PubMed Health⌕ Search

Biomedical subjects

D M Nance

Publications and source records attributed to D M Nance.

At least 73 records · Page 4Linked to original sources
PubMed1984

Further evidence for hypothalamic asymmetry in endocrine control of the ovary.

The differential release of FSH and LH associated with hemigonadectomy (hemi-x) of prepubertal male rats can be blocked by unilateral hypothalamic deafferentation located on the side ipsilateral, but not contralateral, to the hemi-x. Also, ovarian compensatory hypertrophy (OCH) in prepubertal female rats can be blocked by ipsilateral, but not contralateral, hypothalamic hemi-islands. Both these endocrine phenomenon are limited to knife cuts on a particular side of the brain. These results suggest that there are neural connections with the gonads which are involved in endocrine regulation and that hypothalamic control of the endocrine system may be asymmetrically organized. In support of this, the present study shows that in adult female rats, unilateral injections of the excitotoxin kainic acid (1.0 microgram in 1.0 microliter) into the retrochiasmatic area of the hypothalamus can block OCH if the injections are located on the side ipsilateral to the hemi-x. This phenomenon was more apparent if the lesions and hemi-x were located on the right side. In addition, neither hemi-x nor kainic acid injections alone had any effect on vaginal cycles, whereas the combination of these two treatments reduced the incidence of estrus. However, these effects on vaginal cycles were not specifically associated with lesions or hemi-x on a particular side, thus excluding this as an explanation of the different endocrine effects of kainic acid on the two sides of the brain. These results support the evidence for a direct neural contribution to endocrine control and further suggest a functional difference in the two-halves of the hypothalamus in neuroendocrine regulation.

Animals↗
PubMed1983

Psychoneuroendocrine effects of neurotoxic lesions in the septum and striatum of rats.

The psychoneuroendocrine effects of electrolytic septal lesions were compared with neurotoxic lesions in the lateral septum or striatum of rats induced by 6-hydroxydopamine (6-OHDA) or kainic acid (KA). Lesion effects were examined in terms of changes in body weight (BWt) regulation, ovarian compensatory hypertrophy (OCH) and female sexual behavior. Septal injections of 6-OHDA selectively reduced septal levels of dopamine (DA) by 60% whereas striatal injections reduced striatal levels of DA by 77% and septal levels by 30%. Significant effects of these various lesions were relative to controls (1) KA lesions in the septum increased and 6-OHDA lesions in the striatum decreased BWt; (2) 6-OHDA lesions in the striatum reduced ovarian weight and KA lesions in the septum increased OCH; (3) electrolytic septal lesions increased and KA septal lesions decreased female sexual behavior; (4) the effects of estrogen on food intake and BWt were attenuated in KA septal lesioned rats. Since this experiment failed to show an inhibitory role for DA on lordotic behavior, in a second experiment brain levels of DA were depleted by 6-OHDA injections in the ventral tegmental area or substantia nigra. Levels of female sexual behavior for these animals were comparable to controls. Thus, decreases in brain levels of DA previously shown to associated with electrolytic septal lesions may not be causally related to the observed increase in lordotic behavior. Lateral septal damage induced by KA appears to modify a variety of estrogen-sensitive systems.

Animals↗
PubMed1983

The developmental and neural determinants of the effects of estrogen on feeding behavior in the rat: a theoretical perspective.

