Biomedical subjects

G Tavernier

Publications and source records attributed to G Tavernier.

At least 19 recordsLinked to original sources

PubMed2004

Early enterocytic differentiation of HT-29 cells: biochemical changes and strength increases of adherens junctions.

We have characterized the modulation of cell-cell adhesion and the structure of adherens junctions in the human colon adenocarcinoma HT-29 cell line that differentiates into enterocytes after glucose substitution for galactose in the medium. We demonstrate that differentiated cells (HT-29 Gal) rapidly established E-cadherin-mediated interactions in aggregation assays. This effect is not due to an increase in E-cadherin expression during this early stage of cell differentiation, but rather results from the maturation of preexisting adherens junctions. These junctions are characterized by the redistribution of E-cadherin to the basolateral membrane and its co-localization with the actin cytoskeleton. Subcellular fractionation studies indicate that actin-associated E-cadherins bind beta-catenin and p120ctn. Furthermore, the p120ctn/E-cadherin association is upregulated. These data reveal a cooperative interaction between p120ctn and E-cadherin that corresponds to mature functional adherens junctions able to initiate tight cell-cell adhesion required for epithelium architecture and further affirm the gatekeeper role of p120ctn.

Actins↗

PubMed2000

Testis hormone-sensitive lipase expression in spermatids is governed by a short promoter in transgenic mice.

A testicular form of hormone-sensitive lipase (HSL(tes)), a triacylglycerol lipase, and cholesterol esterase, is expressed in male germ cells. Northern blot analysis showed HSL(tes) mRNA expression in early spermatids. Immunolocalization of the protein in human and rodent seminiferous tubules indicated that the highest level of expression occurred in elongated spermatids. We have previously shown that 0.5 kilobase pairs of the human HSL(tes) promoter directs testis-specific expression of a chloramphenicol acetyltransferase reporter gene in transgenic mice and determined regions binding nuclear proteins expressed in testis but not in liver (Blaise, R., Grober, J., Rouet, P., Tavernier, G., Daegelen, D., and Langin, D. (1999) J. Biol. Chem. 274, 9327-9334). Mutation of a SRY/Sox-binding site in one of the regions did not impair in vivo testis-specific expression of the reporter gene. Further transgenic analyses established that 95 base pairs upstream of the transcription start site were sufficient for correct testis expression. In gel retardation assays using early spermatid nuclear extracts, a germ cell-specific DNA-protein interaction was mapped between -46 and -29 base pairs. The DNA binding nuclear protein showed properties of zinc finger transcription factors. Mutation of the region abolished reporter gene activity in transgenic mice, showing that it is necessary for testis expression of HSL(tes).

Animals↗

PubMed2000

The -403 G-->A promoter polymorphism in the RANTES gene is associated with atopy and asthma.

Asthma is a complex inflammatory condition often associated with bronchial hyperreactivity and atopy. Genetic and environmental factors are implicated and several candidate genes have been implicated. Of these, the chemokine RANTES is responsible for the recruitment of inflammatory cells such as eosinophils and T-lymphocytes. We have recently identified a polymorphism within the RANTES promoter (-403 G-->A) and have examined its role, using a PCR-RFLP assay, in the development of atopy and asthma in 201 Caucasian subjects. Atopic status was determined using skin prick testing and serum IgE levels. Severity of airway dysfunction was assessed using spirometric measurement (FEV1) and methacholine challenge (PC20). The -403 A allele was associated with an increased susceptibility to both atopy and asthma. Thus, the proportion of subjects carrying this allele was higher in each of atopic non-asthmatics, non-atopic asthmatics and atopic asthmatics compared with non-atopic, non-asthmatic controls. In particular, this allele was associated with skin test positivity but not IgE level. Homozygosity for the -403 A allele conferred a 6.5-fold increased risk of moderate/severe airway obstruction (FEV1 < or = 80% predicted), a marker for established asthma. Our data, whilst preliminary, indicate that the association of RANTES genotype with both atopy and asthma reflect independent effects, suggesting different mechanisms for the role of this chemokine in atopy and development of airway obstruction.

Adenine↗

PubMed1999

Testis expression of hormone-sensitive lipase is conferred by a specific promoter that contains four regions binding testicular nuclear proteins.

