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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

The effects of administration of bromocriptine on sensory gating in the PFC. Brom 0.313 – bromocriptine 0.313 mg/kg; Brom 0.625 – bromocriptine 0.625 mg/kg; Brom 1.25 – bromocriptine 1.25 mg/kg; CP3 – left parietal lobe; CP4 – right parietal lobe; F3 – left PFC; F4 – right PFC; FT7 – left temporal lobe; FT8 – right temporal lobe; O1 – left occipital area; O2 – right occipital area. The SG ratio (sensory gating ratio = SG[60–90 min]/SG[0–30] min) is shown. With Brom0.313 compared with saline, sensory gating was not significantly different in the eight areas of the brain. In the FT8, sensory gating with Brom0.625 was significantly higher than that in the saline group (P=0.03), and the remaining areas were not significantly different. Compared with the saline group, there were no significant differences in sensory gating in any of the brain areas with Brom 1.25. There was no significant difference in sensory gating between doses (P>0.05). The data are expressed as the mean ±SD. * represents P<0.05, with the one-way repeated-measures ANOVA and LSD post hoc test.
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f1-medscimonit-22-1752: The effects of administration of bromocriptine on sensory gating in the PFC. Brom 0.313 – bromocriptine 0.313 mg/kg; Brom 0.625 – bromocriptine 0.625 mg/kg; Brom 1.25 – bromocriptine 1.25 mg/kg; CP3 – left parietal lobe; CP4 – right parietal lobe; F3 – left PFC; F4 – right PFC; FT7 – left temporal lobe; FT8 – right temporal lobe; O1 – left occipital area; O2 – right occipital area. The SG ratio (sensory gating ratio = SG[60–90 min]/SG[0–30] min) is shown. With Brom0.313 compared with saline, sensory gating was not significantly different in the eight areas of the brain. In the FT8, sensory gating with Brom0.625 was significantly higher than that in the saline group (P=0.03), and the remaining areas were not significantly different. Compared with the saline group, there were no significant differences in sensory gating in any of the brain areas with Brom 1.25. There was no significant difference in sensory gating between doses (P>0.05). The data are expressed as the mean ±SD. * represents P<0.05, with the one-way repeated-measures ANOVA and LSD post hoc test.

Mentions: Bromocriptine (0.313 mg/kg) had no obvious effect on sensory gating in the PFC or other areas compared with the control; therefore, low-dose bromocriptine did not significantly disrupt the gating in the PFC. There was a significant effect of bromocriptine (0.625 mg/kg) in the right temporal lobe relative to the control group (P=0.03). There was no significant difference in sensory gating in any other area. These results showed that the mid-dose bromocriptine disrupted sensory gating in the right temporal lobe, but not in the PFC. There was no significant difference in sensory gating in the presence of bromocriptine (1.25 mg/kg) compared with the control (P>0.05); thus, high-dose bromocriptine did not damage the PFC. With the increase in dose, increases in the ratios in CP3 (left parietal lobe), F3 (left PFC), F4 (rPFC), and FT7 (left temporal lobe) were seen. The ratio was the highest following administration of mid-dose bromocriptine in the rest of the areas, but the differences were not significant (F (1, 15)=1.444; P>0.05) (Figure 1).


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)

The effects of administration of bromocriptine on sensory gating in the PFC. Brom 0.313 – bromocriptine 0.313 mg/kg; Brom 0.625 – bromocriptine 0.625 mg/kg; Brom 1.25 – bromocriptine 1.25 mg/kg; CP3 – left parietal lobe; CP4 – right parietal lobe; F3 – left PFC; F4 – right PFC; FT7 – left temporal lobe; FT8 – right temporal lobe; O1 – left occipital area; O2 – right occipital area. The SG ratio (sensory gating ratio = SG[60–90 min]/SG[0–30] min) is shown. With Brom0.313 compared with saline, sensory gating was not significantly different in the eight areas of the brain. In the FT8, sensory gating with Brom0.625 was significantly higher than that in the saline group (P=0.03), and the remaining areas were not significantly different. Compared with the saline group, there were no significant differences in sensory gating in any of the brain areas with Brom 1.25. There was no significant difference in sensory gating between doses (P>0.05). The data are expressed as the mean ±SD. * represents P<0.05, with the one-way repeated-measures ANOVA and LSD post hoc test.
© Copyright Policy - open-access
Related In: Results  -  Collection

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getmorefigures.php?uid=PMC4920095&req=5

f1-medscimonit-22-1752: The effects of administration of bromocriptine on sensory gating in the PFC. Brom 0.313 – bromocriptine 0.313 mg/kg; Brom 0.625 – bromocriptine 0.625 mg/kg; Brom 1.25 – bromocriptine 1.25 mg/kg; CP3 – left parietal lobe; CP4 – right parietal lobe; F3 – left PFC; F4 – right PFC; FT7 – left temporal lobe; FT8 – right temporal lobe; O1 – left occipital area; O2 – right occipital area. The SG ratio (sensory gating ratio = SG[60–90 min]/SG[0–30] min) is shown. With Brom0.313 compared with saline, sensory gating was not significantly different in the eight areas of the brain. In the FT8, sensory gating with Brom0.625 was significantly higher than that in the saline group (P=0.03), and the remaining areas were not significantly different. Compared with the saline group, there were no significant differences in sensory gating in any of the brain areas with Brom 1.25. There was no significant difference in sensory gating between doses (P>0.05). The data are expressed as the mean ±SD. * represents P<0.05, with the one-way repeated-measures ANOVA and LSD post hoc test.
Mentions: Bromocriptine (0.313 mg/kg) had no obvious effect on sensory gating in the PFC or other areas compared with the control; therefore, low-dose bromocriptine did not significantly disrupt the gating in the PFC. There was a significant effect of bromocriptine (0.625 mg/kg) in the right temporal lobe relative to the control group (P=0.03). There was no significant difference in sensory gating in any other area. These results showed that the mid-dose bromocriptine disrupted sensory gating in the right temporal lobe, but not in the PFC. There was no significant difference in sensory gating in the presence of bromocriptine (1.25 mg/kg) compared with the control (P>0.05); thus, high-dose bromocriptine did not damage the PFC. With the increase in dose, increases in the ratios in CP3 (left parietal lobe), F3 (left PFC), F4 (rPFC), and FT7 (left temporal lobe) were seen. The ratio was the highest following administration of mid-dose bromocriptine in the rest of the areas, but the differences were not significant (F (1, 15)=1.444; P>0.05) (Figure 1).

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