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N T McMullen

Publications and source records attributed to N T McMullen.

6 recordsLinked to original sources
PubMed1990

Postmenopausal hypertrophy of neurons expressing the estrogen receptor gene in the human hypothalamus.

Computer microscopy and in situ hybridization were used to investigate neuronal hypertrophy in the infundibular nucleus of postmenopausal women. In the first experiment, hypothalami from premenopausal (n = 3) and postmenopausal (n = 3) women were formalin fixed, paraffin embedded, serially sectioned, and stained with cresyl violet. Soma areas of more than 3500 neurons were digitized using an image-combining computer microscope. The mean cross-sectional area of infundibular neurons in the postmenopausal women was 30% greater than that in premenopausal women, with no change in cell density. The mean cross-sectional area of mammillary neurons was unchanged, indicating that the infundibular neuronal hypertrophy was not an artifact of tissue processing. In the second experiment, hypothalami from premenopausal (n = 3) and postmenopausal (n = 2) women were frozen, serially sectioned, and incubated with a 48-base synthetic cDNA probe complementary to estrogen receptor (ER) mRNA. Adjacent sections were incubated with a cDNA probe complementary to GnRH mRNA. Morphometric analysis revealed that the mean cross-sectional area of infundibular neurons expressing the ER gene in the postmenopausal women was twice as large as the mean area in premenopausal hypothalami. The hypertrophied neurons did not contain GnRH mRNA. Finally, analysis of the infundibular nucleus from an oophorectomized 38-yr-old woman also revealed hypertrophied neurons containing ER mRNA. These data support the hypothesis that hypertrophy of infundibular neurons in postmenopausal women is secondary to loss of the inhibitory feedback of ovarian steroids.

Adult↗
PubMedDate not supplied

Infant rats: hypothalamic unit activity.

Single-unit recordings were made from lateral hypothalamic area (LHA) neurons of infant (8 through 21 days of age) male and female albino rats. Basal (or spontaneous) firing rates of LHA neurons were recorded for 20 min from rats 8 through 21 days of age, and mean basal firing rates did not differ across ages. Basal firing rates of LHA neurons in infant rats ranged from less than 1 spike/sec up to 27 spikes/sec, with 56% of the basal rates less than 1 spike/sec. Infant rats also received hypertonic saline injections (and control injections) to determine osmosensitivity characteristics of LHA neurons. Across ages, 56%--88% of LHA neurons were osmosensitive, with the highest percentages of osmosensitive units found in rats 14--21 days of age. Infant rats showed LHA unit electrophysiological characteristics that were quite similar to those obtained from LHA neurons in adult rats with respect to basal firing rates and osmosensitivity, however, LHA neuron activity in infants was not modulated by sensory stimuli as is frequently reported for adults. The results are discussed in terms of functional development of the LHA.

Action Potentials↗
PubMedDate not supplied

Ontogeny of drinking behavior of preweanling rats with lateral preoptic damage.

Male (N = 9) and female (N = 7) infant albino rats sustained bilateral lateral preoptic area (LPO) destruction on the tenth day of life. During development and as adults, these brain-damaged rats were subjected to repeated testing of drinking behaviors in response to cellular and extracellular dehydration. Immediately following LPO destruction the pups ceased suckling and most rats required tube-feeding to maintain life; however, all pups were maintaining body weight through voluntary suckling and/or feeding-drinking by 20-21 days of age. Daily water intakes were elevated from 30-42 days of age, following which intakes decreased to control vonse to water deprivation, polyethylene glycol injection and food deprivation treatments. These results are consistent with the suggestion that the LPO contains osmoreceptors for drinking behavior, and the present results suggest that such osmoreceptors, may be functional by the tenth day of life for rats.

Animals↗
PubMedDate not supplied

Ontogeny of lateral preoptic unit activity in rats.

Extracellular single unit recordings were made from units within the lateral preoptic area (LPO) of infant rats from 1 day of age through 31 days of age (postweaning). The rats were anesthetized with dial-urethane and basal (spontaneous) spike rates were recorded for 10--20 min. The rats also received pain-arousal stimulation (tail-pinch and sc injection of formalin solution), and osmotic stimulation (sc or ip injection of hyperosmotic NaCl or sucrose solutions). LPO units were spontaneously active in neonatal rats; however, basal spike rates increased during development. Also increasing during development was the percentage of LPO units which displayed alteration of spike rate in response to hyperosmotic injections (osmosensitive). However, LPO units were found that were responsive to severe pain-arousal stimulation at all ages tested. The developmental changes in LPO unit activity characteristics paralleled the morphological development of LPO neurons and the development of osmotically induced drinking behaviors.

Aging↗
PubMedDate not supplied

Septal destruction in infant rats and the ontogeny of drinking behaviors.

Male and female albino rat pups sustained septal destruction at 10 days of age and body weight and water intakes were measured daily throughout development until 200 days of age. During development the septal and control rats received a battery of drinking tests (e.g., cellular dehydration, hypovolemia, renin). Septal rats (males and females) were hyperdipsic for daily water intakes as early as 31 days of age and the daily hyperdipsia persisted through 200 days of age. On the battery of drinking tests, septal rats consumed water at control volumes on all tests except water deprivation (following which females were hyperdipsic) and food deprivation (during which both males and females were hyperdipsic). Urine output-water intake relationships were determined, and a series of food deprivation tests were conducted during development to determine the etiology of the developmental septal hyperdipsia. All results suggest that hyperdipsia associated with septal destruction during the preweaning period is a primary condition and not secondary to altered output mechanisms, abnormal feeding-drinking patterns, or displacement behavior.

Animals↗