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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

Design of the experimental procedure.A) Timeline of the different experimental steps. The pre-training visual cortical responses to visual stimulation were recorded 4 days (d5) after the implantation of the electrodes and guide cannulas. Visual training was provided for 10 min/day for 7 days (d7-d14) and followed by the recording of the post-training VEPs (d16) (see text for details). B) Schematic diagram illustrating the chronic implantation of the recording electrode and the push-pull guide cannula in V1. The stimulating electrode was implanted in the HDB. C) Schematic representation of the areas of pharmacological agent injection and electrophysiological recording. D) Representative VEP signal traces in response to a 0.12 CPD grating for the sham, pre- and post-training VS/HDB groups. The VEP was evoked by phase inversion after 2 seconds of stimulus presentation (0.25 Hz), and the amplitude was measured by subtracting the negative peak (a or a’) from the positive peak (b or b’). Note that the visual cortical response increased after the VS/HDB training (b’-a’) compared to sham (b-a).
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pone.0141663.g001: Design of the experimental procedure.A) Timeline of the different experimental steps. The pre-training visual cortical responses to visual stimulation were recorded 4 days (d5) after the implantation of the electrodes and guide cannulas. Visual training was provided for 10 min/day for 7 days (d7-d14) and followed by the recording of the post-training VEPs (d16) (see text for details). B) Schematic diagram illustrating the chronic implantation of the recording electrode and the push-pull guide cannula in V1. The stimulating electrode was implanted in the HDB. C) Schematic representation of the areas of pharmacological agent injection and electrophysiological recording. D) Representative VEP signal traces in response to a 0.12 CPD grating for the sham, pre- and post-training VS/HDB groups. The VEP was evoked by phase inversion after 2 seconds of stimulus presentation (0.25 Hz), and the amplitude was measured by subtracting the negative peak (a or a’) from the positive peak (b or b’). Note that the visual cortical response increased after the VS/HDB training (b’-a’) compared to sham (b-a).

Mentions: Recording electrode and injection guide were implanted in and over the rat V1, respectively, prior to VEP recording (day 1). Pre-training VEPs were recorded (day 5) followed by 7 days of VS/HDB training (day 7–14). Post-training VEPs were then recorded (day 16) (Fig 1A). Then, rats were euthanized with an overdose of pentobarbital and perfused with paraformaldehyde 4% in 0.1 M phosphate buffer, pH 7.4.


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

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

Design of the experimental procedure.A) Timeline of the different experimental steps. The pre-training visual cortical responses to visual stimulation were recorded 4 days (d5) after the implantation of the electrodes and guide cannulas. Visual training was provided for 10 min/day for 7 days (d7-d14) and followed by the recording of the post-training VEPs (d16) (see text for details). B) Schematic diagram illustrating the chronic implantation of the recording electrode and the push-pull guide cannula in V1. The stimulating electrode was implanted in the HDB. C) Schematic representation of the areas of pharmacological agent injection and electrophysiological recording. D) Representative VEP signal traces in response to a 0.12 CPD grating for the sham, pre- and post-training VS/HDB groups. The VEP was evoked by phase inversion after 2 seconds of stimulus presentation (0.25 Hz), and the amplitude was measured by subtracting the negative peak (a or a’) from the positive peak (b or b’). Note that the visual cortical response increased after the VS/HDB training (b’-a’) compared to sham (b-a).
© Copyright Policy
Related In: Results  -  Collection

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

pone.0141663.g001: Design of the experimental procedure.A) Timeline of the different experimental steps. The pre-training visual cortical responses to visual stimulation were recorded 4 days (d5) after the implantation of the electrodes and guide cannulas. Visual training was provided for 10 min/day for 7 days (d7-d14) and followed by the recording of the post-training VEPs (d16) (see text for details). B) Schematic diagram illustrating the chronic implantation of the recording electrode and the push-pull guide cannula in V1. The stimulating electrode was implanted in the HDB. C) Schematic representation of the areas of pharmacological agent injection and electrophysiological recording. D) Representative VEP signal traces in response to a 0.12 CPD grating for the sham, pre- and post-training VS/HDB groups. The VEP was evoked by phase inversion after 2 seconds of stimulus presentation (0.25 Hz), and the amplitude was measured by subtracting the negative peak (a or a’) from the positive peak (b or b’). Note that the visual cortical response increased after the VS/HDB training (b’-a’) compared to sham (b-a).
Mentions: Recording electrode and injection guide were implanted in and over the rat V1, respectively, prior to VEP recording (day 1). Pre-training VEPs were recorded (day 5) followed by 7 days of VS/HDB training (day 7–14). Post-training VEPs were then recorded (day 16) (Fig 1A). Then, rats were euthanized with an overdose of pentobarbital and perfused with paraformaldehyde 4% in 0.1 M phosphate buffer, pH 7.4.

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