Species differences in the vasopressin-immunoreactive pathways in the bed nucleus of the stria terminalis and medial amygdaloid nucleus in prairie voles (Microtus ochrogaster) and meadow voles (Microtus pennsylvanicus).

1995 ◽  
Vol 109 (2) ◽  
pp. 305-311 ◽  
Author(s):  
Zuoxin Wang
Keyword(s):  
Species Differences ◽  
Microtus Pennsylvanicus ◽  
Microtus Ochrogaster ◽  
Amygdaloid Nucleus ◽  
Stria Terminalis ◽  
Prairie Voles ◽  
Meadow Voles ◽  
Bed Nucleus ◽  
Medial Amygdaloid Nucleus

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

2003 ◽  
Vol 284 (4) ◽  
pp. R965-R982 ◽  
Author(s):  
Bruce M. King ◽  
Jack T. Cook ◽  
Kirk N. Rossiter ◽  
Bethany L. Rollins
Keyword(s):  
Weight Gain ◽  
Grid Point ◽  
Retrograde Transport ◽  
Ventromedial Hypothalamus ◽  
Lateral Septum ◽  
Female Rats ◽  
Amygdaloid Nucleus ◽  
Stria Terminalis ◽  
Bed Nucleus ◽  
Medial Amygdaloid Nucleus

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 (+21 to +32 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.

scholarly journals Amygdala-lesion obesity: what is the role of the various amygdaloid nuclei?

2000 ◽  
Vol 279 (4) ◽  
pp. R1348-R1356 ◽  
Author(s):  
Bethany L. Rollins ◽  
Bruce M. King
Keyword(s):  
Female Rats ◽  
Amygdaloid Nucleus ◽  
Stria Terminalis ◽  
Bed Nucleus ◽  
Common Area ◽  
Weight Gains ◽  
Bilateral Lesions ◽  
Medial Amygdaloid Nucleus ◽  
Amygdaloid Nuclei

Anatomic descriptions of amygdaloid lesions resulting in hyperphagia and obesity in rats, cats, and dogs have been inconsistent and often contradictory, frequently resulting in failures to replicate. The present study attempted to reconcile these differences by examining common areas of overlap among differently placed lesions in female rats. Small bilateral lesions of the most posterodorsal aspects of the amygdala resulted in substantial weight gains (mean = 45.4 g/10 days). The smallest lesions caused damage limited to the posterodorsal medial amygdaloid nucleus and the bed nucleus of the stria terminalis and were directly in the area where axons are collecting to form the stria terminalis. Larger lesions that extensively damaged the central and/or anterodorsal medial amygdaloid nuclei sometimes resulted in excess weight gains, as did very large lesions of the basolateral nuclei, but substantial weight gains occurred only when the lesions extended (unilaterally or bilaterally) into the posterodorsal amygdala. Examination of previously published brain sections indicated that the hyperphagia and obesity that have been observed after widely differing lesion placements in cats and dogs were also the result of damage to a common area of overlap (i.e., the bed nucleus and/or stria terminalis). In rats, the critical area producing weight gain has extensive reciprocal relations with the medial hypothalamus.

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