I have developed "tennis elbow" from lugging this book around the past four weeks, but it is worth the pain, the effort, and the aspirin. It is also worth the (relatively speaking) bargain price. Including appendixes, this book contains 894 pages of text. The entire panorama of the neural sciences is surveyed and examined, and it is comprehensive in its scope, from genomes to social behaviors. The editors explicitly state that the book is designed as "an introductory text for students of biology, behavior, and medicine," but it is hard to imagine any audience, interested in any fragment of neuroscience at any level of sophistication, that would not enjoy this book. The editors have done a masterful job of weaving together the biologic, the behavioral, and the clinical sciences into a single tapestry in which everyone from the molecular biologist to the practicing psychiatrist can find and appreciate his or

Principles of Neural Science

It has been clear for almost two decades that cortical representations in adult animals are not fixed entities, but rather, are dynamic and are continuously modified by experience. The cortex can preferentially allocate area to represent the particular peripheral input sources that are proportionally most used. Alterations in cortical representations appear to underlie learning tasks dependent on the use of the behaviorally important peripheral inputs that they represent. The rules governing this cortical representational plasticity following manipulations of inputs, including learning, are increasingly well understood. In parallel with developments in the field of cortical map plasticity, studies of synaptic plasticity have characterized specific elementary forms of plasticity, including associative long-term potentiation and long-term depression of excitatory postsynaptic potentials. Investigators have made many important strides toward understanding the molecular underpinnings of these fundamental plasticity processes and toward defining the learning rules that govern their induction. The fields of cortical synaptic plasticity and cortical map plasticity have been implicitly linked by the hypothesis that synaptic plasticity underlies cortical map reorganization. Recent experimental and theoretical work has provided increasingly stronger support for this hypothesis. The goal of the current paper is to review the fields of both synaptic and cortical map plasticity with an emphasis on the work that attempts to unite both fields. A second objective is to highlight the gaps in our understanding of synaptic and cellular mechanisms underlying cortical representational plasticity.

/pdf/cortical-plasticity-from-synapses-to-maps-2j9eoi9428.pdf

CORTICAL PLASTICITY: From Synapses to Maps

We tested a theoretical prediction that patterns of excitatory input activity that consistently fail to activate target neurons sufficiently to induce synaptic potentiation will instead cause a specific synaptic depression. To realize this situation experimentally, the Schaffer collateral projection to area CA1 in rat hippocampal slices was stimulated electrically at frequencies ranging from 0.5 to 50 Hz. Nine hundred pulses at 1-3 Hz consistently yielded a depression of the CA1 population excitatory postsynaptic potential that persisted without signs of recovery for greater than 1 hr after cessation of the conditioning stimulation. This long-term depression was specific to the conditioned input, ruling out generalized changes in postsynaptic responsiveness or excitability. Three lines of evidence suggest that this effect is accounted for by a modification of synaptic effectiveness rather than damage to or fatigue of the stimulated inputs. First, the effect was dependent on the stimulation frequency; 900 pulses at 10 Hz caused no lasting change, and at 50 Hz a synaptic potentiation was usually observed. Second, the depressed synapses continued to support long-term potentiation in response to a high-frequency tetanus. Third, the effects of conditioning stimulation could be prevented by application of NMDA receptor antagonists. Thus, our data suggest that synaptic depression can be triggered by prolonged NMDA receptor activation that is below the threshold for inducing synaptic potentiation. We propose that this mechanism is important for the modifications of hippocampal response properties that underlie some forms of learning and memory.

https://www.pnas.org/content/pnas/89/10/4363.full.pdf

Homosynaptic long-term depression in area CA1 of hippocampus and effects of N-methyl-D-aspartate receptor blockade.

