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The manuscript printed below has been written by Prof Jerzy Konorski around 1970, a few years before his death in 1973. The manuscript has not been published before. It was recently discovered in Konorski's papers deposed in the Library of the Nencki Institute of Experimental Biology. In his critical review Konorski debates advantages and shortcomings of the physiological approach of Pavlov and purely behavioristic approaches advocated by Hull and Skinner. He supports close cooperation o behaviorists with neurophysiologists and neuroanatomists, with focus on the investigation of the neural mechanisms underlying behavior. Konorski's ideas concerning the integration of the study of behavior and neurophysiology anticipated contemporary path of neuroscience. Indeed, his approach, which at that time appeared somewhat controversial, is universally accepted by contemporary neuroscientists. By contrast, physiological theories of higher mental functions formulated by Pavlov as well as deliberately anti-physiological approaches of Skinner and Hull have all but disappeared from serious scientific discourse. However, the same problems such as strongly promoted self-importance of some branches of neuroscience, the lack of inter-communication between different branches and resulting lack of integrating ideas appear to emerge anew in each new generation of scientists. (Editors of Acta Neurobiologiae Experimentalis).
Long term synaptic plasticity underlying learning and memory is believed to require the reversible and dynamic regulation of local protein synthesis, which is dysregulated in fragile x syndrome, the most common form of inherited intellectual disability and autism. Fragile x syndrome is caused by the loss of the Fragile X Mental Retardation, FMRP, an mRNA binding protein involved in the regulation of local protein synthesis at synapses. We elucidated a cooperative role and dynamic interaction between the Fragile X Mental Retardation, FMRP, and microRNAs to repress translation at synapses, which can be rapidly de-repressed in response to activation of gp1 metabotropic glutamate receptors. One FMRP target mRNA of interest has been postsynaptic density-95, PSD-95, which is localized to dendrites and can be translated at synapses in response to activation of mGluRs. More recent work has revealed the role of other microRNAs to regulate FMRP target mRNA translation that appears important for control of neuronal excitability. We speculate that fragile x syndrome may result from synaptic protein imbalances due to dysregulation of microRNAmediated control that is important for control of neuronal development, excitability and plasticity.
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