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Biomedical subjects

M Sommer

Publications and source records attributed to M Sommer.

At least 55 records · Page 3Linked to original sources

[Cardiorespiratory desynchronization after acute myocardial infarct].

The prognosis of cardiac diseases can be estimated from the variability of regulation parameters of the cardiovascular system. Changes in the variability of a regulation parameter causes disturbances in the synchronisation of interacting control loops. Conclusions about the severity of the underlying functional impairment can be drawn from these disturbances. This study investigates the synchronisation of the control loops of the heart rate and respiration (cardiorespiratory synchronisation, CRS) after acute myocardial infarction. We investigated 43 patients after myocardial infarction and 27 healthy controls. To quantify the CRS the synchronisation in phase of respiration and heart rate was assessed. The heart rate variability (HRV) was also assessed. Patients after myocardial infarction have a significantly reduced HRV and CRS. There is a non-linear relationship between HRV and CRS. Patients with left ventricular enlargement and reduced left ventricular ejection fraction (< or = 45%) significantly differed from the other infarct patients and controls in CRS but not in HRV. They had a marked degree of cardiorespiratory desynchronisation and were identified by a threshold value. CRS is a measure of the interaction of respiration control and heart rate control. After myocardial infarction, a reduction of the HRV can be observed. The desynchronisation of the control loops of respiration and heart rate especially appears in large infarcts. This can be quantitatively assessed by the method presented.

Adult↗

PDGF receptor kinase blocker AG1295 attenuates interstitial fibrosis in rat kidney after unilateral obstruction.

The current study was designed to investigate possible effects of the platelet-derived growth factor (PDGF) receptor kinase blocker AG1295 on the development of interstitial fibrosis in rats with unilateral ureteral obstruction (UUO), monitored by ED-A+ fibronectin expression, the number of macrophages, and the presence of myofibroblasts as visualized by immunohistochemistry with monoclonal antibodies (mAb) IST9, mAb ED1, and mAb 1A4, respectively; interstitial fibrosis was quantified by Sirius-Red staining and computer-aided image analysis. Without AG1295 treatment, the Sirius-Red stained area of the control kidneys comprised 6.8 +/- 1.3% of the totally inspected area and increased to 19.0 +/- 1.9% in animals by 14 days and to 23.4 +/- 1.7% by 21 days after UUO. The number of macrophages increased from 4.3 +/- 1.1 in controls to 16.6 +/- 2.6 in animals at 14 days and to 23.2 +/- 4.4 at 21 days after UUO. This was accompanied by an increase in both ED-A+ fibronectin deposition and alpha-smooth muscle actin expression. Treatment with AG1295 (12 mg/kg body weight, daily i.p.) significantly reduced interstitial fibrosis as verified by a smaller Sirius-Red stained area (15.7 +/- 1.9% in animals at 14 days and 17.0 +/- 0.7% at 21 days after UUO) and also by a reduced number of macrophages (12.8 +/- 1.4 in animals at 14 days and 15.5 +/- 3.8 at 21 days after UUO), and by the ED-A+ fibronectin deposition and the number of cells positive for alpha-smooth muscle actin. The study indicates that the PDGF receptor kinase blocker AG1295 is able to decrease interstitial fibrosis in the rat UUO model significantly. The diminution of early fibrosis mediators, i.e., macrophages, ED-A+ fibronectin, and myofibroblast phenotype, points to a modulated fibrosis process via a blockade of PDGF actions.

Actins↗

Immunochemical detection of imidazolone in uremia and rheumatoid arthritis.

The advanced glycation end-product imidazolone is formed by reaction of arginine with 3-deoxyglucosone (3-DG), a reactive intermediate of the Maillard reaction, whose formation is non-oxidative. Using an antibody specific to this 3-DG-derived AGE, we demonstrated the presence of imidazolone-modified proteins in vivo in the urine and dialysate of patients with chronic renal failure, in the synovial fluid of patients with rheumatoid arthritis, as well as in vitro in human serum and human serum albumin incubated with glucose. Furthermore, we could show that in uremic patients the dimeric form of beta(2)-microglobulin is more susceptible to imidazolone modification than the monomeric one. Thus, the immunochemical detection of imidazolone may be a good marker for 3-DG-derived AGE modification in vivo and in vitro permitting a differentiation between the oxidative and the non-oxidative pathway of AGE generation.

