Biomedical subjects

A M Strack

Publications and source records attributed to A M Strack.

34 records · Page 2Linked to original sources

PubMed1995

Glucocorticoids and insulin: complex interaction on brown adipose tissue.

Glucocorticoids and insulin effect long-term reciprocal changes in food intake and body weight. We tested the interactions of corticosterone and insulin on caloric efficiency, white adipose tissue (WAT) stores, and brown adipose tissue (BAT). Two experiments were performed: 1) adrenalectomized rats were treated with corticosterone with or without streptozotocin-induced diabetes and 2) adrenalectomized, corticosterone-treated, diabetic rats were treated with insulin. By 4-5 days later, > or = 50% of the variance in caloric efficiency, plasma triglycerides, and WAT stores was explained by regression of these variables on corticosterone (catabolic) and insulin (anabolic). When the ratio of the hormones was normal, but concentrations high, overall gain of energy stores decreased and energy was redistributed to fat. Both hormones were anabolic on BAT lipid storage; the hormones played a complex role in the regulation of uncoupling protein (UCP) in BAT. Although corticosterone inhibited and insulin stimulated UCP, these effects were only evident in diabetics and with normoglycemia, respectively. For BAT variables, < or = 50% of the variance was explained by regression on corticosterone and insulin, suggesting that the effects of these hormones are mediated through an intermediate such as sympathetic nervous system input to BAT.

Adipose Tissue↗

PubMed1995

Aldosterone and dexamethasone both stimulate energy acquisition whereas only the glucocorticoid alters energy storage.

Corticosteroids stimulate and insulin inhibits energy acquisition (food intake); conversely, corticosteroids inhibit and insulin stimulates energy storage (body weight gain). Thus, together these hormones mediate long-term energy balance. This study tested whether the stimulatory action of corticosteroids on food intake was mediated by association with high affinity mineralocorticoid receptors (MRs) or lower affinity glucocorticoid receptors (GRs). Young male rats were adrenalectomized (ADX) and given vehicle (control) or streptozotocin (diabetic); subgroups of rats were infused with vehicle, aldosterone (Aldo, an MR agonist in vivo), dexamethasone (Dex, a GR agonist in vivo), or Aldo&Dex for the 5 days after ADX. Sham-ADX rats were included. Food intake, body weight gain, and epididymal white adipose and interscapular brown adipose tissue stores were weighed. ADX decreased food intake by approximately 24%, and food intake was not increased by diabetes as it was in sham-ADX rats. In control ADX rats, Dex, but not Aldo, stimulated insulin, and food intake was not significantly affected by either hormone; together, Aldo and Dex restored insulin and food intake to sham-ADX rats. Food intake in diabetic ADX rats was significantly increased by each treatment (ADX < Aldo < Dex < Aldo&Dex = sham). Aldo increased body weight through an increase in fluid volume (estimated by decreased plasma protein concentration); however, fat stores were not different from ADX. Dex reduced body weight in control rats but maintained fat stores; in diabetic rats, body weight and fat stores were less than or similar to ADX. We conclude that: 1) corticosteroids, acting through association with both MRs and GRs, stimulate food intake; 2) insulin counteracts the GR-mediated stimulation of food intake in control rats; and 3) Dex and insulin, which is stimulated by Dex, selectively maintain or increase body fat stores, probably at the expense of protein stores.

Adipose Tissue↗

PubMed1995

Corticosterone regulation of insulin-like growth factor I, IGF-binding proteins, and growth in streptozotocin-induced diabetic rats.

