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Dose-Dependent Changes in Auditory Sensory Gating in the Prefrontal Cortex of the Cynomolgus Monkey.

Huang H, Ya J, Wu Z, Wen C, Zheng S, Tian C, Ren H, Carlson S, Yu H, Chen F, Wang J - Med. Sci. Monit. (2016)

Bottom Line: RESULTS We demonstrated the following: (1) Administration of mid-dose bromocriptine disrupted sensory gating (N100) in the right temporal lobe, while neither low-dose nor high-dose bromocriptine impaired gating. (2) Low-dose haloperidol impaired gating in the right prefrontal cortex.High-dose haloperidol had no obvious effect on sensory gating. (3) Gating was impaired by PCP in the left parietal lobe.The dopaminergic system influenced sensory gating in a dose- and region-dependent pattern, which might modulate the different stages that receive further processing due to novel information.

View Article: PubMed Central - PubMed

Affiliation: Second Department of Neurosurgery, First Affiliation Hospital of Kunming Medical University, Kunming, Yunnan, China (mainland).

ABSTRACT
BACKGROUND Sensory gating, often described as the ability to filter out irrelevant information that is repeated in close temporal proximity, is essential for the selection, processing, and storage of more salient information. This study aimed to test the effect of sensory gating under anesthesia in the prefrontal cortex (PFC) of monkeys following injection of bromocriptine, haloperidol, and phencyclidine (PCP). MATERIAL AND METHODS We used an auditory evoked potential that can be elicited by sound to examine sensory gating during treatment with haloperidol, bromocriptine, and PCP in the PFC in the cynomolgus monkey. Scalp electrodes were located in the bilateral PFC and bilateral temporal, bilateral parietal, and occipital lobes. Administration of bromocriptine (0.313 mg/kg, 0.625 mg/kg, and 1.25 mg/kg), haloperidol (0.001 mg/kg, 0.01 mg/kg, and 0.05 mg/kg), and the N-methyl-D-aspartic acid receptor antagonist PCP (0.3 mg/kg) influenced sensory gating. RESULTS We demonstrated the following: (1) Administration of mid-dose bromocriptine disrupted sensory gating (N100) in the right temporal lobe, while neither low-dose nor high-dose bromocriptine impaired gating. (2) Low-dose haloperidol impaired gating in the right prefrontal cortex. Mid-dose haloperidol disrupted sensory gating in left occipital lobe. High-dose haloperidol had no obvious effect on sensory gating. (3) Gating was impaired by PCP in the left parietal lobe. CONCLUSIONS Our studies showed that information processing was regulated by the dopaminergic system, which might play an important role in the PFC. The dopaminergic system influenced sensory gating in a dose- and region-dependent pattern, which might modulate the different stages that receive further processing due to novel information.

No MeSH data available.