Adult↗

Expression of LFA-1 (CD11a/CD18) and ICAM-1 (CD54) in an animal model of renal interstitial fibrosis induced by unilateral ureteral obstruction.

Unilateral ureteral obstruction (UUO) has been used as an experimental model to induce tubulointerstitial damage and interstitial fibrosis. UUO is characterized by cellular proliferation, accumulation of inflammatory cells, and subsequent replacement of renal parenchyma by fibrous tissue. The influx of inflammatory cells into the renal interstitium is mediated by adhesion molecules. In this study, the development of fibrosis in the UUO model of the rat was examined and its relation to the time course of LFA-1 and ICAM-1 expression was assessed by immunohistochemistry. An increase in interstitial connective tissue was detected on day 10 after UUO, with a maximum on day 35. After unilateral ureteral obstruction, LFA-1 was prominently expressed in interstitial infiltrates, and to a lesser degree in glomerular areas. An initial increase in LFA-1-positive cells was noted already on day 10, with a maximum on day 20 and a decline on day 25. During the time course of 35 days after UUO, we observed an increase in ICAM-1 expression in the vascular endothelium, in tubular epithelium and in interstitial areas. This study shows that LFA-1 expression and ICAM-1 expression are concordant and that this process is associated with increasing interstitial fibrosis. ICAM-1 interstitial tissue may facilitate the homing and persistence of an interstitial infiltrate by ICAM-1/LFA-1 interactions, thereby preceding the development of renal interstitial fibrosis.

Animals↗

Modification of the silent period by double transcranial magnetic stimulation.

OBJECTIVES: To study the time course of the changes of the inhibitory network of the human motor system, we investigated the silent period (SP) in 7 healthy subjects by double suprathreshold transcranial magnetic stimulation (TMS). METHODS: SPs and motor evoked potentials (MEPs) were recorded from the voluntarily activated right abductor digiti minimi muscle. Conditioning and test stimuli were delivered with equal intensity, which was set to yield a baseline SP duration of 130 ms by a single pulse, and with various interstimulus intervals (ISIs). In addition, a control experiment with adjustment of the intensity of single stimuli was performed. RESULTS: At ISIs of 20 and 30 ms the test pulse SP duration was prolonged, without increasing the MEP amplitude. The SP duration shortened at longer ISIs and showed a significant depression between ISIs of 60-110 ms. The shortened SP was accompanied by a diminished MEP. The control experiment revealed that the SPs evoked by the adjusted pulses were significantly shorter than the test pulse SPs. CONCLUSIONS: A conditioning stimulus can prolong and shorten the test pulse SP duration at different ISIs. The prolongation is probably cortically generated, whereas the shortening is likely to occur at a cortical and spinal level.

Adult↗

Pitfalls in the immunohistochemical localization of the cystic fibrosis transmembrane conductance regulator in paraffin embedded sweat glands.

Mutations in the cystic fibrosis transmembrane conductance regulator (CFTR) gene cause the hereditary disease cystic fibrosis. The most frequent mutant deltaF508 has been shown in vitro to be retained in the endoplasmic reticulum. Ex vivo studies using immunohistochemical labelling in cryofixed skin biopsies have confirmed the mislocalization of deltaF508 CFTR in sweat glands. The purpose of this study was to test CFTR antibodies in paraffin-embedded skin biopsies to take advantage of the superior tissue preservation as compared to cryofixation. A panel of 7 CFTR antibodies was applied to skin sections of healthy controls and of cystic fibrosis patients homozygous for the deltaF508 mutation. Sweat gland labelling consistent with CFTR localization and different between control and cystic fibrosis tissue was obtained with 2 antibodies. Conventional staining controls confirmed the labelling specificity. The antibodies were subsequently tested in a series of 237 sections of 16 biopsy specimens. However, the sweat gland labelling pattern proved not to be dependent on CFTR genotype. This finding was the sole indicator of non-specificity of the staining which was revealed only by the size of our random sample. Our results emphasize that CFTR immunolabelling following formalin fixation has to be interpreted with the utmost caution.

Antibodies, Monoclonal↗

Physical exercise-induced expression of inducible nitric oxide synthase and heme oxygenase-1 in human leukocytes: effects of RRR-alpha-tocopherol supplementation.