The experiments reported herein were conducted to determine how corticosterone regulates growth and plasma insulin-like growth factor (IGF) I and IGF-binding protein (IGFBP) concentrations in normal and streptozotocin (STZ)-induced diabetic rats. Males were bilaterally adrenalectomized (Ax) or sham Ax and given intravenous injections of 0, 30, or 65 mg STZ per kg body wt (0, 30, or 65 STZ) to induce varying degrees of insulin deficiency and implanted with 100-mg pellets containing 0, 40, or 80% corticosterone in cholesterol. Changes in plasma IGFBP concentrations were determined by Western ligand blotting or immunoblots. Neither IGFBP-5 nor IG-FBP-6 was detected in any of the treatment groups. Plasma IGFBP-2 was elevated and IGF-I was reduced in the nondiabetic Ax rats compared with sham Ax controls, but plasma IGFBP-3 and -4 were not significantly changed. Adrenalectomy had no affect on tibial growth or plasma IGFBP-1 in these animals. Plasma IGF-I, IGFBP-1 and -3, and tibial growth were equal among 0, 30, and 65 STZ Ax rats that did not receive corticosterone. Plasma IGFBP-4 was inversely related to the amount of STZ injected in these animals, and IGFBP-2 was elevated in those given the high dose of STZ. In the 0 STZ Ax rats, plasma IGF-I and IGFBP-3 increased in proportion to the corticosterone implant dose, but IGFBP-1 was unaffected. By contrast, IGF-I and IGFBP-3 were unaltered by corticosterone in the 30 STZ Ax rats, and IGFBP-1 increased in proportion with the dose of corticosterone.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenalectomy↗

PubMed1994

The diurnal rhythm in adrenocorticotropin responses to restraint in adrenalectomized rats is determined by caloric intake.

There is a diurnal rhythm in ACTH responses to stressors that peaks, in nocturnally feeding rats, at the time of lights on, in the morning (AM). To determine whether this rhythm is subordinate to the rhythm in food intake, we tested the effects of removing food during the night or the day on ACTH responses in the AM or evening (PM) to the stimulus of restraint in 5-day-adrenalectomized rats. An overnight fast reduced the ACTH response to restraint with tail blood sampling in the AM to the low magnitude observed in the PM in rats fed ad libitum; by contrast, a fast of equivalent duration imposed during the day had no effect on the ACTH response to the stressor in the PM. Short term fasts did not alter the normal AM-PM rhythm in basal ACTH levels. The fasts did, however, significantly decrease the pituitary ACTH concentration at both times of day, suggesting that lack of food had stimulated ACTH secretion during the preceding 14 h. Providing calories by either gavage or manipulation of food presentation increased ACTH responses to restraint in fasted adrenalectomized rats in both the AM and PM. Although four of four experiments showed that provision of calories to fasted rats resulted in increased ACTH responses to the stimulus of restraint, none of the manipulations of caloric intake fully restored ACTH responses in fasted rats to the high amplitude observed in ad libitum fed rats in the AM. We conclude that 1) unlike the circadian rhythm in basal activity in the hypothalamic-pituitary-adrenalocortical (HPA) system, the diurnal rhythm in ACTH responsiveness to stimuli is tightly coupled to the endogenous rhythm in energy intake; and 2) caloric deprivation per se appears to activate the HPA system at some time during the 14- to 17-h fast, but does not produce the normal facilitation in the AM response to acute restraint that is induced by chronic or prior stimulation of the HPA axis.

Adrenalectomy↗

PubMed1994

Regulation of activity in the hypothalamo-pituitary-adrenal axis is integral to a larger hypothalamic system that determines caloric flow.

We have previously reported that there are diurnal rhythms in the magnitude of ACTH responses to stressors and in the sensitivity of stress-induced ACTH responses to facilitation induced by prior stress and to corticosterone (B) feedback induced by exogenous B. In all cases ACTH was more responsive in the morning than in the evening in nocturnally feeding rats. We have also shown in adrenalectomized rats that an overnight fast reduces ACTH responses to restraint in the morning compared with rats fed ad libitum, and we have shown that calorie-containing gavage during the fast increases the amplitude of ACTH responses to restraint in fasted rats. Therefore, this diurnal rhythm is not associated with B feedback and is associated with calories. In these studies we asked whether young, male intact rats that were deprived of food overnight had: 1) hypothalamo-pituitary-adrenal (HPA) axis responses during the fasting period; 2) altered basal activity in the HPA axis; 3) altered responsivity of ACTH to restraint; and 4) altered sensitivity of restraint-induced ACTH responses to facilitation or B feedback. Our results show that food deprivation: 1) induces marked ACTH and B responses during the fast that mirrors the pattern of food intake in fed rats, with an approximately 3-h lag; 2) results in essentially no change in basal ACTH in the morning; 3) reduces ACTH responsivity to stress in the morning; and 4) reduces ACTH responsivity to prior stress-induced facilitation and exogenous B-induced feedback. We conclude that: 1) the HPA axis serves as a default pathway to feeding when food is not available; 2) the diurnal rhythms in restraint-induced ACTH secretion are determined by food intake; and 3) the HPA axis is integral to a larger hypothalamic system that mediates energy flow.

