Projections of the Amygdalopiriform Transition Area (APir): A PHA‐L Study in the Rat

Shammah‐Lagnado, Sara J.; Santiago, Adriana C.

doi:10.1111/j.1749-6632.1999.tb09295.x

Cited by 38 publications

(38 citation statements)

References 8 publications

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“…It is of note that, besides being heavily interconnected, layer III of LOT and the rostral part of the basolateral amygdaloid complex share similar telencephalic projections to the ventrolateral striatum and dorsal agranular insular cortex Price, 1977, 1978a;Kelley et al, 1982;Groenewegen et al, 1990;Kita and Kitai, 1990;McDonald, 1991a,b;Brog et al, 1993;Wright et al, 1996;present data). It should also be appreciated that, in accord with the demonstrated specificity of intraamygdaloid projections Pitkä nen, 2000), the olfactory amygdaloid nuclei projections to the basolateral complex are largely segregated: LOT innervates rostral parts of the basolateral complex, the anterior basomedial nucleus (Petrovich et al, 1996;Savander et al, 1996a), and the amygdalopiriform transition area (Shammah-Lagnado and Santiago, 1999;Jolkkonen et al, 2001;Petrovich et al, 2001) project to the posterior basolateral nucleus, and the posterolateral cortical nucleus supplies the ventrolateral and caudomedial divisions of the lateral nucleus Savander et al, 1996b). Collectively, these projections encompass most of the extent of the basolateral complex and represent a possible anatomical substrate for the high proportion of olfactoryresponsive units herein recorded (Cain and Bindra, 1972).…”

Section: Nucleus Of the Lot Efferentsmentioning

confidence: 83%

Efferent connections of the nucleus of the lateral olfactory tract in the rat

Santiago

Shammah‐Lagnado

2004

J of Comparative Neurology

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The efferent connections of the nucleus of the lateral olfactory tract (LOT) were examined in the rat with the Phaseolus vulgaris leucoagglutinin (PHA-L) technique. Our observations reveal that layers II and III of LOT have largely segregated outputs. Layer II projects chiefly ipsilaterally to the olfactory bulb and anterior olfactory nucleus, bilaterally to the anterior piriform cortex, dwarf cell cap regions of the olfactory tubercle and lateral shell of the accumbens, and contralaterally to the lateral part of the interstitial nucleus of the posterior limb of the anterior commissure. Layer III sends strong bilateral projections to the rostral basolateral amygdaloid complex, which are topographically organized, and provides bilateral inputs to the core of the accumbens, caudate-putamen, and agranular insular cortex (dorsal and posterior divisions). Layer II projects also to itself and to layers I and II of the contralateral LOT, whereas layer III projects to itself, to ipsilateral layer II, and to contralateral layer III of LOT. In double retrograde labeling experiments using Fluorogold and cholera toxin subunit b tracers, LOT neurons from layers II and III were found to provide collateral projections to homonymous structures on both sides of the brain. Unlike other parts of the olfactory amygdala, LOT neither projects directly to the extended amygdala nor to the hypothalamus. Thus, LOT seemingly influences nonpheromonal olfactory-guided behaviors, especially feeding, by acting on the olfactory bulb and on ventral striatal and basolateral amygdaloid districts that are tightly linked to lateral prefrontal cortical operations.

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Section: Nucleus Of the Lot Efferentsmentioning

confidence: 83%

Efferent connections of the nucleus of the lateral olfactory tract in the rat

Santiago

Shammah‐Lagnado

2004

J of Comparative Neurology

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“…2E). The amygdalopiriform transition area also sent dense topographically organized projections to the central extended amygdala (Jolkkonen and Pitkä nen, 1998;Shammah-Lagnado and Santiago, 1999). Whereas, in case 13, these projections tended to avoid the dorsal part of the lateral bed nucleus and the lateral part of the central nucleus, the latter territories were innervated heavily in cases 17 and 27.…”

Section: Structures Related To the Central Extended Amygdalamentioning

confidence: 93%

“…No neocortical areas and only a small number of mesocortical and allocortical areas projected to the BSTS. In general, the same cortical areas that innervated the lateral pocket also innervated the central extended amygdala (McDonald, 1998;McDonald et al, 1999;Shammah-Lagnado and Santiago, 1999).…”

Section: Structures Related To the Central Extended Amygdalamentioning

confidence: 97%

Supracapsular bed nucleus of the stria terminalis contains central and medial extended amygdala elements: Evidence from anterograde and retrograde tracing experiments in the rat

et al. 2000

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Neurons that accompany the stria terminalis as it loops over the internal capsule have been termed collectively the supracapsular bed nucleus of the stria terminalis (BSTS). They form two cell columns, a lateral column and a considerably smaller medial column. The lateral column merges rostrally with the lateral bed nucleus of the stria terminalis and caudally with the central amygdaloid nucleus (central extended amygdala components). The medial column is continuous with the medial bed nucleus of the stria terminalis and the medial amygdaloid nucleus (medial extended amygdala districts). The connections of the BSTS were investigated in the rat by placing injections of Phaseolus vulgaris-leucoagglutinin (PHA-L) or retrograde tracers in different parts of the extended amygdala or in structures related to the extended amygdala. BSTS inputs and outputs were identified, respectively, by the presence of varicose fibers and retrogradely labeled neurons within the stria terminalis. The results suggest that the medial-to-lateral compartmentalization of BSTS neurons reflects their close alliance with the medial and central divisions of the extended amygdala. The medial BSTS contains primarily elements that correspond to the posterodorsal part of the medial amygdaloid nucleus and the medial column of the posterior division of the medial bed nucleus of the stria terminalis, and the lateral BSTS contains elements that correspond to the medial and lateral parts of the central amygdaloid nucleus and lateral bed nucleus of the stria terminalis. These results add strong support to the concept of the extended amygdala as a ring-like macrostructure around the internal capsule, and they are of theoretical interest for the understanding of the organization of the basal forebrain.

