One of the most remarkable aspects of an animal's behavior is the ability to modify that behavior by learning, an ability that reaches its highest form in human beings. For me, learning and memory have proven to be endlessly fascinating mental processes because they address one of the fundamental features of human activity: our ability to acquire new ideas from experience and to retain these ideas over time in memory. Moreover, unlike other mental processes such as thought, language, and consciousness, learning seemed from the outset to be readily accessible to cellular and molecular analysis. I, therefore, have been curious to know: What changes in the brain when we learn? And, once something is learned, how is that information retained in the brain? I have tried to address these questions through a reductionist approach that would allow me to investigate elementary forms of learning and memory at a cellular molecular level-as specific molecular activities within identified nerve cells.

/pdf/the-molecular-biology-of-memory-storage-a-dialogue-between-2cym9imp74.pdf

The Molecular Biology of Memory Storage: A Dialogue Between Genes and Synapses

Structure and function of the brain serotonin system.

1. Introduction 2. On the way to the planning theory 3. Plans and practical reasoning 4. Agent rationality: toward a general theory 5. Reconsideration and rationality 6. Agent rationality: the historical theory 7. Commitment revisited 8. Two faces of intention 9. Acting with an intention 10. Intention and expected side effects 11. Conclusion Bibliography Notes Index.

Intention, Plans, and Practical Reason

Food intake is regulated by the hypothalamus, including the melanocortin and neuropeptide Y (NPY) systems in the arcuate nucleus. The NPY Y2 receptor (Y2R), a putative inhibitory presynaptic receptor, is highly expressed on NPY neurons in the arcuate nucleus, which is accessible to peripheral hormones. Peptide YY3-36 (PYY3-36), a Y2R agonist, is released from the gastrointestinal tract postprandially in proportion to the calorie content of a meal. Here we show that peripheral injection of PYY3-36 in rats inhibits food intake and reduces weight gain. PYY3-36 also inhibits food intake in mice but not in Y2r-null mice, which suggests that the anorectic effect requires the Y2R. Peripheral administration of PYY3-36 increases c-Fos immunoreactivity in the arcuate nucleus and decreases hypothalamic Npy messenger RNA. Intra-arcuate injection of PYY3-36 inhibits food intake. PYY3-36 also inhibits electrical activity of NPY nerve terminals, thus activating adjacent pro-opiomelanocortin (POMC) neurons. In humans, infusion of normal postprandial concentrations of PYY3-36 significantly decreases appetite and reduces food intake by 33% over 24 h. Thus, postprandial elevation of PYY3-36 may act through the arcuate nucleus Y2R to inhibit feeding in a gut–hypothalamic pathway.

BRIEF COMMUNICATION ARISING: Gut hormone PYY3-36 physiologically inhibits food intake

Habituation: A dual-process theory.

Morphological and functional properties of identified neurons in the abdominal ganglion of aplysia californica

The notion of the command cell has been highly influential in invertebrate neurobiology, and related notions have been increasingly used in research on the vertebrate nervous system. The term "command neuron" implies that the neuron has some critical function in the generation of a normally occurring behavior. Nevertheless, most authors either explicitly or implicitly use a strictly operational definition, independent of considerations of normal behavioral function. That is, command neurons are often defined as neurons which, when stimulated by the experimenter, evoke some behavioral response. Even when utilizing such an operational definition, investigators frequently differ on what they consider to be the exact characteristics that a neuron must have (or not have) to be considered a command cell. A few authors appear to treat command neurons in relation to normal function, but a precise be- haviorally relevant definition has not been specified. Because of the ambiguity in the definition of command neurons, the term can refer to a wide variety of neurons which may play divergent behavioral roles. In some ways the attempt to label a cell as a command neuron may interfere with the process of discovering the complex causal determinants of behavior. Nevertheless, the notion that indi- vidual cells are responsible for certain behaviors is highly appealing, and an attempt to define the command neuron rigorously could be worthwhile. We suggest that a command neuron be defined as a neuron that is both necessary and sufficient for the initiation of a given behavior. These criteria can by tested by: (1) establishing the response pattern of the putative command neuron during presenta- tion of a given stimulus and execution of a well specified behavior; (2) removing the neuron and showing that the response is no longer elicited by the stimulus (necessary condition); and (3) firing the neuron in its normal pattern and showing that the complete behavioral response occurs (sufficient condition). In some cases, groups of neurons, when treated as a whole, may satisfy the necessity and sufficiency criteria for a given behavior, even though individual neurons of the group fail to meet the criteria. We suggest that such a group be termed a "command system" for the behavior in question. Individual neurons in the command system can be termed "com- mand elements" if, when fired in their normally occurring pattern, they elicit a part of the behavior, or "modulatory elements" if they do not in isolation elicit any response, but alter the behavior produced by other elements in the command system.

https://courses.cit.cornell.edu/bionb4240/Reprints/Kupferman%20and%20Weiss%201978_ocr.pdf

The command neuron concept

We have examinived the nieural correlates of habittuatiotn atid dishabitiuation of tlhe gill-withdrwal reflex in Aplysia. We obtained intracelllular recordings from identified gill motor neurons in the abdominal ganglionz of a semi-intact preparation of Aplysia wlhile we simultaneously recorded behavior responises of the gill. Habituation and dishabituation were not due to peripheral changes in either the sensory receptors or the gill musculature butt were caused by changes in the amplitlude of the excitatory synaptic potentials produced at the gill motor neurons.

https://science.sciencemag.org/content/sci/167/3926/1745.full.pdf

Neuronal Mechanisms of Habituation and Dishabituation of the Gill-Withdrawal Reflex in Aplysia

Feeding behavior in Aplysia: a simple system for the study of motivation.

I. We have studied the central and peripheral functions of the metacerebral cell (MCC) ofAplysia. This research concentrated on the role of the MCC in controlling the ARC muscle, which is representative of a group of muscles that effect the biting and swallowing response of Aplysia. 2. Firing of the MCC produced a slowly rising and slowly decaying excitatory synaptic potential in motoneurons of the ARC muscle and other muscles of the buccal mass. The excitatory synaptic potential was not sufficient to fire motoneurons unless they received another source of depolarization. 3. In isolated buccal ganglia that exhibit periodic burst output, firing of the MCC at low, physiological rates, increased the frequency of occurrence of the burst output. Firing of the MCC was never effective in eliciting sustained burst output from nonbursting ganglia. 4. Although the MCC sends axonal branches to nerves innervating the accessory radula closer (ARC) and other muscles, firing of the MCC produced neither an increase nor decrease of the resting tension of the ARC muscle. Furthermore, firing of the ARC was never associated with any direct depolarizing or hyperpolarizing responses in muscle fibers. 5. Brief firing of the MCC enhanced the muscle contraction produced by firing of ARC motoneurons. The enhancement of contraction was maximum approximately 30 s after termination of a brief burst of MCC spikes (e.g., 30 spikes at 5/s), and the process then gradually decayed over a period of a minute or more. Physiological rates of MCC firing (see below) also enhanced contraction of ARC muscles. 6. The above data suggested that the MCCs might be involved in feeding behavior. To explore this hypothesis, chronic extracellular recordings from a MCC were obtained while ani-

Irving Kupfermann

Papers

Morphological and functional properties of identified neurons in the abdominal ganglion of aplysia californica

The command neuron concept

Neuronal Mechanisms of Habituation and Dishabituation of the Gill-Withdrawal Reflex in Aplysia

Feeding behavior in Aplysia: a simple system for the study of motivation.

Modulatory control of buccal musculature by a serotonergic neuron (metacerebral cell) in Aplysia