The testicular isoform of hormone-sensitive lipase (HSLtes) is encoded by a testis-specific exon and 9 exons common to the testis and adipocyte isoforms. In mouse, HSLtes mRNA appeared during spermiogenesis in round spermatids. Two constructs containing 1.4 and 0.5 kilobase pairs (kb) of the human HSLtes gene 5'-flanking region cloned upstream of the chloramphenicol acetyltransferase gene were microinjected into mouse oocytes. Analyses of enzyme activity in male and female transgenic mice showed that 0.5 kb of the HSLtes promoter was sufficient to direct expression only in testis. Cell transfection experiments showed that CREMtau, a testis-specific transcriptional activator, does not transactivate the HSLtes promoter. Using gel retardation assays, four testis-specific binding regions (TSBR) were identified using testis and liver nuclear extracts. The testis-specific protein binding on TSBR4 was selectively competed by a probe containing a SRY/Sox protein DNA recognition site. Sox5 and Sox6 which are expressed in post-meiotic germ cells bound TSBR4. Mutation of the AACAAAG motif in TSBR4 abolished the binding. Moreover, binding of the high mobility group domain of Sox5 induced a bend within TSBR4. Together, our results showed that 0.5 kb of the human HSLtes promoter bind Sox proteins and contain cis-acting elements essential for the testis specificity of HSL.

Animals↗

PubMed1999

Interspecies differences in the cardiac negative inotropic effects of beta(3)-adrenoceptor agonists.

The aim of the present study was to compare the effects of three preferential (BRL 37344, SR 58611, CL 316 243) and a partial (CGP 12177) beta-adrenoceptor (beta(3)-AR) agonists on the contractility of ventricular strips sampled from various mammalian species including humans. In the human heart, all beta(3)-AR agonists tested decreased contractility by 40 to 60% below control with an order of potency: BRL 37344 > CL 316 243 = SR 58611 >> CGP 12177. In the dog, the negative inotropic effects produced by beta(3)-AR stimulation were less pronounced than in humans, approximately 30% below control. The order of potency of beta(3)-AR agonists was CGP 12177 > BRL 37344 = SR 58611 >> CL 316 243; i.e., very different from that observed in humans. In rat, only BRL 37344 was efficient to decrease contractility. In guinea pig, only CL 316 243 significantly reduced peak tension. In both species, the reduction in peak tension did not exceed 20 to 30%. Finally, in the ferret, none of the agonists tested induced a negative inotropic effect. In dog, the negative inotropic effects of CGP 12177 were not modified by nadolol, but were abolished by bupranolol, a beta(1-3)-AR. beta(3)-AR transcripts were detected in the dog but not in the rat ventricle by using a reverse transcription-polymerase chain reaction assay. We conclude that cardiac negative inotropic effects related to beta(3)-AR agonist stimulation vary markedly depending on the species. A comparable interspecies variation previously has been reported concerning the lipolytic effects of beta(3)-AR agonist stimulation. Our study demonstrates that the pharmacological profile of a beta(3)-AR agonist on the human myocardium cannot be extrapolated from usual animal models.

Adrenergic beta-Agonists↗

PubMed1997

Adrenergic regulation of adipocyte metabolism.

Five adrenoceptor (AR) subtypes (beta 1, beta 2, beta 3, alpha 2 and alpha 1), are involved in the control of white and brown fat cell function. A number of metabolic events are controlled by the adrenergic system in fat cells. The stimulatory effect of catecholamines on lipolysis and metabolism is mainly connected to increments in cAMP levels, cAMP protein kinase activation and phosphorylation of various target proteins. Norepinephrine and epinephrine operate through differential recruitment of alpha 2- and beta-AR subtypes on the basis of their relative affinity for the different subtypes (the relative order of affinity is alpha 2 > beta 1 > or = beta 2 > beta 3 for norepinephrine). Antagonistic actions at the level of cAMP production exist between alpha 2- and beta 1-, beta 2- and beta 3-AR-mediated lipolytic effects in human white fat cells. The role of fat cell alpha 2-ARs, which largely outnumber beta-ARs in fat cells of certain fat deposits, in human and primate has never been clearly understood. The other AR type which is not linked to lipolysis regulation, the alpha 1-AR, is involved in the control of glycogenolysis and lactate production. Pharmacological approaches using in-situ microdialysis and selective alpha 2- and beta-AR agonists and antagonists have revealed sex- and tissue-specific differences in the adrenergic control of fat cell function and nutritive blood flow in the tissue surrounding the microdialysis probe.

