Despite the concern that has been expressed about potential method biases, and the pervasiveness of research settings with the potential to produce them, there is disagreement about whether they really are a problem for researchers in the behavioral sciences. Therefore, the purpose of this review is to explore the current state of knowledge about method biases. First, we explore the meaning of the terms “method” and “method bias” and then we examine whether method biases influence all measures equally. Next, we review the evidence of the effects that method biases have on individual measures and on the covariation between different constructs. Following this, we evaluate the procedural and statistical remedies that have been used to control method biases and provide recommendations for minimizing method bias.

Sources of Method Bias in Social Science Research and Recommendations on How to Control It

The field of neuroscience has, after a long period of looking the other way, again embraced emotion as an important research area. Much of the progress has come from studies of fear, and especially fear conditioning. This work has pin- pointed the amygdala as an important component of the system involved in the acqui- sition, storage, and expression of fear memory and has elucidated in detail how stimuli enter, travel through, and exit the amygdala. Some progress has also been made in understanding the cellular and molecular mechanisms that underlie fear conditioning, and recent studies have also shown that the findings from experimental animals apply to the human brain. It is important to remember why this work on emotion succeeded where past efforts failed. It focused on a psychologically well-defined aspect of emo- tion, avoided vague and poorly defined concepts such as "affect," "hedonic tone," or "emotional feelings," and used a simple and straightforward experimental approach. With so much research being done in this area today, it is important that the mistakes of the past not be made again. It is also time to expand from this foundation into broader aspects of mind and behavior

http://gruberpeplab.com/3131/LeDoux_2000_Emotioncircuitbrain.pdf

Emotion Circuits in the Brain

The adolescent brain and age-related behavioral manifestations

Various chronic antidepressant treatments increase adult hippocampal neurogenesis, but the functional importance of this phenomenon remains unclear. Here, using genetic and radiological methods, we show that disrupting antidepressant-induced neurogenesis blocks behavioral responses to antidepressants. Serotonin 1A receptor null mice were insensitive to the neurogenic and behavioral effects of fluoxetine, a serotonin selective reuptake inhibitor. X-irradiation of a restricted region of mouse brain containing the hippocampus prevented the neurogenic and behavioral effects of two classes of antidepressants. These findings suggest that the behavioral effects of chronic antidepressants may be mediated by the stimulation of neurogenesis in the hippocampus.

https://science.sciencemag.org/content/sci/301/5634/805.full.pdf

Requirement of Hippocampal Neurogenesis for the Behavioral Effects of Antidepressants

This meta-analysis of 172 studies (N = 2,263 anxious, N = 1,768 nonanxious) examined the boundary conditions of threat-related attentional biases in anxiety. Overall, the results show that the bias is reliably demonstrated with different experimental paradigms and under a variety of experimental conditions, but that it is only an effect size of d = 0.45. Although processes requiring conscious perception of threat contribute to the bias, a significant bias is also observed with stimuli outside awareness. The bias is of comparable magnitude across different types of anxious populations (individuals with different clinical disorders, high-anxious nonclinical individuals, anxious children and adults) and is not observed in nonanxious individuals. Empirical and clinical implications as well as future directions for research are discussed.

/pdf/threat-related-attentional-bias-in-anxious-and-nonanxious-2pi60mj0pt.pdf

Threat-related attentional bias in anxious and nonanxious individuals: a meta-analytic study.

