Brain and neuroscience advances最新文献

In this article, we describe our involvement in the early days of research into long-term potentiation. We start with a description of the early experiments conducted in Oslo and London where long-term potentiation was first characterised. We discuss the ways in which the molecular pharmacology of glutamate receptors control the induction and expression of long-term potentiation and its counterpart, long-term depression. We then go on to summarise the extraordinary advances in understanding the cellular mechanisms of synaptic plasticity that have taken place in the subsequent half century. Finally, the increasing evidence that impaired long-term potentiation is a core feature of many brain disorders (LToPathies) is addressed by way of a few selected examples.

Although most people are right-handed and have language in their left cerebral hemisphere, why that is so, and in particular why about ten per cent of people are left-handed, is far from clear. Multiple theories have been proposed, often with little in the way of empirical support, and sometimes indeed with strong evidence against them, and yet despite that have become modern urban myths, probably due to the symbolic power of right and left. One thinks in particular of ideas of being right-brained or left-brained, of suggestions that left-handedness is due to perinatal brain damage, of claims that left-handers die seven years earlier than right-handers, and of the unfalsifiable ramifications of the byzantine Geschwind-Behan-Galaburda theory. This article looks back over the past fifty years of research on brain asymmetries, exploring the different themes and approaches, sometimes in relation to the author's own work. Taking all of the work together it is probable that cerebral asymmetries are under genetic control, probably with multiple genetic loci, only a few of which are now beginning to be found thanks to very large databases that are becoming available. Other progress is also seen in proper meta-analyses, the use of fMRI for studying multiple functional lateralisations in large number of individuals, fetal ultra-sound for assessing handedness before birth, and fascinating studies of lateralisation in an ever widening range of animal species. With luck the next fifty years will make more progress and show fewer false directions than had much of the work in the previous fifty years.

This review provides a distillate of the advances in knowledge about the neurotransmitter functions of acetylcholine over the 50-year period between 1967 and 2017, together with incremental information about the cognate nicotinic and muscarinic acetylcholine receptors, and some brief comments on possible advances in the near future. The text is supplemented by a timelines figure indicating the dates of some key advances in knowledge about acetylcholine receptors and a box-figure providing a snapshot of selected papers about acetylcholine published in the year 1967.

We review the current knowledge about the part that motor cortex plays in the preparation and generation of movement, and we discuss the idea that corticospinal neurons, and particularly those with cortico-motoneuronal connections, act as 'command' neurons for skilled reach-to-grasp movements in the primate. We also review the increasing evidence that it is active during processes such as action observation and motor imagery. This leads to a discussion about how movement is inhibited and stopped, and the role in these for disfacilitation of the corticospinal output. We highlight the importance of the non-human primate as a model for the human motor system. Finally, we discuss the insights that recent research into the monkey motor system has provided for translational approaches to neurological diseases such as stroke, spinal injury and motor neuron disease.

Neuronal oscillations represent the most obvious feature of electrical activity in the brain. They are linked in general with global brain state (awake, asleep, etc.) and specifically with organisation of neuronal outputs during sensory perception and cognitive processing. Oscillations can be generated by individual neurons on the basis of interaction between inputs and intrinsic conductances but are far more commonly seen at the local network level in populations of interconnected neurons with diverse arrays of functional properties. It is at this level that the brain's rich and diverse library of oscillatory time constants serve to temporally organise large-scale neural activity patterns. The discipline is relatively mature at the microscopic (cell, local network) level - although novel discoveries are still commonplace - but requires a far greater understanding of mesoscopic and macroscopic brain dynamics than we currently hold. Without this, extrapolation from the temporal properties of neurons and their communication strategies up to whole brain function will remain largely theoretical. However, recent advances in large-scale neuronal population recordings and more direct, higher fidelity, non-invasive measurement of whole brain function suggest much progress is just around the corner.

The use of cognitive-enhancing drugs by healthy individuals has been a feature for much of recorded history. Cocaine and amphetamine are modern cases of drugs initially enthusiastically acclaimed for enhancing cognition and mood. Today, an increasing number of healthy people are reported to use cognitive-enhancing drugs, as well as other interventions, such as non-invasive brain stimulation, to maintain or improve work performance. Cognitive-enhancing drugs, such as methylphenidate and modafinil, which were developed as treatments, are increasingly being used by healthy people. Modafinil not only affects 'cold' cognition, but also improves 'hot' cognition, such as emotion recognition and task-related motivation. The lifestyle use of 'smart drugs' raises both safety concerns as well as ethical issues, including coercion and increasing disparity in society. As a society, we need to consider which forms of cognitive enhancement (e.g. pharmacological, exercise, lifelong learning) are acceptable and for which groups under what conditions and by what methods we would wish to improve and flourish.

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The late 1960s was a heyday for catecholamine research. Technological developments made it feasible to study the regulation of sympathetic neuronal transmission and to map the distribution of noradrenaline and dopamine in the brain. At last, it was possible to explain the mechanism of action of some important drugs that had been used in the clinic for more than a decade (e.g. the first generation of antidepressants) and to contemplate the rational development of new treatments (e.g. l-dihydroxyphenylalanine therapy, to compensate for the dopaminergic neuropathy in Parkinson's disease, and β₁-adrenoceptor antagonists as antihypertensives). The fact that drug targeting noradrenergic and/or dopaminergic transmission are still the first-line treatments for many psychiatric disorders (e.g. depression, schizophrenia, and attention deficit hyperactivity disorder) is a testament to the importance of these neurotransmitters and the research that has helped us to understand the regulation of their function. This article celebrates some of the highlights of research at that time, pays tribute to some of the subsequent landmark studies, and appraises the options for where it could go next.