Adrenocorticotropic Hormone↗

PubMed1994

Pseudorabies virus as a transneuronal tract tracing tool: specificity and applications to the sympathetic nervous system.

Because of technical shortcomings, neuroanatomical tract tracing methods have been limited in their ability to examine functional pathways. This has been particularly true of the study of the sympathetic nervous system. Peripheral targets of the sympathetic nervous system are innervated by sympathetic ganglion cells which are located in various, discreet ganglia, primarily in the abdomen and thoracic cavity. Each ganglion contains neurons innervating multiple targets. In turn, each ganglion is innervated by preganglionic motor neurons located in the thoracic and lumbar spinal cord. Preganglionic neurons are innervated by neurons from the brainstem and hypothalamus, as well as probably by spinal interneurons. At each of these sites, the ganglia, the preganglionic nuclei of the spinal cord, and the brainstem and hypothalamus, functionally different neurons are intermingled. Therefore, placement of a traditional retrograde marker (i.e. HRP) in any of those sites would generate retrogradely labeled neurons that represent multiple functional pathways, making the study of one functional pathway impossible. A transneuronal retrograde tracer could obviate this problem by passing the original tracer from the first neuron labeled transsynaptically to neurons which synapse on to it. After injection of the transneuronal tracer into a peripheral target, the tracer would be transported, first to the ganglion cell, then to the preganglionic neurons that innervate the ganglion cell, and then to the neurons in the brain that innervate the preganglionic neurons. All the neurons labeled would belong to one functional pathway, specifically involved in control of that target which was injected. There have been attempts to develop such tracers. WGA-HRP, tetanus toxin, and the tetanus toxin C-fragment have been used with limited success (1,2,3,4,5).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1993

Peripheral and central pathways regulating the kidney: a study using pseudorabies virus.

We used the retrograde transneuronal transport of a neurotropic virus, pseudorabies virus (PRV), to identify the neurons in sympathetic ganglia, spinal cord and brain which regulate renal function and renal circulation. PRV was microinjected into the left kidney of 70, pentobarbital-anesthetized, male rats. After an incubation period of 1-4 days, rats were anesthetized and sacrificed. PRV-infected neurons were located immunocytochemically in pre- and paravertebral sympathetic ganglia, the intermediolateral cell column of the T10-T13 segments and several brainstem cell groups: the medullary raphe nuclei, rostral ventrolateral medulla, rostral ventromedial medulla, A5 cell group, and the paraventricular hypothalamic nucleus. In more heavily infected rats, additional labeling was found in the locus coeruleus, periaqueductal gray matter, lateral hypothalamic area, zona incerta, and anterior hypothalamic area. No infected propriospinal neurons were observed in the lateral spinal nucleus or gray matter of the caudal cervical, lumbosacral or thoracic spinal segments not containing infected putative sympathetic preganglionic neurons. The paucity of infected propriospinal neurons in the presence of infected brainstem neurons, even in lightly infected rats, is discussed in reference to the relative importance of descending vs spinal regulation of the sympathetic outflow to the kidney.

Animals↗

PubMed1993

Feast and famine: critical role of glucocorticoids with insulin in daily energy flow.

