scholarly journals Impaired Prepulse Inhibition and Prepulse-Elicited Reactivity but Intact Reflex Circuit Excitability in Unmedicated Schizophrenia Patients: a Comparison With Healthy Subjects and Medicated Schizophrenia Patients

2009 ◽  
Vol 35 (1) ◽  
pp. 244-255 ◽  
Author(s):  
P. A. Csomor ◽  
B. K. Yee ◽  
J. Feldon ◽  
A. Theodoridou ◽  
E. Studerus ◽  
...  
Life ◽  
2021 ◽  
Vol 11 (10) ◽  
pp. 1024
Author(s):  
Yasuhiro Kawano ◽  
Eishi Motomura ◽  
Koji Inui ◽  
Motohiro Okada

An abrupt change in a sound feature (test stimulus) elicits a specific cerebral response, which is attenuated by a weaker sound feature change (prepulse) preceding the test stimulus. As an exploratory study, we investigated whether and how the magnitude of the change of the prepulse affects the degree of prepulse inhibition (PPI). Sound stimuli were 650 ms trains of clicks at 100 Hz. The test stimulus was an abrupt sound pressure increase (by 10 dB) in the click train. Three consecutive clicks, weaker (−5 dB, −10 dB, −30 dB, or gap) than the baseline, at 30, 40, and 50 ms before the test stimulus, were used as prepulses. Magnetic responses to the ten types of stimuli (test stimulus alone, control, four types of tests with prepulses, and four types of prepulses alone) were recorded in 10 healthy subjects. The change-related N1m component, peaking at approximately 130 ms, and its PPI were investigated. The degree of PPI caused by the −5 dB prepulse was significantly weaker than that caused by other prepulses. The degree of PPI caused by further decreases in prepulse magnitude showed a plateau level between the −10 dB and gap prepulses. The results suggest that there is a physiologically significant range of sensory changes for PPI, which plays a role in the change detection for survival.


2015 ◽  
Vol 52 (11) ◽  
pp. 1511-1519 ◽  
Author(s):  
Yunseo Ku ◽  
Joong Woo Ahn ◽  
Chiheon Kwon ◽  
Myung-Whan Suh ◽  
Jun Ho Lee ◽  
...  

2008 ◽  
Vol 38 (11) ◽  
pp. 1651-1658 ◽  
Author(s):  
P. Roussos ◽  
S. G. Giakoumaki ◽  
M. Rogdaki ◽  
S. Pavlakis ◽  
S. Frangou ◽  
...  

BackgroundRecent evidence suggests that dopamine (DA) agonist-induced disruption of prepulse inhibition (PPI) depends on basal PPI values, in a manner that suggests an inverted U-shaped relationship between PPI and prefrontal DA levels. This is the first study to examine possible genetic determinants of PPI and the catechol O-methyltransferase (COMT) Val158Met polymorphism, the main catabolic pathway of released DA in the prefrontal cortex (PFC).MethodPPI was measured in 93 healthy males presented with 75-dB and 85-dB prepulses at 60-ms and 120-ms prepulse–pulse intervals. Subjects were grouped according to their COMT status into a Val/Val, a Val/Met and a Met/Met group.ResultsANOVAs showed that at all prepulse and interval conditions, Val/Val individuals had the lowest PPI, Met/Met the highest, and Val/Met were intermediate.ConclusionsThese results suggest that PPI is regulated by DA neurotransmission in the PFC and its levels depend on the COMT Val158Met gene polymorphism. These findings enhance the value of the PPI paradigm in examining individual variability of early information processing in healthy subjects and psychiatric disorders associated with changes in PFC DA activity and attentional deficits such as schizophrenia.


Author(s):  
R. Chen

ABSTRACT:Cutaneous reflexes in the upper limb were elicited by stimulating digital nerves and recorded by averaging rectified EMG from proximal and distal upper limb muscles during voluntary contraction. Distal muscles often showed a triphasic response: an inhibition with onset about 50 ms (Il) followed by a facilitation with onset about 60 ms (E2) followed by another inhibition with onset about 80 ms (12). Proximal muscles generally showed biphasic responses beginning with facilitation or inhibition with onset at about 40 ms. Normal ranges for the amplitude of these components were established from recordings on 22 arms of 11 healthy subjects. An attempt was made to determine the alterent fibers responsible for the various components by varying the stimulus intensity, by causing ischemic block of larger fibers and by estimating the afferent conduction velocities. The central pathways mediating these reflexes were examined by estimating central delays and by studying patients with focal lesions


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