Projections from the nociceptive area of the central nucleus of the amygdala to the forebrain: a PHA‐L study in the rat

Abstract

The lateral capsular division (CeLC) of the central nucleus (Ce) of the amygdala, in the rat, has been shown to be the main terminal area of a spino(trigemino)-parabrachio-amygdaloid nociceptive pathway [Bernard & Besson (1990) J. Neurophysiol. 63, 473-490; Bernard et al. (1992) J. Neurophysiol. 68, 551-569; Bernard et al. (1993) J. Comp. Neurol. 329, 201-229]. The projections to the forebrain from the CeLC and adjacent regions were studied in the rat by using microinjections of Phaseolus vulgaris leucoagglutinin (PHA-L) restricted in subdivisions of the Ce and the basolateral amygdaloid nucleus anterior (BLA). Our data showed that the entire CeLC projects primarily and extensively to the substantia innominata dorsalis (SId). The terminal labelling is especially dense in the caudal aspect of the SId. The other projections of the CeLC in the forebrain were dramatically less dense. They terminate in the bed nucleus of the stria terminalis (BST) and the posterior hypothalamus (pLH). No (or only scarce) other projections were found in the remaining forebrain areas. The Ce lateral division (CeL) and the Ce medial division (CeM), adjacent to the CeLC, also project to the SId with slightly lower density labelling. However, contrary to the case of the CeLC, both the CeL and the CeM extensively project to the ventrolateral subnucleus of the BST (BSTvl) with a few additional terminals found in other regions of the lateral BST. Only the CeM projects densely to both the interstitial nucleus of the posterior limb of the anterior commissure and the caudal most portion of the pLH. The projections of the BLA are totally different from those of the Ce as they terminate in the dorsal striatum, the accumbens nucleus, the olfactory tubercle, the nucleus of olfactory tract and the rostral pole of the cingulate/frontal cortex. This study demonstrates that the major output of the nociceptive spino(trigemino)-parabrachio-CeLC pathway is to the SId. It is suggested that the CeLC-SId pathway could have an important role in anxiety, aversion and genesis of fear in response to noxious stimuli.

Synaptic Plasticity in the Amygdala in a Model of Arthritic Pain: Differential Roles of Metabotropic Glutamate Receptors 1 and 5

“…As the output nucleus for major amygdala functions, the CeA with its laterocapsular division, also termed the "nociceptive amygdala" because of its high content of nociceptive neurons (Bourgeais et al, 2001;Neugebauer and Li, 2002), is well positioned to contribute to aversive and anxiogenic reactions to noxious stimuli, to participate in autonomic and endocrine aspects of emotional pain behavior, and to influence cortical sensory processing and forebrain mechanisms of pain modulation (Willis, 1991;Casey, 1999;Gallagher and Schoenbaum, 1999;Fields, 2000;LeDoux, 2000;Bourgeais et al, 2001).…”

“…Under microscopic control, the patch-clamp electrode was positioned in the "nociceptive amygdala," which is the lateral capsular part (CeC) of the CeA contralateral to the arthritis (cf. Bourgeais et al, 2001;Neugebauer and Li, 2002). Two stimulation electrodes were arranged for synaptic stimulation of afferent fibers from the pontine PB area providing nociceptive information to the CeA (left; Bernard et al, 1993) and inputs from the lateral-basolateral amygdala (right) providing polymodal information to the CeA from thalamic and cortical areas (part of the netting below the slice can be seen).…”

“…To test whether the arthritic pain behavior is associated with synaptic plasticity in the "nociceptive amygdala" (Bourgeais et al, 2001;Neugebauer and Li, 2002), we performed whole-cell patch-clamp recordings of membrane properties and synaptic transmission in CeA neurons recorded in brain slices obtained from control (normal and sham) rats and arthritic rats.…”

Role of Extracellular Signal-Regulated Kinase in Synaptic Transmission and Plasticity of a Nociceptive Input on Capsular Central Amygdaloid Neurons in Normal and Acid-Induced Muscle Pain Mice

“…It is likely that the use-dependent change in function of overall synaptic inputs onto CeAC neurons might provide a means by which the level of background synaptic conductance can be adjusted, thereby affecting the spike transfer of CeAC neurons. The CeAC is the main output of the amygdala and the axons of CeAC neurons form widespread direct and indirect connections with forebrain and brainstem areas, and the projections of the CeAC to the thalamus and cortical areas are believed to be related to cognitive and conscious components of pain, while the projection to the hypothalamus is believed to be related to autonomic and neuroendocrine pain-like responses (Davis, 1998;LeDoux, 2000;Bourgeais et al, 2001;Price, 2003). Thus, the usedependent enhancement of synaptic function of nociceptive signals from the parabrachial nuclei and other non-nociceptive signals, possibly from the basolateral amygdala, which conveys polymodal signals from the thalamus and the cortex, onto CeAC neurons might increase the gain of the input/output relationship, thereby increasing the output of the central amygdala and partially causing central sensitization of supraspinal origin.…”

Emotional regulation of pain: the role of noradrenaline in the amygdala

“…and the bed nucleus of the stria terminalis, which can influence the autonomic system [49,50]. However, most tracer studies did not distinguish between subnuclei in the CeA, and include the CeM.…”