Daniel L. Alkon

Bio: Daniel L. Alkon is an academic researcher from Marine Biological Laboratory. The author has contributed to research in topics: Associative learning & Hippocampal formation. The author has an hindex of 3, co-authored 4 publications receiving 1640 citations. Previous affiliations of Daniel L. Alkon include University of California, San Diego & Northwestern University.

Learning and memory

Abstract: How the brain codes, stores, and retrieves memories is among the most important and baffling questions in science. The uniqueness of each human being is due largely to the memory store—the biological residue of memory from a lifetime of experience. The cellular basis of this ability to learn can be traced to simpler organisms. In the past generation, understanding of the biological basis of learning and memory has undergone a revolution. It is clear that various forms and aspects of learning and memory involve particular systems, networks, and circuits in the brain, and it now appears possible to identify these circuits, localize the sites of memory storage, and analyze the cellular and molecular mechanisms of memory.

Conditioning-specific membrane changes of rabbit hippocampal neurons measured in vitro (ionic mechanisms/afterhyperpolarization/associative learning/brain slice/nictitating membrane conditioning)

Abstract: Intracellular recordings were made from hip- pocampal CAl pyramidal neurons within brain slices of nictitating membrane conditioned, pseudoconditioned, and naive adult male albino rabbits All neurons included (26 conditioned, 26 pseudoconditioned, and 28 naive) had stable penetration and at least 60 mV action potential amplitudes Mean input resistances were -=60 Mfl for the three groups A marked reduction in the afterhyperpolarization (AHP) follow- ing an impulse was apparent for conditioned (x = -098 mV) as compared to the pseudoconditioned (x = -17 mV) and naive (x = -20 mV) neurons The AHP has been attributed previously to activation of a Ca2+-dependent outward K+ current The distribution of AHP amplitudes for the condi- tioned group included a new lower range of values for which there was little overlap with the other groups The condition- ing-specific reduction of 'AHP may be due to reduction of Ica2+-K+ as shown previously for conditioned Hermissenda neurons This conditioning-induced biophysical alteration of the CAl pyramidal cell must be stored by mechanisms intrinsic to the hippocampal slice and cannot be explained as a conse- quence of changes of presynaptic input arising elsewhere in the brain Our experiments demonstrate the feasibility of analyz- ing cellular mechanisms of associative learning in mammalian brain with the in vitro brain slice technique

Enhancement of synaptic potentials in rabbit CAl pyramidal neurons following classical conditioning (learning and memory/hippocampus/brain slice)

Abstract: A synaptic potential elicited by high-frequen- cy stimulation of the Schaffer collaterals was enhanced In hippocampal CAI pyramidal cells from rabbits that were classically conditioned relative to cells from control rabbits. In addition, confirming previous reports, the after-hyperpolari- zation was reduced in cells from conditioned animals. We suggest that reduced after-hyperpolarization and enhanced synaptic responsiveness in cells from conditioned animals work in concert to contribute to the functioning of hippo- campal CAl pyramidal cells during classical conditioning. Associative memory, the storage of learned relationships, is a fundamental function of nervous systems. Cellular corre- lates of learned behaviors are traces of associative memory and, as such, represent elementary units of memory storage. While there has been success in identifying cellular traces of associative memory in mulluscan neurons (1-3), progress toward this end has been slower in the mammalian brain (4, 5). To overcome the methodological difficulties that have impeded the identification of learning-specific cellular corre- lates in the mammalian brain, we have capitalized on the inherent advantages offered by both the in vitro brain-slice technique (6) and a robust form of associative learning: classical conditioning of the rabbit's eye-blink/nictitating- membrane response (7). By combining these two prepara- tions, previous studies have demonstrated that biophysical and biochemical correlates of classical conditioning are

Design of Everyday Things

Abstract: Revealing how smart design is the new competitive frontier, this innovative book is a powerful primer on how--and why--some products satisfy customers while others only frustrate them.

Learning by expanding: An activity-theoretical approach to developmental research

Abstract: 1. Introduction 2. The emergence of learning activity as a historical form of human learning 3. The zone of proximal development as the basic category of expansive research 4. The instruments of expansion 5. Toward an expansive methodology 6. Epilogue.

On a confusion about a function of consciousness. Author's response

Abstract: of the original article: Consciousness is a mongrel concept: there are a number of very different consciousnesses. Phenomenal consciousness is experience; the phenomenally conscious aspect of a state is what it is like to be in that state. The mark of access-consciousness, by contrast, is availability for use in reasoning and rationally guiding speech and action. These concepts are often partly or totally conflated, with bad results. This target article uses as an example a form of reasoning about a function of consciousness based on the phenomenon of blindsight. Some information about stimuli in the blind field is represented in the brains of blindsight patients, as shown by their correct guesses. They cannot harness this information in the service of action, however, and this is said to show that a function of phenomenal consciousness is somehow to enable information represented in the brain to guide action. But stimuli in the blind field are both access-unconscious and phenomenally unconscious. The fallacy is: an obvious function of the machinery of access-consciousness is illicitly transferred to phenomenal consciousness.

Emotion, plasticity, context, and regulation: perspectives from affective neuroscience.

Abstract: The authors present an overview of the neural bases of emotion. They underscore the role of the prefrontal cortex (PFC) and amygdala in 2 broad approach- and withdrawal-related emotion systems. Components and measures of affective style are identified. Emphasis is given to affective chronometry and a role for the PFC in this process is proposed. Plasticity in the central circuitry of emotion is considered, and implications of data showing experience-induced changes in the hippocampus for understanding psychopathology and stress-related symptoms are discussed. Two key forms of affective plasticity are described--context and regulation. A role for the hippocampus in context-dependent normal and dysfunctional emotional responding is proposed. Finally, implications of these data for understanding the impact on neural circuitry of interventions to promote positive affect and on mechanisms that govern health and disease are considered.