased the amplitude of the control VEPs, suggesting a suppressive effect on cortical responsiveness. However, the M1 mAChR antagonist blocked the increase of the VEP amplitude only for the high spatial frequency (0.3 CPD), suggesting that M1 role was limited to the spread of the enhancement effect to a higher spatial frequency. More generally, all the drugs used did block the VEP increase at 0.3 CPD. Further, use of each of the aforementioned receptor antagonists blocked training-induced changes in gamma and beta band oscillations. These findings demonstrate that visual training coupled with cholinergic stimulation improved perceptual sensitivity by enhancing cortical responsiveness in V1. This enhancement is mainly mediated by nAChRs, M2 mAChRs and GABAARs. The M1 mAChR subtype appears to be involved in spreading the enhancement of V1 cortical responsiveness to adjacent neurons.

No MeSH data available.


Related in: MedlinePlus

Change in VEP amplitudes following pharmacological modulation during visual/cholinergic stimulation (VS/HDB).The histograms represent the VEP difference of amplitude (Post-Pre training) for the different groups for the trained spatial frequency of 0.12 CPD (A) and 0.3 CPD (B). Note that the VEP amplitude enhancement following the visual/cholinergic training was blocked by MEC, AFDX, or PTX injection. (*; one-way ANOVA, post-hoc Dunnett, p < 0.05, compared to VS/HDB group, †; post-hoc Dunnett, p <0.05, compared to VS group). The error bars represent the average deviation. (Abbreviations; PZP: pirenzepine; MEC: mecamylamine; AFDX: AF-DX 116; MUS: muscimol and PTX: picrotoxin).
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pone.0141663.g003: Change in VEP amplitudes following pharmacological modulation during visual/cholinergic stimulation (VS/HDB).The histograms represent the VEP difference of amplitude (Post-Pre training) for the different groups for the trained spatial frequency of 0.12 CPD (A) and 0.3 CPD (B). Note that the VEP amplitude enhancement following the visual/cholinergic training was blocked by MEC, AFDX, or PTX injection. (*; one-way ANOVA, post-hoc Dunnett, p < 0.05, compared to VS/HDB group, †; post-hoc Dunnett, p <0.05, compared to VS group). The error bars represent the average deviation. (Abbreviations; PZP: pirenzepine; MEC: mecamylamine; AFDX: AF-DX 116; MUS: muscimol and PTX: picrotoxin).

Mentions: Blockade of nAChRs (mecamylamine: VS/HDB/MEC) disrupted the VEP amplitude enhancement induced by VS/HDB pairing for the trained 0.12 CPD spatial frequency (F [5,39] = 7.014, ANOVA, post-hoc Dunnett, p = 0.001 compared to VS/HDB) (Fig 3A). Antagonism of the M2 mAChR (AF-DX116) not only disrupted the VEP amplitude enhancement for the trained spatial frequency (p < 0.001) but also appeared to reduce the VEP amplitude compared to the basal level. Comparatively, specific blockade of M1 mAChR with pirenzepine did not disrupt the enhancement effect induced by VS/HDB pairing at 0.12 CPD (Fig 3A, p = 0.414).


Pharmacological Mechanisms of Cortical Enhancement Induced by the Repetitive Pairing of Visual/Cholinergic Stimulation.

Kang JI, Huppé-Gourgues F, Vaucher E - PLoS ONE (2015)

Change in VEP amplitudes following pharmacological modulation during visual/cholinergic stimulation (VS/HDB).The histograms represent the VEP difference of amplitude (Post-Pre training) for the different groups for the trained spatial frequency of 0.12 CPD (A) and 0.3 CPD (B). Note that the VEP amplitude enhancement following the visual/cholinergic training was blocked by MEC, AFDX, or PTX injection. (*; one-way ANOVA, post-hoc Dunnett, p < 0.05, compared to VS/HDB group, †; post-hoc Dunnett, p <0.05, compared to VS group). The error bars represent the average deviation. (Abbreviations; PZP: pirenzepine; MEC: mecamylamine; AFDX: AF-DX 116; MUS: muscimol and PTX: picrotoxin).
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4626033&req=5