The hypothesis proposed in this review is that normal diurnal rhythms in the hypothalamic-pituitary-adrenal (HPA) axis are highly regulated by activity in medial hypothalamic nuclei to effect an interaction between corticosteroids and insulin such that optimal metabolism results in response to changes in the fed or fasted state of the animal. There are marked diurnal rhythms in function of the HPA axis under both basal and stress conditions. The HPA axis controls corticosteroid output from the adrenal and, in turn, forward elements of this axis are inhibited by feedback from circulating plasma corticosteroid levels. Basal activity in the HPA axis of mammals fed ad lib peaks about 2 h before the peak of the diurnal feeding rhythm, and is controlled by input from the suprachiasmatic nuclei. The rhythm in stress responsiveness is lowest at the time of the basal peak and highest at the time of the basal trough in the HPA axis activity. There are also diurnal rhythms in corticosteroid feedback sensitivity of basal and stress-induced ACTH secretion which peak at the time of the basal trough. These rhythms are all overridden when feeding, and thus insulin secretion, is disrupted. Corticosteroids interact with insulin on food intake and body composition, and corticosteroids also increase insulin secretion. Corticosteroids stimulate feeding at low doses but inhibit it at high doses; however, it is the high levels of insulin, induced by high levels of corticosteroids, that may inhibit feeding. The effects of corticosteroids on liver, fat, and muscle cell metabolism, with emphasis on their interactions with insulin, are briefly reviewed. Corticosteroids both synergize with and antagonize the effects of insulin. The effects of stress hormones, and their interactions with insulin on lipid and protein metabolism, followed by some of the metabolic effects of injury stress, with or without nutritional support, are evaluated. In the presence of elevated insulin stimulated by glucocorticoids and nutrition, stress causes less severe catabolic effects. In the central nervous system, regulation of function in the HPA axis is clearly affected by the activity of medial hypothalamic nuclei that also alter feeding, metabolism, and obesity in rats. Lesions of the arcuate (ARC) and ventromedial (VMN) paraventricular (PVN) nuclei result in obesity and hyperactivity in the HPA axis. Moreover, adrenalectomy inhibits or prevents development of the lesion-induced obesity. There are interactions among these nuclei; one mode of communication is via inputs of neuropeptide Y (NPY) cells in the ARC to the VMN, dorsomedial nuclei, and PVN.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

PubMed1993

Lesions of the hippocampal efferent pathway (fimbria-fornix) do not alter sensitivity of adrenocorticotropin to feedback inhibition by corticosterone in rats.

The hypothalamic-pituitary-adrenal (HPA) axis controls the diurnal and stress-induced release of adrenal corticosteroids into the general blood circulation. In turn, corticosteroids inhibit the HPA axis under basal conditions and during stress through occupation of their receptors (types I and II) in the brain by closing a negative feedback loop. The primary site in the brain at which corticosteroids act to inhibit the HPA axis has not been identified. High concentrations of both types of receptors are found in neurons of the hippocampal formation, a structure which has been reported by some, but not others, to control activity within the HPA axis by serving as a major negative feedback site. In many of these past studies, blood was collected after extensive handling or exposure to ether, conditions which do not favor the detection of basal hormone concentrations. To address these controversies, we tested the feedback sensitivity of the anterior pituitary hormone responsible for corticosteroid production, adrenocorticotropin (ACTH), to corticosterone (B), the main corticosteroid in rats, in total fornix- and, as controls, cortex-lesioned rats. All rats were given vascular catheters to avoid any handling-induced differences in plasma B or ACTH when sampling blood. In some experiments, fornix- and cortex-lesioned rats were adrenalectomized and given 1 of 3 doses of exogenous B provided in a subcutaneous pellet to ensure that plasma B was equal in different lesion groups. We hypothesized that if the hippocampal formation were an important site of B-mediated inhibition of the HPA axis, fornix-lesioned rats would have higher plasma B as a result of increased endogenous secretion in the morning or the evening compared to cortex-lesioned rats in rats with adrenal glands. In addition, we hypothesized that adrenalectomized fornix-lesioned rats given the same low to moderate levels of exogenous constant B would have higher basal and stress-induced ACTH than cortex-lesioned rats. Diurnal plasma B was not affected by fornix lesions in intact rats. Moreover, basal ACTH measured in the morning and the evening and stress-induced ACTH was the same in adrenalectomized fornix- and cortex-lesioned rats with constant exogenous B. We conclude, therefore, that information about occupancy of B receptors in the hippocampus carried by the fornix primarily subserves functions which do not directly regulate activity in the HPA axis.

Adrenalectomy↗

PubMed1992

Feedback and facilitation in the adrenocortical system: unmasking facilitation by partial inhibition of the glucocorticoid response to prior stress.