The purpose of the present study was to determine whether lesions of areas projected to by the central amygdaloid nucleus (ACE) would disrupt the classical conditioning of autonomic and/or behavioral emotional responses. The areas studied included 3 projection targets of the ACE: the lateral hypothalamic area (LH), midbrain central gray (CG) region, and bed nucleus of the stria terminalis (BNST). Lesions were made either electrolytically or by microinjection of ibotenic acid, which destroys local neurons without interrupting fibers of passage. Two weeks later, the animals were classically conditioned by pairing an acoustic stimulus with footshock. The next day, conditioned changes in autonomic activity (increases in arterial pressure) and emotional behavior ("freezing," or the arrest of somatomotor activity) evoked by the acoustic conditioned stimulus (CS) were measured during extinction trials. Electrolytic and ibotenic acid lesions of the LH interfered with the conditioned arterial pressure response, but did not affect conditioned freezing. Electrolytic lesions of the rostral CG disrupted conditioned freezing but not conditioned changes in arterial pressure. Ibotenic acid injected into the rostral CG reduced neither the arterial pressure nor the freezing response. Injection of ibotenic acid in the caudal CG, like electrolytic lesions of the rostral CG, disrupted the freezing, but not the arterial pressure response. Injection of ibotenic acid into the BNST had no effect on either response. These data demonstrate that neurons in the LH are involved in the autonomic, but not the behavioral, conditioned response pathway, whereas neurons in the caudal CG are involved in the behavioral, but not the autonomic, pathway. Different efferent projections of the central amygdala thus appear to mediate the behavioral and autonomic concomitants of conditioned fear.

https://www.jneurosci.org/content/jneuro/8/7/2517.full.pdf

Different projections of the central amygdaloid nucleus mediate autonomic and behavioral correlates of conditioned fear

Previous work has implicated projections from the acoustic thalamus to the amygdala in the classical conditioning of emotional responses to auditory stimuli. The purpose of the present studies was to determine whether the lateral amygdaloid nucleus (AL), which is a major subcortical target of projections from the acoustic thalamus, might be the sensory interface of the amygdala in emotional conditioning. Lesions were placed in AL of rats and the effects on emotional conditioning were examined. Lesions of AL, but not lesions of the striatum above or the cortex adjacent to the AL, interfered with emotional conditioning. Lesions that only partially destroyed AL or lesions placed too ventrally that completely missed AL had no effect. AL lesions did not affect the responses elicited following nonassociative (random) training. AL is thus an essential link in the circuitry through which auditory stimuli are endowed with affective properties and may function as the sensory interface of the amygdala during emotional learning.

https://www.jneurosci.org/content/jneuro/10/4/1062.full.pdf

The lateral amygdaloid nucleus: Sensory interface of the amygdala in fear conditioning

Previous work has implicated projections from the acoustic thalamus to the amygdala in the classical conditioning of emotional responses to auditory stimuli. The purpose of the present studies was to determine whether the lateral amygdaloid nucleus (AL), which is a major subcortical target of projections from the acoustic thalamus, might be the sensory interface of the amygdala in emotional conditioning. Lesions were placed in AL of rats and the effects on emotional conditioning were examined. Lesions of AL, but not lesions of the striatum above or the cortex adjacent to the AL, interfered with emotional conditioning. Lesions that only partially destroyed AL or lesions placed too ventrally that completely missed AL had no effect. AL lesions did not affect the responses elicited following nonassociative (random) training. AL is thus an essential link in the circuitry through which auditory stimuli are endowed with affective properties and may function as the sensory interface of the amygdala during emotional learning. Most of the stimuli we encounter in daily life are neither intrinsically good nor bad and only acquire affective qualities through our experiences with them. For example, stimuli that occur at the same time as some unpleasant event can, by association, acquire aversive properties. In laboratory studies, classical conditioning procedures are used to study the brain mechanisms underlying the formation of emotional associations. Typically, a relatively neutral stimulus, such as a tone or light, is paired with an aversive event, such as footshock. After only a few pairings, the previously neutral stimulus becomes aversive and can itself evoke an emotional reaction. The effects of conditioning develop rapidly and persist for long periods of time, reflecting the biological significance of the learning experience for the organism. For these reasons, emotional conditioning is an extremely valuable tool for studying learning mechanisms. Considerable evidence now suggests that the amygdala, and particularly the central nucleus of the amygdala (ACE), is an essential link in the neural circuit underlying aversive emotional conditioning (fear conditioning): lesions or pharmacological ma

Piera Cicchetti

Papers

Different projections of the central amygdaloid nucleus mediate autonomic and behavioral correlates of conditioned fear

The lateral amygdaloid nucleus: Sensory interface of the amygdala in fear conditioning

The Lateral Amygdaloid in Fear Conditioning Nucleus: Sensory Interface Amygdala