Related in: MedlinePlus

Drug-dependent changes in the N100 amplitude of S1 and S2 in different cortical areas. CP3, F4, FT8, and O1 represent the left parietal lobe, rPFC, right temporal lobe, and left occipital lobe, respectively. Saline, saline-1, saline-2, and saline-3 were the control group, representing the values of different areas. S1 and S2 are the first and second sounds, respectively. The amplitude ratio is the amplitude of the S1 or S2 in the 60- to 90-min interval in contrast with that of the 0- to 30-min interval. The decline in the S1 amplitude and increase in the S2 amplitude in the FT8 were compared for bromocriptine 0.625 mg/kg (Brom 0.625) and saline. Haloperidol 0.001 mg/kg (Hal 0.001) compared with saline was tested for increase of S1 and S2 amplitude in the F4. An increase in the amplitude of S1 and S2 in the O1 was recorded in the haloperidol 0.01 mg/kg (Hal 0.01) group compared with the saline group. An increase in the S2 amplitude in the CP3 was recorded in the PCP group compared with the saline group. The data are expressed as the mean ±SD. * represents P<0.05, with the one-way repeated-measures ANOVA and LSD post hoc tests.
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f5-medscimonit-22-1752: Drug-dependent changes in the N100 amplitude of S1 and S2 in different cortical areas. CP3, F4, FT8, and O1 represent the left parietal lobe, rPFC, right temporal lobe, and left occipital lobe, respectively. Saline, saline-1, saline-2, and saline-3 were the control group, representing the values of different areas. S1 and S2 are the first and second sounds, respectively. The amplitude ratio is the amplitude of the S1 or S2 in the 60- to 90-min interval in contrast with that of the 0- to 30-min interval. The decline in the S1 amplitude and increase in the S2 amplitude in the FT8 were compared for bromocriptine 0.625 mg/kg (Brom 0.625) and saline. Haloperidol 0.001 mg/kg (Hal 0.001) compared with saline was tested for increase of S1 and S2 amplitude in the F4. An increase in the amplitude of S1 and S2 in the O1 was recorded in the haloperidol 0.01 mg/kg (Hal 0.01) group compared with the saline group. An increase in the S2 amplitude in the CP3 was recorded in the PCP group compared with the saline group. The data are expressed as the mean ±SD. * represents P<0.05, with the one-way repeated-measures ANOVA and LSD post hoc tests.

Mentions: The mid-dose of bromocriptine impaired sensory gating in the right temporal lobe. The amplitude of S1 was lower in the bromocriptine group than in the control group; however, the amplitude of S2 was not significantly different. Low-dose haloperidol disrupted sensory gating in the rPFC; this was mainly reflected in an increase in the amplitude of S2, while the increase in the amplitude of S1 was smaller. Further examination of the amplitude of S2 with mid-dose haloperidol indicated that when the differences in the amplitude of S2 and S1 in the haloperidol group relative to the control in the left occipital lobe were compared, S1 was increased to a lesser extent. PCP impaired sensory gating in the left parietal lobe, which was mainly reflected in an increase in S2; the change in S1 was not significant (Figure 5).


Dose-Dependent Changes in Auditory Sensory Gating in the Prefrontal Cortex of the Cynomolgus Monkey.

Huang H, Ya J, Wu Z, Wen C, Zheng S, Tian C, Ren H, Carlson S, Yu H, Chen F, Wang J - Med. Sci. Monit. (2016)

Drug-dependent changes in the N100 amplitude of S1 and S2 in different cortical areas. CP3, F4, FT8, and O1 represent the left parietal lobe, rPFC, right temporal lobe, and left occipital lobe, respectively. Saline, saline-1, saline-2, and saline-3 were the control group, representing the values of different areas. S1 and S2 are the first and second sounds, respectively. The amplitude ratio is the amplitude of the S1 or S2 in the 60- to 90-min interval in contrast with that of the 0- to 30-min interval. The decline in the S1 amplitude and increase in the S2 amplitude in the FT8 were compared for bromocriptine 0.625 mg/kg (Brom 0.625) and saline. Haloperidol 0.001 mg/kg (Hal 0.001) compared with saline was tested for increase of S1 and S2 amplitude in the F4. An increase in the amplitude of S1 and S2 in the O1 was recorded in the haloperidol 0.01 mg/kg (Hal 0.01) group compared with the saline group. An increase in the S2 amplitude in the CP3 was recorded in the PCP group compared with the saline group. The data are expressed as the mean ±SD. * represents P<0.05, with the one-way repeated-measures ANOVA and LSD post hoc tests.
© Copyright Policy - open-access
Related In: Results  -  Collection