Conceptually, the neural regulation of feeding behavior is proposed to be a function of the activities of a long-term (day to day) and a short-term (meal to meal) control system. Although these two control systems are presumably involved in a continuous and dynamic interaction, they can be behaviorally and anatomically separated by specific regulatory challenges and brain lesions. Utilizing this general regulatory model for the hypothalamic control of feeding behavior, the effects of estrogen on a variety of behavioral indices of energy regulation are reviewed and discussed. The effects of ovarian hormones on the feeding behavior of both prepubertal and adult female rats when faced with a series of regulatory tests shown to provide specific information about the long- and short-term control of feeding behavior leads to the following conclusions. Modulation of feeding behavior by ovarian hormones is detectable well before the time of puberty in the female rat and is expressed in terms of a 4-day periodicity that is very similar to adult animals. Estrogen appears to modulate feeding behavior primarily by modifying the long-term control of feeding behavior or else the manner in which nutrients are integrated into this long-term system. It is further proposed that estrogen acts upon metabolically specific and unique neural elements in the hypothalamus whose function is to translate error signals derived from the long-term integration of body nutrients into appropriate readjustments in feeding behavior. Although this dual-regulatory model for the hypothalamic control of feeding behavior can account for the majority of the effects of estrogen on feeding behavior, further studies suggest that an "extrahypothalamic" mechanism must mediate certain aspects of the neural control of feeding behavior as well as the behavioral effects of estrogen. Specifically, the present model system can account for the role of carbohydrates in the neural control of feeding behavior, but fats and possibly proteins can modify feeding behavior independent of the hypothalamus. Likewise, estrogen can influence the efficiency with which nutrient loads of fats and proteins can modify subsequent feeding behavior and therefore this proposed "extrahypothalamic" mechanism may mediate those effects of estrogen on feeding behavior that cannot be accounted for by the present dual-regulatory model.

Afferent Pathways↗
PubMed1983

Neural regulation of the ovary: evidence for hypothalamic asymmetry in endocrine control.

The effects of hypothalamic hemi-islands on ovarian compensatory hypertrophy (OCH) were determined in prepubertal female rats. In animals with hypothalamic hemi-islands on the left side, OCH was blocked in rats hemi-ovariectomized on the ipsi- but not the contralateral side. A potential asymmetrical involvement of the hypothalamus in OCH was suggested by the further observation that this phenomenon could not be demonstrated in rats given hypothalamic hemi-islands on the right side and hemi-ovariectomized on the ipsi- or contralateral side. These data suggest that in addition to a possible direct neural contribution to endocrine feedback, the two-halves of the hypothalamus may differ in terms of their sensitivity to various components of endocrine control.

Animals↗
PubMed1983

Origin of insulin-receptive nerve terminals in rat median eminence.

The origin of insulin-receptive axon terminals in the rat median eminence was determined by combining surgical and chemical ablation techniques and the in vivo radioautographic approach, in which labeling of the median eminence with blood-borne [125I]insulin served as a quantifiable marker for the presence of receptive axonal elements. Whereas unilateral deafferentation of the median eminence from the ipsilateral brain produced as much as a 50% ipsilateral loss of insulin-binding sites, transection of axonal projections to median eminence from neurons located lateral to the ventromedial hypothalamic nucleus produced no detectable loss in insulin-binding capacity. Unilateral electrocoagulation of various regions of the medial basal hypothalamus indicated that insulin-receptive axon terminals arise primarily from neurons in and about the hypothalamic arcuate nucleus and from the posterior ventrolateral subdivision of the hypothalamic ventromedial nucleus. A primary site of origin from the arcuate nucleus was confirmed in rats treated neonatally with monosodium L-glutamate, which, in addition to a selective destruction of arcuate neurons, produced a profound reduction in the insulin-specific binding capacity of the median eminence. The results of this study indicate that insulin-binding axon terminals arise from a unique class of tuberoinfundibular neuron with hormone-receptive capacity. These neurons may function to mediate direct interaction of circulating insulin with central autonomical, behavioral, and neuroendocrine systems.

Animals↗
PubMed1982

Changes in estrogen and progestin receptor binding resulting from retrochiasmatic knife cuts.

Retrochiasmatic frontolateral knife cuts (FLC) or sham operations (Sham) were performed with a Halasz-type knife. All animals were primed with estrogen plus 0.5 mg progesterone (P) and tested for lordosis both before and after surgery. Two weeks after the last test they received estradiol (E2) in Silastic capsules and were sacrificed 2 days later for determination of either nuclear estrogen receptors or cytosol progestin receptor binding in brain and pituitary (PIT). Rats which had received FLC showed significantly lower lordosis quotients relative to Shams, and relative to their own pre-surgery scores. Nuclear E2-receptor binding was significantly reduced in the hypothalamus (HYPO) following FLC, but not in preoptic area (POA) or PIT. No changes in cytosol P-receptor binding were observed in HYPO, POA or PIT following FLC. Our results suggest a positive correlation between the number of hypothalamic E2-receptors and the capacity to display lordosis, and emphasize the importance of anterolateral connections to the HYPO for the progesterone-induced facilitation of lordosis.