This study evaluated the effects of RRR-alpha-tocopherol (500 IU/day, 8 days) on in vivo cytokine response and cytoplasmic expression of inducible nitric oxide synthase (iNOS) and the antioxidant stress protein heme oxygenase-1 (HO-1) in human leukocytes after exhaustive exercise. Thirteen men were investigated in a double-blind, placebo-controlled, cross-over study with a wash-out period of 28 days. The exercise procedure consisted of an incremental treadmill test followed by a continuous run until exhaustion at 110% of the individual anaerobic threshold (total duration 28.5 +/- 0.8 min). HO-1 and iNOS protein were assessed in mono- (M), lympho-, and granulocytes (G) using flow cytometry. Plasma interleukin-6 (IL-6) and IL-8 were measured by ELISA. IL-6 rose significantly whereas IL-8 did not exhibit significant changes after exercise. Changes of IL-6 were not affected by RRR-alpha-tocopherol. Exercise induced an increase of iNOS protein primarily in M and G. A small, but significant, increase of HO-1 protein was measured in M and G. RRR-alpha-Tocopherol did not show any significant effects on cytoplasmic expression of iNOS and HO-1 at rest and after exercise. In conclusion, exhaustive exercise induces expression of iNOS and HO-1 in human leukocytes by a mechanism that is not sensitive to RRR-alpha-tocopherol supplementation.

Adult↗

Expression of the inducible nitric oxide synthase (iNOS) in human leukocytes: responses to running exercise.

INTRODUCTION: We examined the influence of two different bouts of vigorous running exercise on the expression of the inducible nitric oxide synthase (iNOS) in leukocytes (LE). METHODS: In study 1, 10 trained runners competed in a half marathon (HM) lasting 90.5 +/- 11.0 min. In study 2, 8 untrained subjects performed a graded treadmill test followed by a continuous run (CR) until exhaustion (11.3 +/- 1.3 min). iNOS mRNA levels were assessed by RT/PCR at rest, 0, 3, and 24 h after HM and CR. In study 2, iNOS was additionally analyzed at the protein level in lympho- (L), mono- (M), and granulocytes (G) by flow cytometry at rest and up to 48 h after CR. RESULTS: Analysis revealed a rise of the iNOS transcript directly after the HM in 8 of 10 subjects. In study 2, the expression of iNOS protein at rest differed between L (mean +/- SE: 30.9 +/- 4.5% iNOS positive cells), M (91.3 +/- 4.0%), and G (64.9 +/- 10.3%): 3 h after CR, expression of iNOS increased in L (67.3 +/- 7.4%) and G (90.3 +/- 2.9%) and was still elevated 48 h post-exercise. However, our measurements failed to detect significant changes of leukocyte iNOS mRNA in response to CR. After the HM, our findings were paralleled by elevated plasma levels of interleukin-8, myeloperoxidase (MPO), and partly of TNF-alpha, whereas CR only induced a low rise of MPO. CONCLUSION: Our investigations revealed an increased expression of iNOS at the transcriptional and translational level in response to vigorous exercise. This reflects an inflammatory response and may contribute to an exercise-induced rise of endogenous nitric oxide production. It remains unclear if these effects serve an in-vivo immunoregulatory or cell-damaging role.

Adult↗

Time course of cytokine mRNA expression in kidneys of rats with unilateral ureteral obstruction.

The development of renal interstitial fibrosis (RIF) is related to the expression and excretion of cytokines and growth factors. Thus, we investigated the time course of mRNA expression of cytokines known as causative factors in a model of RIF in rats before and on day 10 after unilateral ureteral obstruction (UUO), when first signs of fibrosis were visible, as well as during progressive RIF. UUO causes a fivefold increase in mRNA expression of monocyte chemoattractant protein 1 15 days after surgery as compared with contralateral kidneys. The level remains elevated about three-fold up to day 25. The mRNA of the fibrogenic cytokine transforming growth factor beta 1 (TGF-beta1) is increased two- to threefold during the time course, whereas the mRNAs of platelet-derived growth factor B chain (PDGF-B) and its receptor beta (PDGF-Rbeta) increase after UUO, reaching their maxima on days 10-15. PDGF-B mRNA increase up to day 15, marking the onset of fibrosis, and decreases thereafter, whereas the expression of the PDGF-Rbeta mRNA remains elevated more than threefold over the entire study period. Incubation of cultured renal fibroblasts with TGF-beta1 and/or PDGF-B suggests that their specific action on cell growth and proliferation is maintained even when they are used in combination. The sustained elevation of TGF-beta1 and PDGF-B/PDGF-Rbeta mRNA levels confirms the assumption of a particular involvement of these cytokines in the pathogenesis of RIF. The mRNA expression of the gap junctional protein connexin 43 in ureteral ligated kidneys is increased sixfold already 5 days after UUO. In this way, the increased connexin 43 mRNA levels indicate a possible function in the remodeling of the kidney tissue after tubular damage and fibrosis.

