The overwhelming majority of research in the neurosciences employs P-values stemming from tests of statistical significance to decide on the presence or absence of an effect of some treatment variable. Although a continuous variable, the P-value is commonly used to reach a dichotomous decision about the presence of an effect around an arbitrary criterion of 0.05. This analysis strategy is widely used, but has been heavily criticized in the past decades. To counter frequent misinterpretations of P-values, it has been advocated to complement or replace P-values with measures of effect size (MES). Many psychological, biological and medical journals now recommend reporting appropriate MES. One hindrance to the more frequent use of MES may be their scarcity in standard statistical software packages. Also, the arguably most widespread data analysis software in neuroscience, matlab, does not provide MES beyond correlation and receiver-operating characteristic analysis. Here we review the most common criticisms of significance testing and provide several examples from neuroscience where use of MES conveys insights not amenable through the use of P-values alone. We introduce an open-access matlab toolbox providing a wide range of MES to complement the frequently used types of hypothesis tests, such as t-tests and analysis of variance. The accompanying documentation provides calculation formulae, intuitive explanations and example calculations for each measure. The toolbox described is usable without sophisticated statistical knowledge and should be useful to neuroscientists wishing to enhance their repertoire of statistical reporting.

This paper describes experimental techniques with head-fixed, operantly conditioned rodents that allow the control of stimulus presentation and tracking of motor output at hitherto unprecedented levels of spatio-temporal precision. Experimental procedures for the surgery and behavioral training are presented. We place particular emphasis on potential pitfalls using these procedures in order to assist investigators who intend to engage in this type of experiment. We argue that head-fixed rodent models, by allowing the combination of methodologies from molecular manipulations, intracellular electrophysiology, and imaging to behavioral measurements, will be instrumental in combining insights into the functional neuronal organization at different levels of observation. Provided viable behavioral methods are implemented, model systems based on rodents will be complementary to current primate models—the latter providing highest comparability with the human brain, while the former offer hugely advanced methodologies on the lower levels of organization, for example, genetic alterations, intracellular electrophysiology, and imaging.

Palpatory movements ('active' touch) are an integral part of tactile sensing. It is known that tactile signals can be modulated in certain behavioral contexts, but it is still unresolved to what degree this modulation is related to movement kinematics and whether it stems from tactile receptors or from central sources. Using awake, head-fixed rats, trained to contact an object, we measured trajectories of muscle-propelled whisker movement precisely and compared tactile responses to contacts thus accomplished with 'passive' contacts (motionless whisker contacted by object). Multielectrode extracellular recordings in deep layers of barrel cortex revealed that when the animals moved their whiskers actively, tactile processing switched from high response amplitudes, wide cortical representation and low background firing, to low response amplitudes, narrow spatial representation and elevated background firing. Switching was fast (<100 ms) and unrelated to the degree of alertness as assessed by spectral analysis of pre-contact field potentials. Switching persisted when information about whisker kinematics was interrupted by transection of the infraorbital nerve and contacts were mimicked by peripheral electrical stimulation. Taken together, these characteristics render central signals derived from the motor system a likely contributor to the processing of active touch.

General anaesthetics cause sedation, amnesia and hypnosis. Although these clinically desired actions are indicative of an impairment of neocortical information processing, it is widely held that they are to a large part mediated by subcortical neural networks. Anaesthetic action on brain stem, basal forebrain and thalamus, all of which are known to modulate cortical excitability, would thus ultimately converge on neocortex, perturbing and reducing action potential activity therein. However, as neocortex harbours molecular targets of anaesthetics in high densities, notably GABA(A) receptors, neocortex itself should be very sensitive to anaesthetics. Here, we performed experiments to reveal the extent to which neocortex proper is a relevant target of the low concentrations of volatile anaesthetics causing sedation and hypnosis. We compared the effects of isoflurane, enflurane and halothane on spontaneous action potential activity of rat neocortical neurons in vivo and in isolated cortical networks in vitro, i.e. in the presence and absence of subcortical arousal systems. We observed that the anaesthetics decreased spontaneous firing of neurons via intracortical mechanisms; concentrations inducing hypnosis in humans reduced discharge rates both in vivo and in vitro to the same extent, approximately 50%. This decrease in neuronal activity was paralleled by a significant enhancement of neocortical GABA(A) receptor-mediated inhibition. These findings challenge the notion of predominantly subcortical effects of volatile anaesthetics and suggest that intracortical targets, among them neocortical GABA(A) receptors, mediate the sedative and hypnotic properties of volatile anaesthetics.