Faculty Bibliography

The neural mechanisms of emotion and memory have long been thought to reside side by side, if not in overlapping structures, of the limbic system. However, the limbic system concept is no longer acceptable as an account of the neural basis of memory or emotion and is being replaced with specific circuit accounts of specific emotional and memory processes. Emotional memory, a special category of memory involving the implicit (probably unconscious) learning and storage of information about the emotional significance of events, is modeled in rodent experiments using aversive classical conditioning techniques. The neural system underlying emotional memory critically involves the amygdala and structures with which it is connected. Afferent inputs from sensory processing areas of the thalamus and cortex mediate emotional learning in situations involving specific sensory cues, whereas learning about the emotional significance of more general, contextual cues involves projections to the amygdala from the hippocampal formation. Within the amygdala, the lateral nucleus (AL) is the sensory interface and the central nucleus the linkage with motor systems involved in the control of species-typical emotional behaviors and autonomic responses. Studies of cellular mechanisms in these pathways have focused on the direct relay to the lateral amygdala from the auditory thalamus. These studies show that single cells in AL respond to both conditioned stimulus and unconditioned stimulus inputs, leading to the notion that AL might be a critical site of sensory-sensory integration in emotional learning. The thalamo-amygdala pathway also exhibits long-term potentiation, a form of synaptic plasticity that might underlie the emotional learning functions of the circuit. The thalamo-amygdala pathway contains and uses the amino acid glutamate in synaptic transmission, suggesting the possibility that an amino-acid mediated form of synaptic plasticity is involved in the emotional learning functions of the pathway. We are thus well on the way to a systems level and a cellular understanding of at least one form of emotional learning and memory

Stimuli associated with painful or otherwise unpleasant events acquire aversive emotional properties in animals and humans. Subsequent presentation of the stimulus alone (in the absence of the unpleasant event) leads to the eventual extinction of the aversive reaction. Although the neural basis of emotional learning has been studied extensively, considerably less is known about the neural basis of emotional extinction. In the present study, we show that the medial prefrontal cortex plays an important role in the regulation of fear extinction in rats, a finding that may help elucidate the mechanisms and, possibly, the treatment of disorders of uncontrolled fear, such as anxiety, phobic, panic and posttraumatic stress disorders in humans

The neural system underlying the conditioning of autonomic and behavioral fear responses to auditory stimuli is now understood in some detail. It involves projections through the auditory system to the medial geniculate body and from there directly to the amygdala. The lateral nucleus is the sensory interface and the central nucleus the motor interface of the amygdala. The lateral nucleus projects to the central nucleus indirectly, by way of the basolateral nucleus. Projections from the amygdala central nucleus to the midbrain central gray region mediate the behavioral responses whereas projections from the amygdala central nucleus to the lateral hypothalamus mediate the autonomic responses. Emotional memories established through such pathways bypass the neocortex and may contribute to the unconscious processing of emotion. Such memories are indelible (highly resistant to extinction). The sensory input pathway exhibits long-term synaptic potentiation and appears to utilize glutamate in synaptic transmission. An excitatory amino acid-mediated form of synaptic plasticity in the lateral amygdala may be responsible in part for emotional learning

Corticocortical and corticoamygdaloid connections of temporal cortext and perirhinal cortex (PRh) were examined in the rat with the anterograde tracer Phaseolus vulgaris leucoagglutinin (PHA-L). Iontophoretic injections of PHA-L into area TE1 resulted in columnar axonal terminations in surrounding and contralateral regions of temporal neocortex and in the striatum, but not in the amygdala. Within temporal neocortex, labeled fibers were present locally in adjacent regions of TE1, as well as in TE2d, TE1v, TE3v, and TE2c. Injection of cortical areas TE1v, TE3v, and TE2c, which received projections from TE1, or injections of perirhinal periallocortex, which received projections from TE1v, TE2v, and TE3v, resulted in projections to the amygdala. The pattern of corticocortical and corticoamygdaloid projections differed among the divisions of auditory cortex. TE1 exhibited extensive ipsilateral and contralateral projections to temporal cortical regions and no projections to the amygdala. In contrast, areas of temporal neocortex ventral and posterior to TE1, including TE1v, TE3v, TE2c, and PRh, had more limited ipsi- and contralateral corticocortical projections but had an increased connectivity with the subcortical forebrain, especially the lateral nucleus of the amygdala (AL). There was a topographic organization to the AL afferents. The dorsal subdivision of AL received projections from TE1v, TE3v, TE2c, and PRh, while the ventrolateral division received projections from TE3v, TE2c, and PRh. The ventromedial division received projections only from PRh, which, unlike other temporal cortical areas, also projected to the basolateral and basomedial nuclei of the amygdala. These findings define the complete sequence of connections linking primary auditory cortex with the amygdala in the rat. In addition, the findings indicate that the ventral portion of TE1, designated TE1v, has connections that distinguish it from dorsal TE1, namely, dense projections to AL and a diminished number of corticocortical projections ipsilaterally and contralaterally. Finally, the results suggest a topographic organization to the cortical terminations within the amygdala