Previously stressed animals remain responsive to subsequent stressors, despite secreting an adequate corticosteroid signal during the first stress which should act to damp the response to a second stress. We have previously postulated that stress acts to facilitate subsequent responses in the adrenocortical system, and that this facilitation is balanced by the corticosteroid feedback signal. To test this hypothesis directly, we treated young male rats with cyanoketone (CK) to partially block the adrenal capacity to synthesize corticosterone (B). Subsequently, groups of CK- or vehicle (VEH)-treated rats were exposed to the FIRST stress of 30-min restraint with small blood samples collected at 0, 15, and 30 min. The FIRST stress was given to subgroups of rats 12, 9, 6, or 3 h before lights off (12 h) or lights on (24 h). At 12 or 24 h, rats were again restrained with blood samples at 0 ("basal") and 30 min (SECOND stress). Control groups were stressed for the first time when the experimental groups received their SECOND stress. Plasma ACTH and B concentrations were measured. Although in the absence of stress, basal B concentrations were normal in CK-treated compared to VEH-treated rats throughout the day, the B response to the FIRST stress was reduced by 60% in the CK- compared to the VEH-treated group. When the FIRST stress was performed during the time of lights on, "basal" plasma ACTH was elevated in CK groups at 12 h (lights off) compared to levels in both previously stressed VEH groups and unstressed CK controls. There was no difference at this time of day in the magnitude of the ACTH response to the SECOND stress in CK rats compared to that in CK rats receiving their only stress (controls) or that in VEH-treated rats receiving the SECOND stress. When first stress was performed during the time of lights off, "basal" plasma ACTH at 24 h (lights on) in CK and VEH rats were not different compared to levels in their respective unstressed controls. The ACTH response to the SECOND stress at 24 h was elevated in all previously stressed CK groups compared to that in either CK control or VEH groups. At neither time of day were SECOND stress ACTH concentrations in VEH rats different from those in control VEH rats. At 12 h (lights off), but not at 24 h (lights on), "basal" ACTH was significantly elevated in VEH rats above the unstressed VEH control values.(ABSTRACT TRUNCATED AT 400 WORDS)

Adrenal Cortex↗

PubMed1992

Feedback sensitivity of the rat hypothalamo-pituitary-adrenal axis and its capacity to adjust to exogenous corticosterone.

Chronic stress causing elevated morning (AM) corticosterone (B) concentrations of 2-8 micrograms B/dl does not appear to inhibit subsequent activity in the hypothalamic-pituitary-adrenal (HPA) axis, a surprising finding in view of the known depression in AM basal ACTH by only 3 micrograms B/dl in adrenalectomized rats. To distinguish between the possibilities that either intact rats are less sensitive to B feedback than adrenalectomized rats, or that chronic stress facilitates responses in the HPA axis, we elevated basal B levels in young male rats with slow-release B pellets in the absence of stress. Between 4-6 days after implantation of B pellets at three doses that elevated basal AM (diurnal trough) plasma B to approximately 1.2, 4, and 10 micrograms/dl, we studied basal ACTH and B at trough (AM) and peak evening (PM) times of the diurnal cycle, as well as the responses to the stress of restraint and blood collection from the tail at each time of day. We also determined mean daily plasma B, insulin, and glucose from samples collected at six intervals during the day. Adrenal, thymus, and body wts were measured as were transcortin (CBG) and adrenal phenylethanolamine-N-methyl transferase activity. Compared to controls implanted with wax pellets, all doses of B inhibited adrenal wt and AM stress responses and tended to inhibit pituitary ACTH content and adrenal phenylethanolamine-N-methyl transferase activity. Inhibition with the middle dose B pellet was close to maximally effective for these endpoints. Plasma glucose and thymus wt were significantly decreased and insulin was significantly increased in the middle and highest B pellet groups, with significantly greater effects at the highest dose. The gain in body wt and transcortin concentrations were significantly decreased only in the highest dose groups, in which mean daily plasma B was approximately 10 micrograms/dl, a level that clearly overwhelmed the capacity of the adrenocortical system to respond to any stimulus tested. By contrast, rats with low and middle dose B pellets appeared to adjust HPA axis function by decreasing the peak diurnal increase in B, so that 24-h mean B levels did not differ from control, and were maintained at approximately 5 micrograms/dl. Both of these groups also had inhibited ACTH responses to stress applied during the diurnal trough (AM). By contrast, neither group had inhibited ACTH responses to stress applied during the diurnal peak (PM). We conclude that: 1) The HPA axis of intact rats is extremely sensitive to exogenous B.(ABSTRACT TRUNCATED AT 400 WORDS)

