Sprawozdanie

Sprawozdanie z VI Międzynarodowego Sympozjum Naukowego Polskiego Towarzystwa Psychologii Behawioralnej, Kraków, 19–20 marca 201

Acquisition of emotional responses : reconstruction and revision of the Little Albert

In 1920 John B. Watson and Rosalie Rayner published the results of the study experiment describing how they had conditioned an 11-month-old boy (known as Little Albert) to fear a rat. The experiment is one of the best known and the most frequently cited empirical studies in the history of psychology. Many studies and theories suggesting the role of learning processes in the development of emotional responses were initiated by the Little Albert experiment. The article summarizes the procedures and results of the experiment reported by J.B. Watson and R. Rayner. The importance and impact of the results of the experiment on the development of psychological theories and research is discussed. Errors in the discussions of the Little Albert experiment in Polish psychological literature are identifi ed. The results of the latest historical research on the Little Albert experiment are summarized and their consequences are discussed

Nabywanie reakcji emocjonalnych: rekonstrukcja i rewizja eksperymentu z udziałem Małego Alberta

In 1920 John B. Watson and Rosalie Rayner published the results of the study experiment describing how they had conditioned an 11-month-old boy (known as Little Albert) to fear a rat. The experiment is one of the best known and the most frequently cited empirical studies in  the history of psychology. Many studies and theories suggesting the role of learning processes in the development of emotional responses were initiated by the Little Albert experiment.  The article summarizes the procedures and results of the experiment reported by J.B. Watson and R. Rayner. The importance and impact of the results of the experiment on the development of psychological theories and research is discussed. Errors in the discussions of the Little Albert experiment in Polish psychological literature are identifi ed. The results of the latest historical research on the Little Albert experiment are summarized and their consequences are discussed

PSD-95 in CA1 area regulates spatial choice depending on age

Cognitive processes that require spatial information rely on synaptic plasticity in the dorsal CA1 area (dCA1) of the hippocampus. Since the function of the hippocampus is impaired in aged individuals, it remains unknown how aged animals make spatial choices. Here, we used IntelliCage to study behavioural processes that support spatial choices of aged female mice living in a group. As a proxy of training-induced synaptic plasticity, we analysed the morphology of dendritic spines and expression of a synaptic scaffold protein, PSD-95. We observed that spatial choice training in young adult mice induced correlated shrinkage of dendritic spines and downregulation of PSD-95 in dCA1. Moreover, long-term depletion of PSD-95 by shRNA in dCA1 limited correct choices to a reward corner, while reward preference was intact. In contrast, old mice used behavioural strategies characterised by an increased tendency for perseverative visits and social interactions. This strategy resulted in a robust preference for the reward corner during the spatial choice task. Moreover, training decreased the correlation between PSD-95 expression and the size of dendritic spines. Furthermore, PSD-95 depletion did not impair place choice or reward preference in old mice. Thus, our data indicate that while young mice require PSD-95-dependent synaptic plasticity in dCA1 to make correct spatial choices, old animals observe cage-mates and stick to a preferred corner to seek the reward. This strategy is resistant to the depletion of PSD-95 in the CA1 area. Overall, our study demonstrates that aged mice combine alternative behavioral and molecular strategies to approach and consume rewards in a complex environment

Chronic Obstructive Pulmonary Disease and Lung Cancer: Underlying Pathophysiology and New Therapeutic Modalities

Chronic obstructive pulmonary disease (COPD) and lung cancer are major lung diseases affecting millions worldwide. Both diseases have links to cigarette smoking and exert a considerable societal burden. People suffering from COPD are at higher risk of developing lung cancer than those without, and are more susceptible to poor outcomes after diagnosis and treatment. Lung cancer and COPD are closely associated, possibly sharing common traits such as an underlying genetic predisposition, epithelial and endothelial cell plasticity, dysfunctional inflammatory mechanisms including the deposition of excessive extracellular matrix, angiogenesis, susceptibility to DNA damage and cellular mutagenesis. In fact, COPD could be the driving factor for lung cancer, providing a conducive environment that propagates its evolution. In the early stages of smoking, body defences provide a combative immune/oxidative response and DNA repair mechanisms are likely to subdue these changes to a certain extent; however, in patients with COPD with lung cancer the consequences could be devastating, potentially contributing to slower postoperative recovery after lung resection and increased resistance to radiotherapy and chemotherapy. Vital to the development of new-targeted therapies is an in-depth understanding of various molecular mechanisms that are associated with both pathologies. In this comprehensive review, we provide a detailed overview of possible underlying factors that link COPD and lung cancer, and current therapeutic advances from both human and preclinical animal models that can effectively mitigate this unholy relationship

Sprawozdanie

Sprawozdanie z III Sympozjum Naukowego Polskiego Towarzystwa Psychologii Behawioralnej, Kraków, 17–18 marca 200

Sprawozdanie

Sprawozdanie z VI Międzynarodowego Sympozjum Naukowego Polskiego Towarzystwa Psychologii Behawioralnej, Kraków, 19–20 marca 201

Simulation of memory impairment: The nature, origin and detection with neuro-psychological tests

Głównym tematem artykułu jest problematyka symulowania zaburzeń funkcjonowania pamięci. DSM-IV (APA, 1994) definiuje symulowanie jako zamierzone tworzenie pozornych lub znacznie wyolbrzymionych objawów somatycznych i/lub psychicznych, motywowane czynnikami zewnętrznymi, takimi jak chęć uniknięcia służby wojskowej lub pracy, uzyskania rekompensaty finansowej, uniknięcia odpowiedzialności karnej lub zdobycia narkotyków. W pierwszej części artykułu przedstawiono trzy główne modele wyjaśniające zjawisko symulowania, które opierają się na analizie motywacji leżącej u podłoża zjawiska. Druga część została poświęcona problematyce wykrywania symulowania zaburzeń pamięci. Opisano tu podstawowe plany badawcze oraz metody wykrywania symulowania, oparte na analizach sposobu reagowania i wyników uzyskanych w standardowych testach neuropsychologicznych.The article presents a theoretical analysis of the phenomenon of simulation of memory impairment. According to the DSM-IV (APA, 1994) the essential features of simulation involve intentional or grossly exaggerated presentation of physical symptoms, motivated by external incentives such as avoiding military duty, avoiding work, obtaining financial compensation, evading criminal prosecution, or obtaining drugs. First, three main explanatory models of malingering are presented, then the issue of detection of memory impairment simulation is analyzed. The main research designs employed in the studies on simulation are discussed and detection strategies based on the analysis of the results on standard neuropsychological tests are presented