Animals↗

Applicability of different antibodies for immunohistochemical localization of CFTR in sweat glands from healthy controls and from patients with cystic fibrosis.

The hereditary disease cystic fibrosis (CF) is caused by mutations in the cystic fibrosis transmembrane conductance regulator (CFTR) gene. Understanding of the consequences of CFTR gene mutations is derived chiefly from in vitro studies on heterologous cell cultures and on cells hyperexpressing CFTR. Data from ex vivo studies on human tissue are scarce and contradictory, a fact which is in part explained by secondary tissue destruction in most affected organs. The purpose of this study was to establish conditions under which wild-type and mutated CFTR can be studied in affected human tissue. Sweat glands carry the basic defect underlying CF and are not affected by tissue destruction and inflammation. Therefore, we used this tissue to test a panel of eight different CFTR antibodies under various fixation techniques. The antibodies were tested on skin biopsy sections from healthy controls, from CF patients homozygous for the most common mutation, DeltaF508, and from patients carrying two nonsense mutations. Of the eight CFTR antibodies, only three-M3A7, MATG 1104, and cc24-met the criteria necessary for immunolocalization of CFTR in sweat glands. The labeling pattern in the CF sweat glands was consistent with the postulated processing defect of DeltaF508 CFTR. The antibodies exhibited different sensitivities for detecting DeltaF508 CFTR.

Acetone↗

DeltaF508 CFTR protein expression in tissues from patients with cystic fibrosis.

Heterologous expression of the cystic fibrosis transmembrane conductance regulator (CFTR) provided evidence that the major cystic fibrosis (CF) mutation DeltaF508 leads to defective protein folding in the endoplasmic reticulum, which prevents its processing and targeting to the cell surface. In this study, we investigated endogenous CFTR expression in skin biopsies and respiratory and intestinal tissue specimens from DeltaF508 homozygous and non-CF patients, using immunohistochemical and immunoblot analyses with a panel of CFTR antibodies. CFTR expression was detected at the luminal surface of reabsorptive sweat ducts and airway submucosal glands, at the apex of ciliated cells in pseudostratified respiratory epithelia and of isolated cells of the villi of duodenum and jejunum, and within intracellular compartments of intestinal goblet cells. In DeltaF508 homozygous patients, expression of the mutant protein proved to be tissue specific. Whereas DeltaF508 CFTR was undetectable in sweat glands, the expression in the respiratory and intestinal tracts could not be distinguished from the wild-type by signal intensity or localization. The tissue-specific variation of DeltaF508 CFTR expression from null to apparently normal amounts indicates that DeltaF508 CFTR maturation can be modulated and suggests that determinants other than CFTR mislocalization should play a role in DeltaF508 CF respiratory and intestinal disease.

Amino Acid Sequence↗

Dopamine receptor subtypes modulate olfactory bulb gamma-aminobutyric acid type A receptors.

The gamma-aminobutyric acid type A (GABAA) receptor is the predominant Cl- channel protein mediating inhibition in the olfactory bulb and elsewhere in the mammalian brain. The olfactory bulb is rich in neurons containing both GABA and dopamine. Dopamine D1 and D2 receptors are also highly expressed in this brain region with a distinct and complementary distribution pattern. This distribution suggests that dopamine may control the GABAergic inhibitory processing of odor signals, possibly via different signal-transduction mechanisms. We have observed that GABAA receptors in the rat olfactory bulb are differentially modulated by dopamine in a cell-specific manner. Dopamine reduced the currents through GABA-gated Cl- channels in the interneurons, presumably granule cells. This action was mediated via D1 receptors and involved phosphorylation of GABAA receptors by protein kinase A. Enhancement of GABA responses via activation of D2 dopamine receptors and phosphorylation of GABAA receptors by protein kinase C was observed in mitral/tufted cells. Decreasing or increasing the binding affinity for GABA appears to underlie the modulatory effects of dopamine via distinct receptor subtypes. This dual action of dopamine on inhibitory GABAA receptor function in the rat olfactory bulb could be instrumental in odor detection and discrimination, olfactory learning, and ultimately odotopic memory formation.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗

Riluzole does not have an acute effect on motor thresholds and the intracortical excitability in amyotrophic lateral sclerosis.