Adrenal Glands↗

PubMed1990

Pseudorabies virus: a highly specific transneuronal cell body marker in the sympathetic nervous system.

The present report presents a series of experiments using Bartha's K strain of pseudorabies virus (PRV) designed to test the specificity of this virus as a retrograde transneuronal marker in the sympathetic nervous system of rats. Three experiments were performed. First, an injection of PRV was made in the anterior chamber of the eye, followed 24 hr later by an injection of WGA-HRP. PRV infected neurons in the superior cervical ganglion (SCG) always contained WGA-HRP. This dual labeling of SCG neurons suggests that the PRV cell body labeling does not nonspecifically infect nearby neurons. Second, after PRV injections into the pinna or eye, a specific segmental distribution of the transneuronal cell body labeling occurred in the intermediolateral cell column and related spinal areas. After eye injections, the majority of transneuronally labeled neurons were in the T1-T3 segments. After pinna injections, the majority of labeled cells were in the T2-T5 segments. Since the SCG cells innervating these 2 end organs lie in close proximity to each other within the ganglion, these results suggest that a specific transfer of the virus to the preganglionic neurons occurred, possibly via a transsynaptic mechanism. Third, virally infected glial cells were rarely found in the SCG or spinal cord. In summary, Bartha's K strain of PRV is a specific transneuronal retrograde grader marker in the sympathetic nervous system.

Animals↗

PubMed1989

CNS cell groups regulating the sympathetic outflow to adrenal gland as revealed by transneuronal cell body labeling with pseudorabies virus.

The CNS cell groups that innervate the sympathoadrenal preganglionic neurons of rats were identified by a transneuronal viral cell body labeling technique combined with neurotransmitter immunohistochemistry. Pseudorabies virus was injected into the adrenal gland. This resulted in retrograde viral infections of the ipsilateral sympathetic preganglionic neurons (T4-T13) and caused retrograde transneuronal cell body infections in 5 areas of the brain: the caudal raphe nuclei, ventromedial medulla, rostral ventrolateral medulla, A5 cell group, and paraventricular hypothalamic nucleus (PVH). In the spinal cord, the segmental distribution of virally infected neurons was the same as the retrograde cell body labeling observed following Fluoro-gold injections in the adrenal gland except there was almost a 300% increase in the number of cells labeled and a shift in cell group distribution. These results imply there are local interneurons that regulate the sympathoadrenal preganglionic neurons. In the medulla oblongata, serotonin (5-HT)-, substance P (SP)-, thyrotropin-releasing hormone-, Met-enkephalin-, and somatostatin-immunoreactive neurons of the raphe pallidus and raphe obscurus nuclei and the ventromedial medulla were infected. In the ventromedial and rostral ventrolateral medulla, immunoreactive phenylethanolamine-N-methyltransferase, SP, neuropeptide Y, somatostatin, and enkephalin neurons were infected. The A5 noradrenergic cells were labeled, as were some somatostatin-immunoreactive neurons in this area. In the were infected. The A5 noradrenergic cells were labeled, as were some somatostatin-immunoreactive neurons in this area. In the hypothalamus, tyrosine hydroxylase- and SP-immunoreactive neurons of the dorsal parvocellular PVH were infected. Only a few immunoreactive vasopressin, oxytocin, Met-enkephalin, neurotensin, and somatostatin PVH neurons were labeled.

Adrenal Glands↗

PubMed1989

A general pattern of CNS innervation of the sympathetic outflow demonstrated by transneuronal pseudorabies viral infections.