Animals↗
PubMed1982

Ipsilateral hypothalamic deafferentation blocks the increase in serum FSH following hemi-castration.

In two experiments hypothalamic hemi-islands or sham surgeries were produced on the right side of prepubertal male rats with an extrudable Halàsz-type knife (1.5 mm radius). Animals were then sham castrated or else hemi-castrated on the contralateral or ipsilateral side with respect to brain surgery. Eight or 21 days later, hemi-castrated rats given sham knife cuts showed a significant increase in serum FSH, relative to sham animals with intact testes. Also, animals given hypothalamic hemi-islands and hemi-castrated on the contralateral side showed a significant increase in serum FSH comparable to that seen in hemi-castrated rats with sham brain surgeries. However, hypothalamic hemi-island rats which were hemi-castrated on the ipsilateral side failed to show an increase in serum FSH and were similar to sham operated controls with both gonads. Serum LH levels were comparable among all groups, verifying a clear dissociation between LH and FSH secretion associated with hemi-castration in prepubertal males. In addition, the differences between contralateral and ipsilateral hemi-castrated animals with identical unilateral brain surgeries strongly suggest that FSH release is, in part, under direct neural control. However, in a third experiment, differences in FSH release between ipsi- and contralateral hemi-castrated rats were not found in animals with hypothalamic hemi-islands on the left side of the brain. Thus the hypothalamus may be asymmetrically involved in various components of neuroendocrine control.

Afferent Pathways↗
PubMed1981

Frontolateral hypothalamic knife cuts: interruption of paraventricular efferents to the thoracolumbar cord.

Bilateral thoracolumbar cord injections of the fluorescent tracer bisbenzimide produced extensive retrograde labelling of cell bodies in the paraventricular nucleus of the hypothalamus. Unilateral retrochiasmatic knife cuts (1.5 mm radius) located anterolateral to the paraventricular nucleus dramatically reduced or eliminated the labelling of paraventricular neurons on the ipsilateral side following bilateral bisbenzimide injections into the thoracolumbar cord. Thus paraventricular efferents to the thoracolumbar cord must project in a lateral direction at the level of the nucleus prior to descending toward the spinal cord. Changes in endocrine function, reproductive and feeding behavior reported following similar hypothalamic knife cuts may be related to this efferent system.

Animals↗
PubMed1981

Neural damage following retrochiasmatic knife cuts in the rat.

In order to define neuronal damage produced by sham, frontal and frontolateral hypothalamic knife cuts known to effect neuroendocrine and behavioral variables, we designed a retractable knife capable of delivering horseradish peroxidase as a cut was being produced. Damaged neurons filled with homogeneous reaction product were found in virtually all hypothalamic nuclei. A similar distribution of damage was produced by frontolateral (FLC), frontal (FC) or sham cuts--the primary differences being the greater density of damaged neurons in hypothalamic nuclei and labeling of the ventral tegmental area of Tsai in FLC and FC animals. The difference between FC and FLC animals was primarily one of degree of damage. The amount of damage produced by the sham surgery is consistent with the idea that sham surgeries produce endocrine dysfunctions intermediate between frontal cut animals and unoperated controls. It is interesting to note that a number of nuclei damaged by these surgeries provide aminergic innervation to the hypothalamus.

Animals↗
PubMed1979

Experiments with a reported anorexigenic tripeptide: pyro-Glu-His-Gly-OH.

A newly described tripeptide, pyro-Glu-His-Gly-OH, which was reported to produce profound and long-term anorexia and weight loss in female mice, was initially tested in female rats. After total dose of either 8, 16, or 32 microgram SC of the peptide, administered across an eight day interval, there was no detectable effect on food intake, body weight, or estrous cycles of female rats. In a second study, we attempted to verify the anorexigenic potency of this peptide in mice. Total doses of 3.4 and 6.8 microgram, injected across a 20 day period, had no effect on the food intake or body weight of S/W albino female mice. Thus, the anorexigenic potency of pyro-Glu-His-Gly-OH has yet to be established.

Animals↗