Intracortical excitability in amyotrophic lateral sclerosis (ALS) is impaired. The effectiveness of the glutamate antagonist riluzole (Rilutek, Rhône-Poulenc Rorer) in ALS has been shown in clinical studies. In healthy subjects it modifies intracortical excitability in a frequently used double-stimulus paradigm of transcranial magnetic stimulation (TMS). Under riluzole intracortical inhibition is enhanced in healthy individuals, although not always significantly, whereas intracortical facilitation has been described as reduced [10, 11]. We wanted to find out whether riluzole affects and potentially rebalances impaired intracortical excitability in ALS. We, therefore, enrolled 13 patients with clinically and electromyographically confirmed ALS into this study. Five patients had to be excluded because motor thresholds were too high to get reliable motor evoked potentials (MEPs). In the remaining 8 patients, mean age was 59.9 +/- 11.9 years (+/- standard deviation) and mean symptom duration 9.6 +/- 2.5 months. Intracortical excitability was assessed before and 1.5 hours after the first intake of a loading dose of 100 mg of riluzole using a conventional paired-pulse TMS paradigm with interstimulus intervals (ISI) ranging from 1-30 ms and intensities adjusted to yield MEPs of 1.0 mV for test pulses and of 90% active motor threshold for conditioning pulses. Patients' baseline results were compared to those of 9 age-matched, healthy control subjects. Before drug intake, motor thresholds did not differ between groups, but there was significantly less intracortical inhibition in the ALS patient group. Riluzole intake did not significantly alter motor thresholds or intracortical excitability in the ALS patients. We conclude that riluzole does not immediately influence intracortical excitability in ALS. Our results are in contrast to the findings of Stefan et al (1998) [14] where a partial normalization of intracortical inhibition in ALS was observed after at least 5 days of drug intake. The difference between that study and our result may indicate a delayed onset of riluzole's influence on intracortical excitability.

Aged↗

[Virologic diagnosis of herpes zoster].

Diagnosis of herpes zoster needs to be rapid when effective antiviral chemotherapy is being considered. Patients with atypical clinical features can often only be diagnosed by virological methods. In the present study, vesicle specimens of 100 patients with zoster were analysed by detecting viral DNA using polymerase chain reaction (PCR). The findings were compared with those obtained by traditional virological and serological methods. PCR results confirmed the clinical diagnosis of zoster in 95%. Primers selected from varicella-zoster virus (VZV) gene 28 proved to be most sensitive. The sensitivity of virus culture was 20% (specificity 100%) and of direct immunofluorescent VZV-specific antigen staining in vesicle samples 82% (specificity 76%). There was a serological response to specific IgM and IgA antibodies in 48% within four days after the onset of rash. These findings suggest that PCR is the method of choice for rapid laboratory diagnosis of zoster.

Adolescent↗

Cell cultures from cryopreserved renal biopsies and other tissue samples.

Answering questions regarding research or clinical aspects, histological and histochemical examinations of tissue specimens are playing an increasing role. The same is true for cell cultures obtained from organ specimens. In most cases, tissue samples are obtained only once and have to be examined immediately. This is often impracticable and therefore, it is necessary to store tissue samples or cells from established cell cultures so as to be able to continue examinations at a later time. Very rare reports exist on the preservation of tissue for performing cell culture examinations and they exclusively refer to tumour tissue and bone marrow, but not to normal organ tissue and biopsy samples. Therefore, in this study cell cultures from several organs have been prepared immediately after obtaining the tissue and compared with those established after cryopreservation several months later. The tissue specimens were obtained from rats (kidney, skin, heart) and from humans (kidney, placenta) or were biopsy specimens from the kidney and skin. From all these cryopreparations, typical cells were cultured. There was no significant difference in the mean population doubling time (MPD) and regarding morphological cell criteria between cell cultures obtained from fresh tissue samples after biopsy and those prepared several months after cryopreservation. There was nearly the same ratio between most cell types present in the tissue. From these results we can conclude that in the examined organs cells from cryopreserved tissue can be cultured even months or more than one year later. At least, these results make it possible to answer new questions and repeat different experiments at any time.