pone.0141663.g003: Change in VEP amplitudes following pharmacological modulation during visual/cholinergic stimulation (VS/HDB).The histograms represent the VEP difference of amplitude (Post-Pre training) for the different groups for the trained spatial frequency of 0.12 CPD (A) and 0.3 CPD (B). Note that the VEP amplitude enhancement following the visual/cholinergic training was blocked by MEC, AFDX, or PTX injection. (*; one-way ANOVA, post-hoc Dunnett, p < 0.05, compared to VS/HDB group, †; post-hoc Dunnett, p <0.05, compared to VS group). The error bars represent the average deviation. (Abbreviations; PZP: pirenzepine; MEC: mecamylamine; AFDX: AF-DX 116; MUS: muscimol and PTX: picrotoxin).
Mentions: Blockade of nAChRs (mecamylamine: VS/HDB/MEC) disrupted the VEP amplitude enhancement induced by VS/HDB pairing for the trained 0.12 CPD spatial frequency (F [5,39] = 7.014, ANOVA, post-hoc Dunnett, p = 0.001 compared to VS/HDB) (Fig 3A). Antagonism of the M2 mAChR (AF-DX116) not only disrupted the VEP amplitude enhancement for the trained spatial frequency (p < 0.001) but also appeared to reduce the VEP amplitude compared to the basal level. Comparatively, specific blockade of M1 mAChR with pirenzepine did not disrupt the enhancement effect induced by VS/HDB pairing at 0.12 CPD (Fig 3A, p = 0.414).

Bottom Line: The post-training VEP amplitude was significantly increased compared to the pre-training values for the trained spatial frequency and to adjacent spatial frequencies up to 0.3 CPD, suggesting a long-term increase of V1 sensitivity.However, the M1 mAChR antagonist blocked the increase of the VEP amplitude only for the high spatial frequency (0.3 CPD), suggesting that M1 role was limited to the spread of the enhancement effect to a higher spatial frequency.These findings demonstrate that visual training coupled with cholinergic stimulation improved perceptual sensitivity by enhancing cortical responsiveness in V1.

View Article: PubMed Central - PubMed

Affiliation: École d'optométrie, Université de Montréal, CP 6128 succursale centre-ville, Montréal, Qc, H3C 3J7, Canada; Département de Neuroscience, Université de Montréal, CP 6128 succursale centre-ville, Montréal, Qc, H3C 3J7, Canada.

ABSTRACT
Repetitive visual training paired with electrical activation of cholinergic projections to the primary visual cortex (V1) induces long-term enhancement of cortical processing in response to the visual training stimulus. To better determine the receptor subtypes mediating this effect the selective pharmacological blockade of V1 nicotinic (nAChR), M1 and M2 muscarinic (mAChR) or GABAergic A (GABAAR) receptors was performed during the training session and visual evoked potentials (VEPs) were recorded before and after training. The training session consisted of the exposure of awake, adult rats to an orientation-specific 0.12 CPD grating paired with an electrical stimulation of the basal forebrain for a duration of 1 week for 10 minutes per day. Pharmacological agents were infused intracortically during this period. The post-training VEP amplitude was significantly increased compared to the pre-training values for the trained spatial frequency and to adjacent spatial frequencies up to 0.3 CPD, suggesting a long-term increase of V1 sensitivity. This increase was totally blocked by the nAChR antagonist as well as by an M2 mAChR subtype and GABAAR antagonist. Moreover, administration of the M2 mAChR antagonist also significantly decreased the amplitude of the control VEPs, suggesting a suppressive effect on cortical responsiveness. However, the M1 mAChR antagonist blocked the increase of the VEP amplitude only for the high spatial frequency (0.3 CPD), suggesting that M1 role was limited to the spread of the enhancement effect to a higher spatial frequency. More generally, all the drugs used did block the VEP increase at 0.3 CPD. Further, use of each of the aforementioned receptor antagonists blocked training-induced changes in gamma and beta band oscillations. These findings demonstrate that visual training coupled with cholinergic stimulation improved perceptual sensitivity by enhancing cortical responsiveness in V1. This enhancement is mainly mediated by nAChRs, M2 mAChRs and GABAARs. The M1 mAChR subtype appears to be involved in spreading the enhancement of V1 cortical responsiveness to adjacent neurons.

No MeSH data available.


Related in: MedlinePlus