Abstract
A hypothesis is proposed for five visual fear signaling pathways in humans, based on an analysis of anatomical connectivity from primate studies and human functional connectvity and tractography from brain imaging studies. Earlier work has identified possible subcortical and cortical fear pathways known as the “low road” and “high road,” which arrive at the amygdala independently. In addition to a subcortical pathway, we propose four cortical signaling pathways in humans along the visual ventral stream. All four of these traverse through the LGN to the visual cortex (VC) and branching off at the inferior temporal area, with one projection directly to the amygdala; another traversing the orbitofrontal cortex; and two others passing through the parietal and then prefrontal cortex, one excitatory pathway via the ventral-medial area and one regulatory pathway via the ventral-lateral area. These pathways have progressively longer propagation latencies and may have progressively evolved with brain development to take advantage of higher-level processing. Using the anatomical path lengths and latency estimates for each of these five pathways, predictions are made for the relative processing times at selective ROIs and arrival at the amygdala, based on the presentation of a fear-relevant visual stimulus. Partial verification of the temporal dynamics of this hypothesis might be accomplished using experimental MEG analysis. Possible experimental protocols are suggested.
Highlights
Understanding the neurological basis of human emotional processing is a challenging problem, because observed neural correlates span cortical and subcortical structures, and because experimental data may come from many different sources, including anatomical studies, functional magnetic resonance imaging, diffusion tensor imaging (DTI), electroencephalography (EEG), magnetoencephalography (MEG), positron emission tomography (PET), and electrophysiology
This study focuses on the signaling pathways between activated neural correlates of fear responses, and less so on recurrent and sustained activity
In addition to activation of the ventrolateral PFC (vlPFC) and down-regulation of the amygdala during some effortful regulation tasks with negative emotional stimuli, some studies have found possible mediation via the ventromedial PFC (vmPFC) (Urry et al, 2006; Johnstone et al, 2007). While this may be similar to pathway p4, it does not explain lateral OFC (lOFC) activity in some studies (Phillips et al, 2003; Carlsson et al, 2004; Wager et al, 2008; Golkar et al, 2012)
Summary
Understanding the neurological basis of human emotional processing is a challenging problem, because observed neural correlates span cortical and subcortical structures, and because experimental data may come from many different sources, including anatomical studies, functional magnetic resonance imaging (fMRI), diffusion tensor imaging (DTI), electroencephalography (EEG), magnetoencephalography (MEG), positron emission tomography (PET), and electrophysiology. From IT, the ventral visual stream splits and propagates to several regions, including the parietal cortex (Distler et al, 1993; Webster et al, 1994), the LA and B nuclei of the amygdala (Webster et al, 1991; Baizer et al, 1993; Cheng et al, 1997; Ghashghaei and Barbas, 2002; Stefanacci and Amaral, 2002; Freese and Amaral, 2005), the lateral OFC (lOFC) (Webster et al, 1994; Kondo et al, 2003; Barbas, 2007) and the frontal eye fields (FEF) in the PFC (Webster et al, 1994; Schall et al, 1995). While this signaling is not incompatible with recurrent activity through the thalamus and pulvinar, we do not explicitly represent the replicated cortical connectivity of the thalamus in the pathways, except for some connectivity within the visual stream
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