Actins↗

The effect of flavophospholipol (Flavomycin) and salinomycin sodium (Sacox) on the excretion of Clostridium perfringens, Salmonella enteritidis, and Campylobacter jejuni in broilers after experimental infection.

Intestinal colonization and shedding of pathogenic bacteria in animal feces is an important factor in both human food safety and animal health. The effect of broiler feed additives flavophospholipol (FPL; Flavomycin, bambermycins) and salinomycin sodium (SAL; Sacox) given singly on the excretion of Salmonella enteritidis, Campylobacter jejuni, and Clostridium perfringens was studied following controlled infection. The incidence of shedding (number of birds with positive fecal cultures) and the degree of shedding (cfu per gram of feces in positive birds) were measured to determine the influence of these two common feed additive antibiotics on shedding rates of potential pathogens. A total of 216 Ross broiler chickens, housed in battery cages, were fed either an unmedicated feed (controls), feed containing FPL, or feed containing SAL. Feed treatment groups were subdivided into three bacterial challenge groups of 24 chicks, each receiving only one of the pathogens. Bacterial challenge was administered orally on Days 11 and 12 for Salmonella and Campylobacter and on Days 2 and 3 for Clostridium. Fecal samples were collected weekly up to 6 wk of age and cultured for presence of the target organism. The shedding rate was determined by decimal dilutions of the fecal samples. Feeding FPL resulted in a reduced (P < or = 0.05) degree and incidence of Salmonella and Clostridium shedding at 6 wk. Feeding SAL reduced (P < or = 0.05) the incidence of Salmonella shedding at 6 wk. Neither feed additive affected the incidence nor the degree of Campylobacter shedding. The results of this study indicate that these feed additives may reduce the incidence of these potential human and animal pathogens in preslaughter broilers.

Animal Feed↗

Characterization of Varicella-Zoster virus glycoprotein K (open reading frame 5) and its role in virus growth.

Varicella-zoster virus (VZV) is an alphaherpesvirus that is the causative agent of chickenpox and herpes zoster. VZV open reading frame 5 (ORF5) encodes glycoprotein K (gK), which is conserved among alphaherpesviruses. While VZV gK has not been characterized, and its role in viral replication is unknown, homologs of VZV gK in herpes simplex virus type 1 (HSV-1) and pseudorabies virus (PRV) have been well studied. To identify the VZV ORF5 gene product, we raised a polyclonal antibody against a fusion protein of ORF5 codons 25 to 122 with glutathione S-transferase and used it to study the protein in infected cells. A 40,000-molecular-weight protein was detected in cell-free virus by Western blotting. In immunogold electron microscopic studies, VZV gK was in enveloped virions and was evenly distributed in the cytoplasm in infected cells. To determine the function of VZV gK in virus growth, a series of gK deletion mutants were constructed with VZV cosmid DNA derived from the Oka strain. Full and partial deletions in gK prevented viral replication when the gK mutant cosmids were transfected into melanoma cells. Insertion of the HSV-1 (KOS) gK gene into the endogenous VZV gK site did not compensate for the deletion of VZV gK. The replacement of VZV gK at a nonnative AvrII site in the VZV genome restored the phenotypic characteristics of intact recombinant Oka (rOka) virus. Moreover, gK complementing cells transfected with a full gK deletion mutant exhibited viral plaques indistinguishable from those of rOka. Our results are consistent with the studies of gK proteins of HSV-1 and PRV showing that gK is indispensable for viral replication.

Amino Acid Sequence↗

Learning in Parkinson's disease: eyeblink conditioning, declarative learning, and procedural learning.

OBJECTIVE: To assess the degree of learning ability in Parkinson's disease. METHODS: Three different learning tasks: eyeblink classical conditioning with delay and trace paradigms, the California verbal learning test (CVLT), and a serial reaction time task (SRTT) were studied in patients with Parkinson's disease and normal (control) subjects. RESULTS: In the eyeblink conditioning tasks, both patients and normal subjects showed significant learning effects without between group differences. In the CVLT, patients remembered significantly fewer words than normal subjects in both short term and long term cued recall tasks. In the SRTT, normal subjects had significantly reduced response time and error rates across blocks of repeated sequence trials, whereas patients had significantly reduced error, but not response time rates. CONCLUSION: Impairment of nigrostriatal pathways selectively affects performance in complex learning tasks that are competitive and require alertness such as the SRTT, but not in simple learning procedures such as eyeblink conditioning.

Adult↗