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“…As with the degeneration in the shell of the accumbens (discussed previously), this degeneration is likely to arise from extrinsic sources such as the basomedial nucleus (81), the posterior basolateral amygdaloid nucleus (56,67,88,92,93), or the amygdalopiriform transition area (67,94), whose axons might have been inadvertently damaged by our lesions.…”

Section: Anterograde Degeneration and Retrograde Tracing Experimentsmentioning

confidence: 99%

“…It is noteworthy that the meager projection to accumbens emanating from the MePD (8,10) and the limited evidence for input from the BSTIA (8, present results) suggest that the dense degeneration seen in the shell was not primarily the result of damage to these two structures. Other potential sources of these terminals include the amygdalopiriform transition area (8,94), the ventral subiculum (13), the posterior basolateral amygdaloid nucleus (8,56,66), and the basomedial nucleus, which also projects densely to the VMH (81). The anterodorsal medial amygdala is another possible source of afferents to the shell of the accumbens (12,36), but the virtual lack of degeneration in the mitral layer of the accessory olfactory bulb and lateral hypothalamus indicates that our lesions largely spared the anterior part of the medial amygdaloid nucleus.…”

Section: Anterograde Degeneration and Retrograde Tracing Experimentsmentioning

confidence: 99%

Obesity-inducing amygdala lesions: examination of anterograde degeneration and retrograde transport

King

Cook

Rossiter

et al. 2003

American Journal of Physiology-Regulatory, Integrative and Comp

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King, Bruce M., Jack T. Cook, Kirk N. Rossiter, and Bethany L. Rollins. Obesity-inducing amygdala lesions: examination of anterograde degeneration and retrograde transport. Am J Physiol Regul Integr Comp Physiol 284: R965-R982, 2003. First published November 14, 2002 10.1152/ajpregu.00249.2002.-Small lesions centered in the posterodorsal region of the medial amygdala resulted in excessive weight gains in female rats. Unilateral lesions were nearly as effective as bilateral lesions in the first 48 h after surgery (ϩ21 to ϩ32 g). Assessment of lesion damage was done by both qualitative evaluation and by a quantitative grid-point counting method. The critical sites for weight gain were the intra-amygdaloid bed nucleus of the stria terminalis and the posterodorsal medial amygdaloid nucleus. Incidental damage to the overlying globus pallidus was negatively related to weight gain. The cupric silver method for demonstrating axonal degeneration was applied to brains with obesity-inducing lesions. A dense pattern of degenerating terminals was found in the lateral septum, amygdala, ventral striatum, and ventromedial hypothalamus. Degeneration in the paraventricular nucleus of the hypothalamus was scarce or absent. Small retrograde tracer injections made in either the intra-amygdaloid bed nucleus of the stria terminalis or in the posterodorsal medial amygdaloid nucleus labeled cells in the amygdala, lateral septum, and hypothalamus, reciprocating the anterograde projections from the amygdala to these areas. The data suggest that subdivisions of the posterodorsal amygdala participate in the regulation of feeding in a manner that is similar to the better-known role of this part of the brain in mediating reproductive behavior. Although topographical differences may exist within the amygdaloid and hypothalamic subdivisions regulating these two sexually dimorphic behaviors, the relays engaged by feeding-related connections and those related to reproduction are remarkably parallel. nucleus accumbens; hypothalamus; stria terminalis SEVERAL RECENT STUDIES have demonstrated that bilateral electrolytic lesions of the amygdala in female rats can result in marked hyperphagia and excessive weight gains. Daily food intake nearly doubles, and weight gains of 20-30 g during the first 3 days after lesions are not unusual (e.g., 45, 50-53, 84). Weight gains of Ն100 g in 20-25 days have been observed (50, 51). The lesions result in a marked preference for carbohydrates (53). Although food intake eventually returns to normal, the excessive weight gain is maintained indefinitely, with a marked increase in adipose tissue (50).These results are similar to those reported many years ago for cats, dogs, and primates (including humans) given amygdaloid lesions or temporal lobectomies (e.g., 9, 32, 37, 70, 103). In the rat, the effective lesion site for hyperphagia and obesity has recently been identified as the posterodorsal part of the medial amygdaloid nucleus (MePD) and the intra-amygdaloid bed nucleus of the stria terminalis (BSTIA), together ...

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Projections of the Amygdalopiriform Transition Area (APir): A PHA‐L Study in the Rat

Cited by 38 publications

References 8 publications

Efferent connections of the nucleus of the lateral olfactory tract in the rat

Efferent connections of the nucleus of the lateral olfactory tract in the rat

Supracapsular bed nucleus of the stria terminalis contains central and medial extended amygdala elements: Evidence from anterograde and retrograde tracing experiments in the rat

Obesity-inducing amygdala lesions: examination of anterograde degeneration and retrograde transport

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