https://homepages.inf.ed.ac.uk/pseries/Neuroinformatics/Uhlhaas&Singer2006.pdf

Neural Synchrony in Brain Disorders: Relevance for Cognitive Dysfunctions and Pathophysiology

http://ski.clps.brown.edu/papers/CavanaghFrank_TICS.pdf

Frontal theta as a mechanism for cognitive control

Nonlinear dynamical analysis of EEG and MEG: Review of an emerging field

1. Clarification: The 2013 Guidelines make a distinction between euthanasia, humane killing, and slaughter, and state that neither slaughter nor humane killing is covered in the document P.68, S6.1.1. Not included among the definitions of these terms are ending the lives of healthy animals or scientific collection of animals. For clarification, whatever the term used, classification of the method, or reason given for killing animals: euthanasia, humane killing, slaughter, harvest, depopulation, scientific collection, or research-related, the Council on Accreditation’s foremost concern, in all situations, is with humane technique. The goal of humane technique is to minimize pain, distress, and the negative effect to the animal. The technique employed should result in rapid loss of consciousness followed by cardiac or respiratory arrest and, ultimately, a loss of brain function. Although complete absence of pain and distress is preferred, it is understood that it cannot always be achieved P7.13.2.

https://works.bepress.com/cheryl_greenacre/14/download/

AVMA Guidelines for the Euthanasia of Animals: 2013 Edition

Grouping of brain rhythms in corticothalamic systems

Walkers target article proposes a refinement of the well known two-stage model of memory formation to explain the positive effects of sleep on consolidation. After a first stage in which a labile memory representation is formed, a further stabilisation of the memory trace takes place in the second stage. which is dependent on (REM) sleep. Walker has refined the latter stage into a stage in which a consolidation-based enhancement occurs. It is not completely clear what consolidation-based enhancement implies and how it can be dissociated from a stage for memory-stabilisation. A more serious consideration, however, is whether a second stage in memory consolidation that is solely dependent on sleep is really necessary. The classical, passive, interference theory is able to explain adequately the findings related to the effects of sleep and memory, and can lead perhaps better to an understanding of the highly variable data in this field.

/pdf/where-is-the-classic-interference-theory-for-sleep-and-4bl0njbnhe.pdf

Where is the classic interference theory for sleep and memory

Adolf Beck, co-founder of the EEG: An essay in honour on his 150th birthday

Publisher Summary This chapter describes the behavioral pharmacology of sleep. The sensitivity of sleep parameters to the effects of psychoactive drugs makes the behavioral pharmacology of EEG and sleep an interesting tool for research of the central nervous system. Major progress has been made in the discovery of nonbenzodiazepine hypnotics with fewer unwanted effects. Twenty years of sleep research has also resulted in a much better understanding of sleep. The two-process model of sleep, with an emphasis on the power of the delta waves as its main parameter, provides a new way of thinking with consequences for the behavioral pharmacology of sleep. The chapter presents a methodological overview of the basic problems and questions in the pharmacology of preclinical sleep research. A behavioral definition of sleep is presented, followed by a definition in terms of electrophysiological parameters. New developments are briefly introduced, which are expected to have major impact on the evaluation of putative hypnotic compounds. The chapter describes different animal models followed by an introduction to the different procedures available to the sleep researcher. It also presents an analysis of some of the critical problems encountered in the behavioral pharmacology of sleep.

The behavioral pharmacology of sleep

Chronic experimental allergic encephalomyelitis (CEAE) is an established experimental model for multiple sclerosis (MS). The demyelinating lesions in the white matter of the central nervous system observed in CEAE and in MS are accompanied by various neurophysiological alterations. Among the best defined electrophysiological abnormalities are the changes in event-related potentials, in particular evoked potentials involving the spinal cord, i.e. motor and sensory evoked potentials. Less familiar are the changes observed in the electroencephalogram of CEAE-affected animals, which are also encountered in the human equivalent, MS. In the present experiment we evaluated the therapeutic value of a neurotrophic peptide treatment [H-Met(O2)-Glu-His-Phe-D-Lys-Phe-OH, an ACTH4-9 analogue] and its effect on the delayed flash visual evoked potentials (VEP) and power spectra of the electroencephalogram, during a 17-week follow-up of CEAE. CEAE animals treated with the neurotrophic peptide were protected against the development of neurological symptoms during the course of the demyelinating syndrome. VEPs of animals suffering from CEAE showed a delay of the latencies of the late components which was significantly counteracted by peptide treatment. The peak-to-peak amplitude of the VEP afterdischarge recorded from CEAE animals was significantly increased during the course of CEAE and correlated closely with the progression of the myelinopathy. Furthermore, CEAE animals showed an increase of electroencephalogram (EEG) beta activity of up to 500% as compared with the age-matched control group. This increase in beta power mainly consisted of a prevailing 20-21 Hz peak, a frequency that normally is not dominant in control EEG recordings of the rat during passive wakefulness. All these electrophysiological phenomena were absent in ACTH4-9 analogue-treated animals. The present findings underscore the potential importance of a neurotrophic peptide treatment in the pharmacotherapy of central demyelinating syndromes, and possibly of MS.

/pdf/neurotrophic-acth4-9-analogue-therapy-normalizes-45n5p5fkiq.pdf

Anton M.L. Coenen

Papers

Where is the classic interference theory for sleep and memory

Adolf Beck, co-founder of the EEG: An essay in honour on his 150th birthday

The behavioral pharmacology of sleep

Neurotrophic ACTH4-9 analogue therapy normalizes electroencephalographic alterations in chronic experimental allergic encephalomyelitis.

Effect of appetitive Pavlovian conditioning on the N150 of the amygdalar Auditory Evoked Potential in the rat