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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 compared with haloperidol in the PFC. Hal 0.001 – haloperidol 0.001 mg/kg; Hal 0.01 – haloperidol 0.01 mg/kg; Hal 0.05 – haloperidol 0.05 mg/kg. Brom 0.313, Brom 0.625, and Brom 1.25 – bromocriptine 0.313 mg/kg, bromocriptine 0.625 mg/kg, and bromocriptine 1.25 mg/kg, respectively. 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 lobe; O2 – right occipital lobe. SG ratio (sensory gating ratio = SG[60–90] min/SG[0–30] min) is shown. Sensory gating in the bromocriptine group was obviously lower than that in the haloperidol group in the left parietal lobe (P<0.05) and the rPFC (P=0.055) at the low dose. At the high dose, gating in the bromocriptine group was significantly higher than that in the haloperidol group in the rPFC (P<0.05) and the left temporal lobe (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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f3-medscimonit-22-1752: The effects of administration of bromocriptine compared with haloperidol in the PFC. Hal 0.001 – haloperidol 0.001 mg/kg; Hal 0.01 – haloperidol 0.01 mg/kg; Hal 0.05 – haloperidol 0.05 mg/kg. Brom 0.313, Brom 0.625, and Brom 1.25 – bromocriptine 0.313 mg/kg, bromocriptine 0.625 mg/kg, and bromocriptine 1.25 mg/kg, respectively. 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 lobe; O2 – right occipital lobe. SG ratio (sensory gating ratio = SG[60–90] min/SG[0–30] min) is shown. Sensory gating in the bromocriptine group was obviously lower than that in the haloperidol group in the left parietal lobe (P<0.05) and the rPFC (P=0.055) at the low dose. At the high dose, gating in the bromocriptine group was significantly higher than that in the haloperidol group in the rPFC (P<0.05) and the left temporal lobe (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: In contrast to haloperidol, bromocriptine had a significant effect on the sensory gating ratio in the low-dose group in the left parietal lobe (P<0.05) and the rPFC (P=0.055). Sensory gating following bromocriptine treatment was obviously lower than that following haloperidol administration. In the high-dose treatment, bromocriptine, in contrast to haloperidol, had significant effects on the rPFC (P<0.05) and the left temporal lobe (P<0.05). Sensory gating following bromocriptine was significantly higher than it was following haloperidol. The dose effects of bromocriptine and haloperidol in the PFC and other areas differed between drug treatments. Increasing the dose of bromocriptine was followed by an increase in gating, but sensory gating with the haloperidol treatments declined (Figure 3).


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 compared with haloperidol in the PFC. Hal 0.001 – haloperidol 0.001 mg/kg; Hal 0.01 – haloperidol 0.01 mg/kg; Hal 0.05 – haloperidol 0.05 mg/kg. Brom 0.313, Brom 0.625, and Brom 1.25 – bromocriptine 0.313 mg/kg, bromocriptine 0.625 mg/kg, and bromocriptine 1.25 mg/kg, respectively. 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 lobe; O2 – right occipital lobe. SG ratio (sensory gating ratio = SG[60–90] min/SG[0–30] min) is shown. Sensory gating in the bromocriptine group was obviously lower than that in the haloperidol group in the left parietal lobe (P<0.05) and the rPFC (P=0.055) at the low dose. At the high dose, gating in the bromocriptine group was significantly higher than that in the haloperidol group in the rPFC (P<0.05) and the left temporal lobe (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

Show All Figures
getmorefigures.php?uid=PMC4920095&req=5

f3-medscimonit-22-1752: The effects of administration of bromocriptine compared with haloperidol in the PFC. Hal 0.001 – haloperidol 0.001 mg/kg; Hal 0.01 – haloperidol 0.01 mg/kg; Hal 0.05 – haloperidol 0.05 mg/kg. Brom 0.313, Brom 0.625, and Brom 1.25 – bromocriptine 0.313 mg/kg, bromocriptine 0.625 mg/kg, and bromocriptine 1.25 mg/kg, respectively. 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 lobe; O2 – right occipital lobe. SG ratio (sensory gating ratio = SG[60–90] min/SG[0–30] min) is shown. Sensory gating in the bromocriptine group was obviously lower than that in the haloperidol group in the left parietal lobe (P<0.05) and the rPFC (P=0.055) at the low dose. At the high dose, gating in the bromocriptine group was significantly higher than that in the haloperidol group in the rPFC (P<0.05) and the left temporal lobe (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: In contrast to haloperidol, bromocriptine had a significant effect on the sensory gating ratio in the low-dose group in the left parietal lobe (P<0.05) and the rPFC (P=0.055). Sensory gating following bromocriptine treatment was obviously lower than that following haloperidol administration. In the high-dose treatment, bromocriptine, in contrast to haloperidol, had significant effects on the rPFC (P<0.05) and the left temporal lobe (P<0.05). Sensory gating following bromocriptine was significantly higher than it was following haloperidol. The dose effects of bromocriptine and haloperidol in the PFC and other areas differed between drug treatments. Increasing the dose of bromocriptine was followed by an increase in gating, but sensory gating with the haloperidol treatments declined (Figure 3).

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