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Please use this identifier to cite or link to this item: http://hdl.handle.net/123456789/14567

Title: Effects of bromocriptine and haloperidol on prepulse inhibition; comparison of the acoustic startle eyeblink response and the N1/P2 auditory evoked response in man.
Authors: K.A.J. Abduljawad
C.M., & Szabadi,
Keywords: acoustic startle response; auditory-evoked potential; bromocriptine; D2 dopamine receptors; eyeblink; haloperidol; N1/P2 complex; prepulse inhibition
Issue Date: 1999
Publisher: British Journal of psychopharm
Abstract: Experiments with animals have shown that D2 dopamine receptors are involved in regulating prepulse inhibition (PPI) of the acoustic startler reflex (suppression of there reflex response evoked by a loud sound by prior presentation of a low-intensitystimulus). Recently we found that PPI of the human eyeblink startle response could be suppressed by a D2 receptor agonist, bromocriptine, and that this suppression could be reversed by a D receptor-blocking neuroleptic, haloperidol. The present work attempted to replicate this finding and to extend it to PPI of the N1/P2 component of the auditory-evoked potential. Eleven healthy males (18-30years) participated in four sessions in which they received oral doses of placebo, bromocriptine 1.25mg, haloperidol 3mg and combined treatment with bromocriptine 1.25mg + haloperidol 3mg, according to a balanced double-blind protocol. Thirty-minute simultaneous recording soft heel ectromyographic(EMG) haloperidol 3mg and combined treatment with bromocriptine 1.25mg + haloperidol 3mg, according to a 120min after ingestion of haloperidol and/or 90min after ingestion of bromocriptine. Sound stimuli(1-kHz) were presented in 60 trials separated by variable intervals (mean25sec): (i) 40msec 115dB (`pulsealone':20 trials); (ii) 40msec 85dB (20trials); (iii) 40msec 85dB, followed after 120msec by 40msec 115dB (`prepulse/ pulse': 20trials). The amplitudes of the EMG and N1/P2 responses were not altered significantly by any of the treatments. Bromocriptine attenuated PPI of the EMG response significantly, this attenuation being absent following combined haloperidol/bromocriptine treatment. Neither bromocriptine nor haloperidol significantly altered PPI of the N1/P2 complex. Bromocriptine suppressed and haloperidol elevated serum prolactin levels, these changes being absent when the two drugs were given in combination. The results suggest that different mechanisms maybe involved in regulating PPI of the eyeblink and the N1/P2 component of the auditory-evoked potential, and that D2 receptors maybe involved in the former case, but not the latter.
URI: http://hdl.handle.net/123456789/14567
Appears in Collections:College of Applied Medical Sciences

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