02433nas a2200241   4500008004100000022001400041245007500055210006900130260001200199300001400211490000800225520167700233653003001910653001201940653002701952653001101979653002401990653001302014653001302027100002402040700001802064856010902082       2022                        eng d  a1469-779300aHeksor: the central nervous system substrate of an adaptive behaviour.0 aHeksor the central nervous system substrate of an adaptive behav  c08/2022  a3423-34520 v6003 a<p>Over the past half-century, the largely hardwired central nervous system (CNS) of 1970 has become the ubiquitously plastic CNS of today, in which change is the rule not the exception. This transformation complicates a central question in neuroscience: how are adaptive behaviours - behaviours that serve the needs of the individual - acquired and maintained through life? It poses a more basic question: how do many adaptive behaviours share the ubiquitously plastic CNS? This question compels neuroscience to adopt a new paradigm. The core of this paradigm is a CNS entity with unique properties, here given the name heksor from the Greek hexis. A heksor is a distributed network of neurons and synapses that changes itself as needed to maintain the key features of an adaptive behaviour, the features that make the behaviour satisfactory. Through their concurrent changes, the numerous heksors that share the CNS negotiate the properties of the neurons and synapses that they all use. Heksors keep the CNS in a state of negotiated equilibrium that enables each heksor to maintain the key features of its behaviour. The new paradigm based on heksors and the negotiated equilibrium they create is supported by animal and human studies of interactions among new and old adaptive behaviours, explains otherwise inexplicable results, and underlies promising new approaches to restoring behaviours impaired by injury or disease. Furthermore, the paradigm offers new and potentially important answers to extant questions, such as the generation and function of spontaneous neuronal activity, the aetiology of muscle synergies, and the control of homeostatic plasticity.</p>10aAdaptation, Psychological10aAnimals10acentral nervous system10aHumans10aNeuronal Plasticity10aPlastics10aSynapses1 aWolpaw, Jonathan, R1 aKamesar, Adam  uhttps://neurotechcenter.org/publications/2022/heksor-central-nervous-system-substrate-adaptive-behaviour01807nas a2200229   4500008004100000022001400041245014300055210006900198260001200267300001400279490000700293520108100300653001701381653002701398653001901425653001901444653001201463100002101475700001901496700001501515856004701530       1989                        eng d  a0197-846200aChronic exposure of primates to 60-Hz electric and magnetic fields: I. Exposure system and measurements of general health and performance.0 aChronic exposure of primates to 60Hz electric and magnetic field  c01/1989  a277–2880 v103 aWe exposed pigtailed macaques (Macaca nemestrina) to electric (E) and magnetic (B) fields at strengths of 3 kV/m and 0.1 G, 10 kV/m and 0.3 G, and 30 kV/m and 0.9 G for three 21 day segments. These three exposure segments were preceded and followed by 21 day sham exposure segments. Additional animals received only sham exposure for five 21 day segments. Detailed description of the exposure chamber and field generation apparatus is given. We evaluated measures of animal well-being, including weight, blood chemistry, blood cell counts, and performance on a simple motor task, and performed postmortem examinations. Reliable and consistent results were obtained throughout data collection. None of the measures evaluated was significantly affected by E- and B-field exposures. Data obtained during actual exposure segments were not distinguishable from those obtained during the initial and final sham exposure segments, nor were they different from data obtained from the sham-exposed animals. Thus, field exposure had no apparent effects on general health or performance.10a60-Hz fields10acentral nervous system10aelectric field10amagnetic field10aprimate1 aWolpaw, Jonathan1 aSeegal, R., F.1 aDowman, R.  uhttp://www.ncbi.nlm.nih.gov/pubmed/2751702