Disease relevance of P200

• N100, P200, and N200 ERP components did not differ in latency or amplitude between migraine patients and controls [1].
• Patients with DAT and demented patients with Parkinson's disease had normal SSEPs as well as normal P100, and N140 latencies, but patients with vascular dementia showed prolonged N140 and P200 latencies in addition to a prolonged central conduction time (CCT) [2].
• In tinnitus patients, the magnetic wave M200 (corresponding to the electric wave P200, or P2) is delayed and only poorly developed or even completely missing, while the amplitude of the magnetic wave M100 (corresponding to the electric wave N100, or N1) is significally augmented [3].
• P200 latency and N100 latency were unaffected by hypoxia [4].
• Hypercapnia increased the peak end-inspiratory mouth pressure (Ppeak) during complete airway occlusion and the pressures at 100, 200, and 300 ms after the onset of inspiration (P100, P200, P300) [5].

Psychiatry related information on P200

• As a group, subjects with PTSD showed no such increase in P200 response magnitude [6].
• For all but one subject with no psychopathology and for all subjects with a history of alcohol abuse or major depression (but no PTSD), the Cz amplitude of the P200 response component showed augmentation as a nearly linear function of tone intensity [6].
• Measurements and Results: In the tonic period of REM sleep (the period without REM), P200 and P400 were elicited by deviant stimuli, with scalp distributions maximal at central and occipital sites, respectively [7].
• Reaction time and N100/P200 amplitudes and latency were analyzed as a function of memory load [8].
• Analysis of N140 and P200 components of somatosensory ERPs may be important for evaluation of patients with vascular dementia [2].

High impact information on P200

• Human syncytiotrophoblast cell membranes prepared by differential ultracentrifugation were extracted with 3 M KCl, solubilized in 1% deoxycholate, and chromatographically separated into two peaks by passage through a column of Bio-Gel P-200 [9].
• Sa-I was isolated by ultrafiltration, Sephadex G-25, and diethylaminoethyl-Sephacel chromatography, whereas, Sa-II, the major allergen, was purified by successive chromatography on diethylaminoethyl-Sephacel, Bio-Gel P-200, and Sepharose 4B columns [10].
• Significant negative linear correlations were found between the P300 amplitude and both HVA and hypoxanthine, and between the P200 slope and both 5HIAA and hypoxanthine [11].
• Urinary MHPG changes paralleled the changes in P200 amplitude [12].
• Ten patients in each group received 50 mg (P50), 100 mg (P100), 200 mg (P200) of pethidine or prilocaine (5 mg/ml) + adrenaline (4 mg/ml) (PC), injected intra-articularly (i.a.) before surgery [13].

Chemical compound and disease context of P200

• ERPs for cues and targets (P50, N100, P200, late slow wave), and negative slow potentials between cues and targets were assessed.RESULTS: Target reaction times for valid cues were significantly shorter than for invalid cues, with intermediate values for neutral cues [14].
• The effects of .7 ml/kg alcohol and 200 mg caffeine on the P200, N200, P300 and N500 difference wave components of the event-related potential and on reaction time (RT) were examined in 16 females who performed both simple and choice RT tasks [15].

Biological context of P200

• OBJECTIVE: The purpose of this study was to explore the relationship between combat-related posttraumatic stress disorder (PTSD) and specific augmentation versus reduction patterns for the N100 and P200 components of auditory event-related potentials evoked by tones of increasing intensity [6].
• Morphological abnormalities of the mid-latency auditory evoked responses (MLAERs; P50, N100, P200), on the other hand, received very little attention [16].
• This study attempted to replicate and extend earlier work that reported that the amplitude of the P200 peak of the human somatosensory evoked potential (SEP) can be increased and decreased when reward is made contingent upon change and that these changes are accompanied by alterations in pain sensitivity [17].
• N100, P200, and P300 to the CSs revealed that psychopaths were not deficient in information processing and showed even better anticipatory responding than the HC group indicated by the terminal contingent negative variation (tCNV), that lacked, however, CS+ and CS- differentiation [18].
• Right visual field left hemisphere P200 reduction predicted suppression of behavioral response (button press) to hypnotically obstructed targets in both hemifields [19].

Anatomical context of P200

• Anti-IFA, a monoclonal antibody that recognizes an epitope common to all classes of intermediate filaments, binds to P200 and P60 [20].
• Twenty-one subjects were able to make the amplitude of the P200 peak evoked by sural nerve stimulation larger during increased training (up-training) than during decreased training (down-training) [17].
• This finding demonstrates that the change in P200 amplitude was not due to a change in stimulus efficacy, but rather to a change within the central nervous system [17].
• It was found that the source of each component is located on the superior surface of the temporal lobe and that the source of the P200 component is anterior to the N100 source in all subjects using both procedures [21].
• As the correctly classified schizophrenics showed increased frontally pronounced delta-activity and decreased signal power of the N100/P200 amplitude, it was concluded that these schizophrenics show dysfunction of the frontal lobe [22].

Associations of P200 with chemical compounds

• When axoplasm is incubated with [32P]Pi, the major phosphorylated polypeptides are P200 and Band 1 [20].
• P200 latency was sped by yohimbine and slowed by clonidine, and the frontal P3a was shifted in tandem [23].
• Sensory gating of the P50, the N100, and the P200 were deficient in cocaine-dependent subjects [24].
• Effects of ACTH 4-10 on the AEPs to inattended stimuli, however, differed from influences of the synthetic analog in that they did not affect a rather wide latency range but concentrated on the latency range of the P200 component [25].
• Sulpiride shortened the P200 latency for frequent stimuli, but tended to increase the N200 and P300 latencies for rare stimuli [26].

Enzymatic interactions of P200

• The proteinase preferentially cleaves P200 and Band 1, liberating the phosphorylated domains [20].

Other interactions of P200

• ANOVA results revealed no significant attention or stimulus intensity effects for N150 but highly significant differences in P200 and P300 amplitudes between attended and ignored stimuli [27].
• Pairing reduced blink, and midline P50, N100 and P200 amplitudes; reductions were greater at the longer interval [28].
• CONCLUSIONS: Brain potentials in MCI subjects during target detection have certain features similar to healthy aging (RP, N100, P200, N200), and other features similar to Alzheimer's disease (delayed P300 latency, slower reaction time) [29].

Analytical, diagnostic and therapeutic context of P200

• Analysis of proteolysed filaments by electron microscopy and gel electrophoresis shows that most of P200 and Band 1 can be cleaved while still maintaining intact filaments [20].
• For 3HThy autoradiography, quokkas aged P1-P200 were injected with 3HThy and killed either 6-20 hours later (pulse-kill) or at P100 or P250 (pulse-leave) [30].
• In the EEG recording, face-specific components, positive at the vertex, P200 (Cz), and the negative at the temporal areas, N190 (T5') and N190 (T6'), were clearly recorded [31].
• Analyses revealed statistical significant reductions in P200 amplitudes for the angry facial expression on both frontal and parietal electrode sites [32].
• The PTSD group showed ERP disturbances to target stimuli (reduced P200 and P300 and increased N200 amplitude, increased N200 and P300 latency) and reduced P200 amplitude to common stimuli compared to the control group [33].

References