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getmorefigures.php?uid=PMC4920095&req=5

f5-medscimonit-22-1752: Drug-dependent changes in the N100 amplitude of S1 and S2 in different cortical areas. CP3, F4, FT8, and O1 represent the left parietal lobe, rPFC, right temporal lobe, and left occipital lobe, respectively. Saline, saline-1, saline-2, and saline-3 were the control group, representing the values of different areas. S1 and S2 are the first and second sounds, respectively. The amplitude ratio is the amplitude of the S1 or S2 in the 60- to 90-min interval in contrast with that of the 0- to 30-min interval. The decline in the S1 amplitude and increase in the S2 amplitude in the FT8 were compared for bromocriptine 0.625 mg/kg (Brom 0.625) and saline. Haloperidol 0.001 mg/kg (Hal 0.001) compared with saline was tested for increase of S1 and S2 amplitude in the F4. An increase in the amplitude of S1 and S2 in the O1 was recorded in the haloperidol 0.01 mg/kg (Hal 0.01) group compared with the saline group. An increase in the S2 amplitude in the CP3 was recorded in the PCP group compared with the saline group. The data are expressed as the mean ±SD. * represents P<0.05, with the one-way repeated-measures ANOVA and LSD post hoc tests.
Mentions: The mid-dose of bromocriptine impaired sensory gating in the right temporal lobe. The amplitude of S1 was lower in the bromocriptine group than in the control group; however, the amplitude of S2 was not significantly different. Low-dose haloperidol disrupted sensory gating in the rPFC; this was mainly reflected in an increase in the amplitude of S2, while the increase in the amplitude of S1 was smaller. Further examination of the amplitude of S2 with mid-dose haloperidol indicated that when the differences in the amplitude of S2 and S1 in the haloperidol group relative to the control in the left occipital lobe were compared, S1 was increased to a lesser extent. PCP impaired sensory gating in the left parietal lobe, which was mainly reflected in an increase in S2; the change in S1 was not significant (Figure 5).

Bottom Line: RESULTS We demonstrated the following: (1) Administration of mid-dose bromocriptine disrupted sensory gating (N100) in the right temporal lobe, while neither low-dose nor high-dose bromocriptine impaired gating. (2) Low-dose haloperidol impaired gating in the right prefrontal cortex.High-dose haloperidol had no obvious effect on sensory gating. (3) Gating was impaired by PCP in the left parietal lobe.The dopaminergic system influenced sensory gating in a dose- and region-dependent pattern, which might modulate the different stages that receive further processing due to novel information.

View Article: PubMed Central - PubMed

Affiliation: Second Department of Neurosurgery, First Affiliation Hospital of Kunming Medical University, Kunming, Yunnan, China (mainland).

ABSTRACT
BACKGROUND Sensory gating, often described as the ability to filter out irrelevant information that is repeated in close temporal proximity, is essential for the selection, processing, and storage of more salient information. This study aimed to test the effect of sensory gating under anesthesia in the prefrontal cortex (PFC) of monkeys following injection of bromocriptine, haloperidol, and phencyclidine (PCP). MATERIAL AND METHODS We used an auditory evoked potential that can be elicited by sound to examine sensory gating during treatment with haloperidol, bromocriptine, and PCP in the PFC in the cynomolgus monkey. Scalp electrodes were located in the bilateral PFC and bilateral temporal, bilateral parietal, and occipital lobes. Administration of bromocriptine (0.313 mg/kg, 0.625 mg/kg, and 1.25 mg/kg), haloperidol (0.001 mg/kg, 0.01 mg/kg, and 0.05 mg/kg), and the N-methyl-D-aspartic acid receptor antagonist PCP (0.3 mg/kg) influenced sensory gating. RESULTS We demonstrated the following: (1) Administration of mid-dose bromocriptine disrupted sensory gating (N100) in the right temporal lobe, while neither low-dose nor high-dose bromocriptine impaired gating. (2) Low-dose haloperidol impaired gating in the right prefrontal cortex. Mid-dose haloperidol disrupted sensory gating in left occipital lobe. High-dose haloperidol had no obvious effect on sensory gating. (3) Gating was impaired by PCP in the left parietal lobe. CONCLUSIONS Our studies showed that information processing was regulated by the dopaminergic system, which might play an important role in the PFC. The dopaminergic system influenced sensory gating in a dose- and region-dependent pattern, which might modulate the different stages that receive further processing due to novel information.

No MeSH data available.


Related in: MedlinePlus