3',5'-Cyclic-AMP Phosphodiesterases↗

PubMed1996

Functional beta3-adrenoceptor in the human heart.

Beta3-adrenoceptors are involved in metabolism, gut relaxation, and vascular vasodilation. However, their existence and role in the human heart have not been documented. We investigated the effects of several beta-adrenoceptor agonists and antagonists on the mechanical properties of ventricular endomyocardial biopsies. In the presence of nadolol, a beta1- and beta2-adrenoceptor antagonist, isoprenaline produced consistent negative inotropic effects. Similar negative inotropic effects also resulted from the action of beta3-adrenoceptor agonists with an order of potency: BRL 37344 > SR 58611 approximately CL 316243 > CGP 12177. The dose-response curve to BRL 37344-decreasing myocardial contractility was not modified by pretreatment with nadolol, but was shifted to the right by bupranolol, a nonselective beta-adrenoceptor antagonist. Beta3-adrenoceptor agonists also induced a reduction in the amplitude and an acceleration in the repolarization phase of the human action potential. Beta3-adrenoceptor transcripts were detected in human ventricle by a polymerase chain reaction assay. These results indicate that: (a) beta3-adrenoceptors are present and functional in the human heart; and (b) these receptors are responsible for the unexpected negative inotropic effects of catecholamines and may be involved in pathophysiological mechanisms leading to heart failure.

Action Potentials↗

PubMed1996

Beta 3-adrenoceptor in guinea pig brown and white adipocytes: low expression and lack of function.

In the guinea pig, cold acclimation induced a conversion of unilocular to multilocular adipocytes in interscapular (IS) and retroperitoneal (RP) fat depots but not in the epididymal (EP) fat pad. The conversion was associated with an increase in mitochondriogenesis and the appearance of the uncoupling protein. The maximal lipolytic responses to norepinephrine and dibutyryl adenosine 3',5'-cyclic monophosphate were decreased in IS cells, unchanged in RP cells, and increased in EP cells, suggesting a site-specific regulation of lipolysis at the postreceptor level. beta 3-Adrenergic agonists were not lipolytic regardless of the depot and the thermal environment of the animal. These agents did not inhibit glucose transport and lipogenesis, as was previously reported for rodents. Cloning and sequencing of the guinea pig beta 3-adrenoceptor gene revealed a slightly higher amino acid sequence similarity with the human than with the rodent beta 3-adrenoceptors. beta 3-Adrenoceptor transcripts were present at a very low level in guinea pig adipocytes, and mRNA levels did not increase to a significant extent after cold acclimation. The guinea pig thus differs from rodents by an absence of beta 3-adrenergic effects and by low beta 3-adrenoceptor expression in brown and white adipose tissues.

Acclimatization↗

PubMed1996

Expression of beta3-adrenoceptors with low lipolytic action in human subcutaneous white adipocytes.

Beta3-Adrenoceptors are involved in the control of catecholamine-induced lipolysis in rodent adipose tissues. The expression and function of human beta3-adrenoceptors were investigated in subcutaneous white adipocytes of young healthy women. In these cells, beta3-adrenoceptor mRNAs represent 20% of total amount of beta-adrenoceptor transcripts and less than half of beta1-adrenoceptor transcripts. Among beta3-agonists known to stimulate beta3-adrenoceptor-mediated lipolysis in rodent fat cells, only CGP12177 was able to mediate such activity in human fat cells. In in vitro lipolysis experiments and in situ microdialysis studies, CGP12177 had a 4- to 5-times lower lipolytic efficacy than isoprenaline, a nonselective beta-adrenoceptor agonist. CGP12177-induced lipolysis was antagonized in vitro by bupranolol, a beta-adrenergic antagonist potent on rodent beta3-adrenoceptors but not by nadolol, a beta1- and beta2-adrenoceptor antagonist. The in vitro blockade of isoprenaline-stimulated lipolysis by nadolol showed that the agonist acted solely via beta1- and beta2-adrenoceptors. Isoprenaline and CGP12177 were able to increase the nutritive blood flow suggesting an interaction of these molecules with receptors present in adipose tissue vessels. In conclusion, beta3-adrenoceptors are expressed in human subcutaneous white adipocytes but do not significantly contribute to isoprenaline-induced lipolysis.

