Affect is a form of cognition: A neurobiological analysis

Abstract

In this paper, we suggest that affect meets the traditional definition of “cognition” such that the affect–cognition distinction is phenomenological, rather than ontological. We review how the affect–cognition distinction is not respected in the human brain, and discuss the neural mechanisms by which affect influences sensory processing. As a result of this sensory modulation, affect performs several basic “cognitive” functions. Affect appears to be necessary for normal conscious experience, language fluency, and memory. Finally, we suggest that understanding the differences between affect and cognition will require systematic study of how the phenomenological distinction characterising the two comes about, and why such a distinction is functional.

Acknowledgements

Preparation of this manuscript was supported by NIMH grant K02 MH001981 and NIA grant ROI AG030311 to LFB.

During the preparation of this article the authors benefited from discussions with Elizabeth Kensinger, Ann Kring, and Luiz Pessoa.

Notes

¹Based upon neuroanatomical studies of rodents, it is typically assumed that the ability to detect a valenced stimulus under the threshold of awareness is mediated by the projections from the thalamus to the amygdala (i.e., the “low-road”; LeDoux, 1996). It has been argued, however, that the “low road” is impoverished in primates (for reviews, see Pessoa & Ungerleider, 2004; Rolls, 2000). It is possible that objective awareness of valenced stimuli is mediated by activity in the ventral stream that is directed by the amygdala. Subliminal presentations of valenced stimuli might be associated with increased activation in the amygdala and ventral visual stream, but such activation may not be sufficient (i.e., too few neurons fire, or neurons do not fire for a sufficient duration) for the neural activation to reach the threshold of conscious awareness. The degree of conscious awareness for a valenced stimulus is most likely modulated by the degree of activity in the ventral stream, such that conscious and non-conscious perceptions of valenced stimuli involve the same circuitry (rather than by two different circuits).

²For example, cholinergic projections from basal forebrain augment neural responses to motivationally relevant sensory events, and enhance their storage in long-term memory; noradrenergic innervations from locus coeruleus increase the signal-to-noise ratio and precision of neuronal firing to such events; dopaminergic projections from substantia nigra and ventral tegmental area mark the salience of an event and gate access to voluntary motor outputs; and serotonergic projections from the rostral raphe nucleus reduce distractibility and gate the processing of motivationally relevant sensory cues (Mesulam, 2000; Parvizi & Damasio, 2001).

³We are not claiming that sensory input is inaccessible to core affective circuitry in blindsight patients. Sensory information could still cause changes in core affective experience, helping blindsight patients to make affect-based discriminations in their environment such as categorising facial configurations depicting fear—as observed by de Gelder and colleagues (de Gelder, Morris, & Dolan, 2005). Our discussion focuses on the output from core affective circuitry to sensory cortex.