Fiber outgrowth from fetal vasopressin neurons of the suprachiasmatic nucleus, bed nucleus of the stria terminalis, and medial amygdaloid nucleus transplanted into adult Brattleboro rats

1991 ◽  
Vol 64 (1-2) ◽  
pp. 200-204 ◽  
Author(s):  
Hussien Ali Al-Shamma ◽  
Geert J. De Vries
Keyword(s):  
Suprachiasmatic Nucleus ◽  
Amygdaloid Nucleus ◽  
Stria Terminalis ◽  
Brattleboro Rats ◽  
Bed Nucleus ◽  
Vasopressin Neurons ◽  
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.

Amygdaloid lesion-induced obesity: relation to sexual behavior, olfaction, and the ventromedial hypothalamus

2006 ◽  
Vol 291 (5) ◽  
pp. R1201-R1214 ◽  
Author(s):  
Bruce M. King
Keyword(s):  
Sexual Behavior ◽  
Nodal Point ◽  
Ventromedial Hypothalamus ◽  
Female Rats ◽  
Male Rats ◽  
Amygdaloid Nucleus ◽  
Stria Terminalis ◽  
Bed Nucleus ◽  
Normal Feeding ◽  
Medial Amygdaloid Nucleus

Lesions of the amygdala have long been known to produce hyperphagia and obesity in cats, dogs, and monkeys, but only recently have studies with rats determined that the effective site is the posterodorsal amygdala (PDA)—the posterodorsal medial amygdaloid nucleus and the intra-amygdaloid bed nucleus of the stria terminalis. There is a sex difference; female rats with PDA lesions display greater weight gain than male rats. In the brains of female rats with obesity-inducing PDA lesions, there is a dense pattern of axonal degeneration in the capsule of the ventromedial hypothalamus (VMH) and other targets of the stria terminalis. Transections of the dorsal component of the stria terminalis also result in hyperphagia and obesity in female rats. Similar to rats with VMH lesions, rats with PDA lesions are hyperinsulinemic during food restriction and greatly prefer high-carbohydrate diets. The PDA is also a critical site for some aspects of rodent sexual behavior, particularly those that depend on olfaction, and the pattern of degeneration observed after obesity-inducing PDA lesions is remarkably parallel to the circuit that has been proposed to mediate sexual behavior. Medial amygdaloid lesions disrupt the normal feeding pattern and result in impaired responses to caloric challenges, and there is evidence that these behavioral changes are also due to a disruption of olfactory input. With its input from the olfactory bulbs and connections to the VMH, the PDA may be a nodal point at which olfactory and neuroendocrine stimuli are integrated to affect feeding behavior.

Steroid Dependency of Vasopressin Neurons in the Bed Nucleus of the Stria Terminalis byin SituHybridization*

Endocrinology ◽  
1989 ◽  
Vol 125 (5) ◽  
pp. 2335-2340 ◽  
Author(s):  
MARGARET A. MILLER ◽  
JANICE H. URBAN ◽  
DANIEL M. DORSA
Keyword(s):  
Stria Terminalis ◽  
Bed Nucleus ◽  
Steroid Dependency ◽  
Vasopressin Neurons

Electroacupuncture Reduces Stress-Induced Expression of c-Fos in the Brain of the Rat

2004 ◽  
Vol 32 (05) ◽  
pp. 795-806 ◽  
Author(s):  
Hye-Jung Lee ◽  
Bombi Lee ◽  
Sun-Hye Choi ◽  
Dae-Hyun Hahm ◽  
Mi-Rye Kim ◽  
...  
Keyword(s):  
Immobilization Stress ◽  
Plasma Catecholamines ◽  
Inhibitory Effect ◽  
Lateral Septum ◽  
Hypothalamic Nucleus ◽  
Amygdaloid Nucleus ◽  
Bed Nucleus ◽  
Fos Expression ◽  
Medial Amygdaloid Nucleus ◽  
The Brain

We have previously shown that electroacupuncture (EA) at Shaohai and Neiguan ( HT 3- PC 6) points significantly attenuated stress-induced peripheral responses, including increases in blood pressure, heart rate and plasma catecholamines. In this study, we examined the central effect of EA on the expression of c-fos, one of the immediate-early genes in the brain of rats subjected to immobilization stress. Immobilization stress (180 minutes) preferentially produced a significant increase in Fos-like immunoreactivity (FLI) in stress-relevant regions including the paraventricular hypothalamic nucleus (PVN), arcuate nucleus (ARN), supraoptic nucleus (SON), suprachiasmatic nucleus (SCN), medial amygdaloid nucleus (AMe), bed nucleus of the stria terminalis (BST), hippocampus, lateral septum (LS), nucleus accumbens, and the locus coeruleus (LC). EA (3 Hz, 0.2 ms rectangular pulses, 20 mA) at HT 3- PC 6 on the heart and pericardium channels for 30 minutes during stress, significantly attenuated stress-induced FLI in the parvocellular PVN, SON, SCN, AMe, LS and the LC. However, EA stimulations at HT 3- PC 6 had no effect on FLI in the magnocelluar PVN, ARN, BST or the hippocampus. EA stimulation at HT 3- PC 6 had a greater inhibitory effect on stress-induced FLI than that at TE 5- LI 11, the triple energizer and large intestine meridian, or non-acupoints. These results demonstrated that EA attenuated stress-induced c-fos expression in brain areas. These results suggest that decreased c-fos expression in hypothalamic and LC neurons, among stress-related areas, may reflect the integrative action of acupuncture in stress response.

scholarly journals Neurochemical Characterization of Neurons Expressing Estrogen Receptor β in the Hypothalamic Nuclei of Rats Using in Situ Hybridization and Immunofluorescence

2019 ◽  
Vol 21 (1) ◽  
pp. 115 ◽  
Author(s):  
Moeko Kanaya ◽  
Shimpei Higo ◽  
Hitoshi Ozawa
Keyword(s):  
In Situ Hybridization ◽  
High Ratio ◽  
Estrogen Signaling ◽  
Stria Terminalis ◽  
Bed Nucleus ◽  
Hypothalamic Nuclei ◽  
Vasopressin Neurons ◽  
The Brain

Estrogens play an essential role in multiple physiological functions in the brain, including reproductive neuroendocrine, learning and memory, and anxiety-related behaviors. To determine these estrogen functions, many studies have tried to characterize neurons expressing estrogen receptors known as ERα and ERβ. However, the characteristics of ERβ-expressing neurons in the rat brain still remain poorly understood compared to that of ERα-expressing neurons. The main aim of this study is to determine the neurochemical characteristics of ERβ-expressing neurons in the rat hypothalamus using RNAscope in situ hybridization (ISH) combined with immunofluorescence. Strong Esr2 signals were observed especially in the anteroventral periventricular nucleus (AVPV), bed nucleus of stria terminalis, hypothalamic paraventricular nucleus (PVN), supraoptic nucleus, and medial amygdala, as previously reported. RNAscope ISH with immunofluorescence revealed that more than half of kisspeptin neurons in female AVPV expressed Esr2, whereas few kisspeptin neurons were found to co-express Esr2 in the arcuate nucleus. In the PVN, we observed a high ratio of Esr2 co-expression in arginine-vasopressin neurons and a low ratio in oxytocin and corticotropin-releasing factor neurons. The detailed neurochemical characteristics of ERβ-expressing neurons identified in the current study can be very essential to understand the estrogen signaling via ERβ.

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