Adipocytes↗

PubMed1995

A DNA fingerprinting method for individual characterization of Toxoplasma gondii strains: combination with isoenzymatic characters for determination of linkage groups.

The genetic polymorphism of Toxoplasma gondii was evaluated for 14 strains by isoenzyme and DNA analysis. The 14 strains belonged to 5 different zymodemes defined by the variable patterns of 6 enzyme systems. A restriction-fragment-length polymorphism analysis was carried out with two endonucleases (Sal I and Pst I) and two repetitive probes (TGR1E and TGR6). This kind of repetitive probe allowed an individual identification of strain, with 13 schizodemes being observed among 14 strains. Only two strains were found to be totally identical when DNA and isoenzyme characters were considered. The numerical taxonomy methods applied to the results obtained for both types of characters allowed determination of linkage groups. Strain clustering obtained by numerical analysis of DNA characters alone is similar to the clustering obtained by analysis of isoenzyme and DNA characters together. A relationship was observed between the defined groups and virulence in Swiss mice.

Animals↗

PubMed1995

Regulation of beta 3-adrenoceptor expression in white fat cells.

Catecholamines (adrenaline and noradrenaline) stimulate adipocyte lipolysis via three beta-adrenoceptor subtypes beta 1, beta 2 and beta 3. beta 3-adrenoceptor-mediated lipolysis varies according to the species. Rodent adipocytes exhibit the strongest response to beta 3 agonists while human fat cells are poorly responsive. The species-related differences can partly be explained by lower beta 3-adrenoceptor mRNA levels in human adipocytes compared to rat adipocytes. Poor coupling efficiency of human adipocyte beta 3-adrenoceptors cannot, however, be ruled out. The regulation of beta 3-adrenoceptor gene expression has been studied in the adipocytes of the murine cell line 3T3-F442A which express high levels of beta 3-adrenoceptors. Insulin and glucocorticoids down-regulate beta 3-adrenoceptor expression through a transcriptional effect. The impairment of beta 3-adrenoceptor gene expression in adipocytes of congenitally obese ob/ob mice could be related to the higher glucocorticoid plasma levels when compared to lean littermates although the direct involvement of glucocorticoids remains to be demonstrated. In the rat and the rabbit, the beta 3-adrenergic responsiveness varies according to the anatomical location of the fat pad. There is a marked decrease in beta 3-adrenergic response in rabbit retroperitoneal fat cells during ageing. cAMP modulates the beta 3-adrenergic response in white adipocytes at different levels. Human beta 3-adrenoceptor expression seems to be up-regulated by cAMP through an interaction with the promoter of the gene. It has been shown in cells transfected with cDNAs for the different beta-adrenoceptors that the beta 3-adrenoceptor is less prone to desensitization than the beta 1 and beta 2-subtypes. This observation is in agreement with the absence of desensitization of the beta 3-adrenoceptor response in isolated rat fat cells. Continuous infusion of noradrenaline for six days into hamsters does not lead to an alteration of the beta-adrenergic response. A similar treatment undertaken in the guinea pig, a species, unlike the hamster, devoid of beta 3-adrenoceptor responsiveness, promoted strong desensitization of the beta-adrenergic response through down-regulation of beta 1- and beta 2-adrenoceptors. From these observations, it could be hypothesized that the beta 3-adrenoceptor, that shows a low affinity for catecholamines, is the "emergency" beta-adrenoceptor which is essential under conditions of strong and sustained sympathetic nervous system activation.

Adipocytes↗

PubMed1995

Molecular mechanisms underlying regional variations of catecholamine-induced lipolysis in rat adipocytes.

The mechanisms underlying catecholamine control of lipolysis were studied in rat white adipocytes from epididymal, retroperitoneal, and subcutaneous fat depots. Sensitivity of subcutaneous adipocytes to selective beta 3-adrenoceptor agonists was lower than that of internal adipocytes. beta 3-Adrenoceptor mRNA levels were lower in subcutaneous adipocytes. A decreased beta 1/beta 2-adrenoceptor-mediated lipolysis was also observed in these adipocytes, and the number of beta 1/beta 2-adrenoceptors was lower than in the internal adipocytes. The number of alpha 2-adrenoceptors was higher in subcutaneous adipocytes without a marked difference in alpha 2-adrenoceptor-mediated antilipolysis between the depots. Subcutaneous adipocytes were also characterized by a lower maximal lipolytic response to drugs acting at different levels of the lipolytic cascade, suggesting differences at the postreceptor level. Lower hormone-sensitive lipase activity and mRNA levels in subcutaneous adipocytes were in agreement with the lipolysis data. These results suggest that the pattern of expression of the genes of the lipolytic pathway varies with the anatomic location of the fat depot.