Developmental mechanisms that generate precise patterns of neuronal connectivity

Synaptic plasticity: LTP and LTD

Our intuition tells us that we, our conscious selves, cause our own voluntary acts. Yet scientists have long questioned this; Thomas Huxley, for example, in 1874 compared mental events to a steam whistle that contributes nothing to the work of a locomotive. New experimental evidence (most notable, work by Benjamin Libet and Daniel Wegner) has brought the causal status of human behavior back to the forefront of intellectual discussion. This multidisciplinary collection advances the debate, approaching the question from a variety of perspectives. The contributors begin by examining recent research in neuroscience that suggests that consciousness does not cause behavior, offering the outline of an empirically based model that shows how the brain causes behavior and where consciousness might fit in. Other contributors address the philosophical presuppositions that may have informed the empirical studies, raising questions about what can be legitimately concluded about the existence of free will from Libet's and Wegner's experimental results. Others examine the effect recent psychological and neuroscientific research could have on legal, social, and moral judgments of responsibility and blame -- in situations including A Clockwork Orange-like scenario of behavior correction. Contributors: William P. Banks, Timothy Bayne, Sarah-Jayne Blakemore, Suparna Choudhury, Walter J. Freeman, Shaun Gallagher, Susan Hurley, Marc Jeannerod, Leonard V. Kaplan, Hakwan Lau, Sabine Maasen, Bertram F. Malle, Alfred R. Mele, Elisabeth Pacherie, Richard Passingham, Susan Pockett, Wolfgang Prinz, Peter W. Ross

Does consciousness cause behavior

T he word “pain” encompasses several phenomena, which probably have several different mechanisms. Immediately after a noxious stimulus there comes an initial, short-lasting component of pain, which is described well by the gate-control theory. A little later comes a slow-onset, long-lasting component mediated by C-fibers from deep tissue, if that has been injured. This may be combined with sensitization of peripheral receptors and their continued activation by products of peripheral inflammatory processes. Relatively rarely, a pathologic state of chronic pain may develop, which can involve more or less permanent changes in the central nervous system (CNS), persisting long after the original injury has healed(l). Various forms of synaptic plasticity that may underlie these pathologic CNS changes are the subject of this review. There has been much interest recently in the involvement of spinal cord synaptic plasticity in the hyperalgesia and allodynia of chronic pain syndromes (2,3). Several forms of activity-dependent plasticity have been described in the spinal cord. Well established cases that have been widely associated with chronic pain are “windup” (4), which lasts seconds to minutes, and increases (5,6) or decreases (7) in the excitability of spinal reflexes lasting 1 to 3 h. More recently, long-term potentiation and depression of synaptic transmission, of the same types that occur in the hippocampus and neocortex (where they have been shown to last for days), have also been described in several regions of the spinal cord (8-10). Until now, there has been little cross-fertilization between the literature on spinal cord changes concerned with chronic pain and that on long-term potentiation and depression. It is, therefore, useful to summarize very briefly what is known of the mechanisms of these various forms of physiologic plasticity in such a way as to allow comparison between them and to clarify similarities and differences.

Spinal cord synaptic plasticity and chronic pain.

https://cdn.auckland.ac.nz/assets/psych/about/our-people/documents/sue-pockett/pockett-bold-freeman-2009.pdf

EEG synchrony during a perceptual-cognitive task: Widespread phase synchrony at all frequencies

https://www.psy.lmu.de/allg2/download/schoenbrodt/ws1011/2002_pockett-2.pdf

On subjective back-referral and how long it takes to become conscious of a stimulus: a reinterpretation of Libet's data.

The aim of this study was to see whether long-term potentiation (LTP) and/or long-term depression (LTD) of synaptic efficacy could be induced in the ventral horn of the rat spinal cord. Transverse slices were cut from neonatal rat spinal cords and maintained in vitro. Field potentials were recorded in the ventral horn in response to stimulation of the dorsal horn-intermediate nucleus region of the slice. Tetanic stimulation at 100 Hz (6 bursts of 50 pulses with 10 s between bursts) resulted in long-term potentiation in 25% of slices, long-term depression in 33% of slices and no long-lasting change of field potential amplitude in the rest. The long-term changes lasted at least 2.5 hours. The principal conclusion of the work is that LTP and LTD can be elicited in the ventral horn.

Susan Pockett

Papers

Does consciousness cause behavior

Spinal cord synaptic plasticity and chronic pain.

EEG synchrony during a perceptual-cognitive task: Widespread phase synchrony at all frequencies

On subjective back-referral and how long it takes to become conscious of a stimulus: a reinterpretation of Libet's data.

Long-term potentiation and depression in the ventral horn of rat spinal cord in vitro.