In the present study we analyzed the organization of the thalamocortical projections of the specific auditory relay nucleus of the thalamus, the ventral division of the medial geniculate body (MGv), using the anterograde axonal tracer Phaseolus vulgaris leucoagglutinin. All injections of MGv produced dense labeling of axonal fibers in temporal cortex. In all cases, labeled axons were predominantly concentrated in cortical layers III and IV and, to a lesser extent, at the junction of layers V and VI. Injections confined to the medial regions of MGv, and specifically to the ovoid nucleus of MGv (OV, pars ovoidea), resulted in anterograde labeling of TE1, with minor labeling of the ventral quarter of TE1, designated subarea TE1v. Injections placed in lateral regions of MGv and occupying the lateral ventral subnucleus (LV), or injections in the mediolateral center of MGv and occupying parts of LV and OV, also resulted in labeling of area TE1 and minor labeling of TE1v. However, these injections also produced labeling in areas TE2 and TE3. Thus, area TE1 (excluding subarea TE1v) receives heavy projections from all aspects of MGv and appears to be the core target of MGv. While regions of MGv also project to surrounding cortical belt areas, these projections tend to be lighter and to vary depending on the region of MGv examined. These results, together with other connectional findings, and cytoarchitectonic and physiological studies, suggest that TE1 (possibly excluding subarea TE1v) is the primary auditory cortex in the rat

Acoustic responses of single units were examined in awake, freely behaving rats in the lateral nucleus of the amygdala (AL). Recordings were made from a movable bundle of 9 microwires. Most cells had very low rates of spontaneous activity (about 3 spikes/s average). Firing rates increased during sleep states. Short-latency auditory responses (12-25 ms) were found in the dorsal subnucleus (ALd) of the AL. Cells in the ALd most typically responded in a sustained fashion. Some of the cells in the ALd showed preferences for high frequencies, tone bursts, or frequency-modulated stimuli with center frequencies above 12 kHz. Response latencies were considerably longer in other areas of the amygdala. Our results corroborate the main findings of a previous study (F. Bordi & J. LeDoux, 1992) that examined the acoustic response properties of single cells in the AL in anesthetized rats. Together the findings from awake and anesthetized rats provide the most precise information about sensory processing in amygdala neurons available to date.

Previous studies have shown that the lateral nucleus of the amygdala (AL) is essential in auditory fear conditioning and that neurons in the AL respond to auditory stimuli. The goals of the present study were to determine whether neurons in the AL are also responsive to somatosensory stimuli and, if so, whether single neurons in the AL respond to both auditory and somatosensory stimulation. Single-unit activity was recorded in the AL in anesthetized rats during the presentation of acoustic (clicks) and somatosensory (footshock) stimuli. Neurons in the dorsal subdivision of the AL responded to both somatosensory and auditory stimuli, whereas neurons in the ventrolateral AL responded only to somatosensory stimuli and neurons in the ventromedial AL did not respond to either stimuli. These findings indicate that the dorsal AL is a site of auditory and somatosensory convergence and may therefore be a locus of convergence of conditioned and unconditioned stimuli in auditory fear conditioning

Comments on W. G. Parrott and J. Schulkin's (see record 1993-28335-001) article on cognition vs emotion from the perspective of a separatist. J. E. LeDoux suggests that the processes providing inputs to emotional systems must be distinguished from the emotional functions of the systems and proposes a distinction between cognition and affective computation. (PsycINFO Database Record (c) 2008 APA, all rights reserved)