Adipocytes↗

PubMed1993

Effects of clonidine, dihydralazine and splanchnic nerve stimulation on the release of neuropeptide Y, MET-enkephalin and catecholamines from dog adrenal medulla.

Various neuropeptides are costored together with catecholamines in the adrenal medulla. The concurrent release (evaluated by adrenal vein plasma levels) of these neuropeptides [neuropeptide Y (NPY), met-enkephaline (ME)] and catecholamines [adrenaline (A) and noradrenaline (NA)] from the adrenal gland was examined in chloralose-anesthetized dogs after intravenous administration of clonidine (10 micrograms/kg) and dihydralazine (1 mg/kg). These results were compared to those obtained after the stimulation of the right splanchnic nerve at 1, 5 and 10 Hz frequencies. The increment in the release of catecholamines and neuropeptides was evaluated for dihydralazine and splanchnic nerve stimulation. Dihydralazine (at its maximal effect) induced a significant preferential increase in catecholamines (expressed as mean (SEM): NA: 17.3 (5.4) fold, A: 13.1 (2.6) fold) and ME (16.0 (7.1) fold) versus basal values. However, the significant increase in NPY-LI was only 2.0 (0.4) times the baseline. Splanchnic nerve stimulation induced a frequency-dependent increase in catecholamines and neuropeptides. When the stimulation frequency was increased from 1 Hz to 5 Hz, NA and A levels increased 17.9 (4.3) and 14.0 (2.2) fold, respectively and ME levels 14.1 (3.0) fold. By contrast, NPY-LI was increased only 2.3 (0.3) fold under the same conditions. Increasing the stimulation frequency from 5 Hz to 10 Hz resulted in similar elevations of NA, ME, and NPY-LI adrenal plasma levels (about 4 times) whereas A only increased twice. Clonidine decreased catecholamine and ME adrenal plasma levels (the maximal percent decrease when compared with control values was about 75%) whereas NPY adrenal plasma levels remained unchanged.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenal Medulla↗

PubMed1993

A study of alpha 1- and alpha 2-adrenoceptor responsiveness in diabetic insipidus dogs.

The present study was performed to investigate the participation of circulating vasopressin in alpha-adrenoceptor responsiveness. Thus, we compared the pressor responses induced by selective alpha 1-or alpha 2-adrenoceptor stimulation in two groups of conscious dogs: a) normal animals and b) animals with surgically-induced diabetes insipidus. In addition, platelet alpha 2-adrenoceptors labelled with (3H)RX821002 were compared in the two groups. The pressor response to alpha 1-adrenoceptor stimulation [ie successive doses of noradrenaline (0.5, 1, 2, 4 micrograms/kg i.v.) after propranolol (1 mg/kg i.v.) plus yohimbine (0.5 mg/kg i.v.)] was significantly (P < 0.05) less pronounced in diabetic insipidus than in normal dogs. In contrast, the magnitude of the pressor effects of alpha 2-adrenoceptor stimulation [ie noradrenaline after propranolol plus prazosin (1 mg/kg i.v.)] was the same in the two groups of animals. Bmax and Kd values for (3H)RX821002 binding on platelets were similar in diabetic insipidus and normal dogs. This study shows that alpha 1- (but not alpha 2-) adrenoceptor responsiveness is decreased in diabetic insipidus suggesting the involvement of vasopressin in the mechanisms of the vascular alpha 1-adrenoceptor pressor response.

Amino Acid Sequence↗

PubMed1993

[Co-release of neuropeptides and catecholamines by adrenal medulla].