Pseudorabies virus (PRV) injections of various sympathetic ganglia and the adrenal gland were made in rats. These produced immunohistochemically detectable retrograde viral infections of ipsilateral sympathetic preganglionic neurons (SPNs) and transneuronal infections of the specific sets of second order neurons in the spinal cord and brain that innervate the infected SPNs. Five cell groups in the brain appear to regulate the entire sympathetic outflow: the paraventricular hypothalamic nucleus (PVH), A5 noradrenergic cell group, caudal raphe region, rostral ventrolateral medulla, and ventromedial medulla. In addition, local interneurons in laminae VII and X of the spinal cord are also involved. Other CNS areas also became transneuronally labeled after infections of certain sympathetic ganglia, most notably the superior cervical and stellate ganglia. These areas include the central gray matter and lateral hypothalamic area. The zona incerta was uniquely labeled after stellate ganglion infections. The cell body labeling was specific. This specificity was demonstrated in the PVH where the neurons of the parvocellular PVH that form the descending sympathetic pathway were labeled in a topographic fashion. Finally, we demonstrate that the retrograde transneuronal viral cell body labeling method can be used simultaneously with either neuropeptide transmitter or transmitter synthetic enzyme immunohistochemistry.

Animals↗

PubMed1988

Spinal origin of sympathetic preganglionic neurons in the rat.

The segmental distribution of sympathetic preganglionic neurons (SPNs) and dorsal root ganglion cells (DRGs) was studied after Fluoro-gold injections into the major sympathetic ganglia and adrenal gland in rats. A quantitative assessment of the segmental and nuclear locations was made. Four general patterns of innervation were apparent: (1) a large number of SPNs (1000-2000/ganglion) innervate the sympathetic ganglia which control head or thoracic organs and a relatively small number of SPNs (100-400/ganglion) innervate the sympathetic ganglia controlling the gut, kidney, and pelvic organs; this difference in density of innervation probably relates to the level of fine control that can occur in these end organs by the SPNs; (2) the reverse pattern is seen in the DRG labeling where a large number of DRGs were labeled after Fluoro-gold injections into the preaortic ganglia (celiac, superior, and inferior mesenteric) and a small number were labeled after injections into the cervical sympathetic ganglia; (3) the intermediolateral cell column is the main source of SPNs except for the inferior mesenteric ganglion which is innervated predominantly by SPNs originating in the central autonomic nucleus (75%); the lateral funiculus is a source of SPNs mainly for the cervical sympathetic ganglia; and (4) each sympathetic ganglion and the adrenal gland receives a multisegmental SPN and DRG input with one segment being the predominant source of the innervation. The adrenal gland shows an intermediate position in terms of the density of SPN input (approximately 800 cells) and dorsal root input (approximately 300 cells); it has a widespread segmental input (T4-T12) with the T8 segment being the major source.

Animals↗

PubMed1986

Renin heterogeneity in stroke-prone hypertensive and normotensive rats.

Six forms of renin are found in the rat kidney. We studied their secretion in renal slices from spontaneously hypertensive stroke-prone rats (SHRSP) and Wistar-Kyoto rats (WKY). Incubation media from renal slices were subjected to isoelectric focusing. Six peaks of renin activity with different isoelectric points were found. The renin concentration of each form was expressed as a percentage of the total recovered from the gel. We established that the forms secreted by renal slices of SHRSP differed from those of WKY: SHRSP slices released a higher proportion of forms focusing at the more acidic pH. The distribution of the six renin forms and of blood pressure (BP) among animals of the F1, F2, and backcross progenies resulting from the cross of SHRSP and WKY rats were studied. In the F1, BP, percentage of renin form 2, and a combination of the percentage of forms 4 + 5 + 6 were intermediate between the parental lines. The backcross rats showed BP and percentages of forms closer to their SHRSP or WKY parent. In the F2, the distribution of BP, percentage of forms 2 and 4 + 5 + 6 take the form of a unimodal distribution with a significantly larger variance than F1. The increase in the correlation between percentage of renin forms and BP, and between renin concentration of BP, in the segregating progenies over that observed in the parental lines and the F1, are support for the hypothesis that these traits are under the control of common genetic mechanisms.

Animals↗