Different neuropeptides are costored together with catecholamines in the adrenal medulla. The concurrent release of these neuropeptides [neuropeptide Y (NPY), met-enkephalin (ME)] and catecholamines (adrenaline and noradrenaline) from the adrenal gland was examined in chloralose-anesthetized dogs after intravenous administration of dihydralazine (1 mg/kg) and insulin (0.3 U/kg). These results were compared to those obtained after the stimulation of the right splanchnic nerve at 1, 5 and 10 Hz frequencies. Baroreflex involvement or hypoglycemia induced a significant preferential increase in CA and ME versus basal values: around 16 fold for dihydralazine and 28 fold after insulin administration. In opposite, increase in NPY was only two times baseline. Splanchnic nerve stimulation induced a frequency-dependent increase in catecholamines and neuropeptides. At the lower frequencies (1 to 5 Hz), splanchnic nerve stimulation elicited a parallel increase in catecholamines and ME (13 to 17 fold basal values). By contrast, NPY increases 2 fold in the same conditions. At the higher frequencies (5 to 10 Hz), we observed a parallel (4 fold) increase in NA, ME and NPY adrenal plasma levels. In conclusion, the present data indicate that both adrenal ME and catecholamines (mainly NA) always exhibit a parallel fashion of corelease which is not the case for NPY and that different populations of chromaffin vesicles could be preferentially mobilized according to different physiological and pharmacological patterns.

Adrenal Medulla↗

PubMed1992

Release of neuropeptide Y and noradrenaline during afferent nerve stimulation.

The present study was carried out to investigate the possibility that noradrenaline (NA) and neuropeptide Y (NPY) are co-released after afferent vagal or saphenous stimulation (1, 5, 10 and 20 Hz) in chloralose-anaesthetized dogs. Electrical stimulation of the vagus elicited an increase in plasma NA levels for the 5, 10 and 20 (but not 1) Hz frequencies. Blood pressure only increased after a 20-Hz stimulation. In contrast, no change in plasma NPY levels was observed whatever the frequency of stimulation. Electrical stimulation of the saphenous nerve failed to change plasma NA and NPY levels. The present data suggest that (1) the release of NA varies according to the frequency of stimulation of nociceptive fibres, (2) NPY release does not seem to be involved in the pressor effect elicited by the stimulation of nociceptive-sensitive fibres, and (3) NPY and NA release are not necessarily linked.

Animals↗

PubMed1992

Is neuropeptide Y co-released with catecholamines in experimental arterial hypertension following sinoaortic denervation?

The release of catecholamines and their coneurotransmitter neuropeptide Y (NPY) was investigated in conscious dogs with neurogenic arterial hypertension elicited by sinoaortic denervation. One month after denervation, an elevation of catecholamine levels (measured by HPLC) without elevation of NPY-like immunoreactivity (NPY-LI) levels in plasma (evaluated by RIA) has been found. This dissociation could be explained by 1) a transient release of NPY during the first weeks after surgery, 2) a depletion of neuronal NPY due to the permanent sympathetic stimulation, or 3) an insufficient increase in sympathetic tone. To test these hypotheses, we investigated the time courses of catecholamine and NPY-LI levels in arterial plasma during the first five weeks after sinoaortic denervation and responses to yohimbine (an alpha 2 antagonist which enhances transmitter release). Resting NPY-LI levels in plasma remained normal during the first five weeks after sinoaortic denervation. In normal dogs, a high dose of yohimbine (0.5 mg/kg i.v.) elevated both catecholamine (6-fold) and NPY-LI levels (1.5-fold), whereas a lower dose (0.05 mg/kg i.v.) induced a two fold elevation of catecholamine levels without changing NPY-LI concentrations. In sinoaortically denervated dogs, yohimbine elicited elevation of both catecholamines and NPY-LI whatever the dose used. Thus, neurogenic arterial hypertension in dogs seems to involve catecholamines but not NPY. Moreover, the present work suggests that a high level of sympathetic stimulation is required for a co-release of catecholamines and NPY.

Animals↗

PubMed1992

Effects of multiple reference points in spatial stimulus-response compatibility.

In two experiments, spatial stimulus-response compatibility effects in situations where the stimulus could appear in eight different locations were investigated. The locations were obtained as a result of orthogonal manipulation of hemispace, visual hemifield within hemispace, and relative position within hemifield. In the first experiment, only relative position within hemifield was relevant for selecting one of two responses (left or right). The results showed that both hemifield and relative position formed the basis of compatibility effects. In the second experiment, which was in most respects identical to the first, all spatial information was irrelevant. Only the geometrical shape of the stimulus determined the correct response. The results showed three S-R compatibility effects, based on hemispace, hemifield, and relative position. These results contradict earlier findings, and have implications for models of stimulus-response compatibility.

Adult↗