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E M Stricker

Publications and source records attributed to E M Stricker.

At least 37 records · Page 2Linked to original sources
PubMed1996

Area postrema lesions in rats appear to disrupt rapid feedback inhibition of fluid intake.

Area postrema lesions (APX) were produced by vacuum aspiration in adult male rats. After systemic administration of hypertonic saline solutions, significantly more water was consumed by rats with APX than by intact control rats. Similarly enhanced water intake by rats with APX also was observed when marked hypovolemia was induced by s.c. administration of a hyperoncotic colloidal solution. In both conditions, the increased water intake occurred within the first 15 min of the drinking tests. Intakes of liquid diet or 10% sucrose solution after food deprivation by rats with APX also were considerably larger than those of control rats. These and other results suggest that rats with APX experience less inhibition of ingestion while drinking. Thus, the AP may be important for the detection of early, inhibitory signals generated by fluid ingestion, and after its ablation increased drinking may occur because the feedback inhibition provided by such signals is diminished.

Animals↗
PubMed1995

Cholecystokinin activates catecholaminergic neurons in the caudal medulla that innervate the paraventricular nucleus of the hypothalamus in rats.

Stimulation of gastric vagal afferents by systemic administration of cholecystokinin octapeptide (CCK) inhibits gastric motility, reduces food intake, and stimulates pituitary secretion of oxytocin and adrenocorticotropic hormone in rats. To characterize further the central neural circuits responsible for these effects, the present study used triple-labeling immunocytochemical methods to determine whether or not exogenous CCK activates cFos expression in catecholaminergic neurons in the caudal medulla that project to the paraventricular nucleus of the hypothalamus (PVN). To identify these neurons, the retrograde tracer fluorogold (FG) was iontophoresed into the PVN of anesthetized rats under stereotaxic guidance. After 2 weeks, rats were injected with CCK (100 micrograms/kg, i.p.) and then anesthetized and killed 1 hour later by perfusion fixation. Medullary sections were processed for triple immunocytochemical localization of cFos, retrogradely transported FG, and tyrosine hydroxylase (TH). In rats with FG injections centered in the PVN (n = 10), approximately 70% of the FG-labeled neurons in the caudal nucleus of the solitary tract (NST) and ventrolateral medulla (VLM) expressed cFos. Of these activated PVN-projecting neurons, approximately 78% in the NST and 89% in the VLM were catecholaminergic (TH positive). These results indicate that PVN-projecting catecholaminergic neurons within the caudal medulla are activated by peripheral administration of CCK, further implicating these ascending catecholaminergic pathways in the neuroendocrine, physiological, and behavioral effects produced by gastric vagal stimulation.

Afferent Pathways↗
PubMed1995

Central oxytocin and ANP receptors mediate osmotic inhibition of salt appetite in rats.

These studies evaluated the involvement of central oxytocin (OT) and atrial natriuretic peptide (ANP) receptors in the osmotic inhibition of hypovolemia-induced salt appetite. Rats were pretreated centrally with the A chain of the cytotoxin ricin conjugated to OT (rAOT) or ANP (rAANP) to selectively inactivate cells bearing these respective receptors, or rats were pretreated with the unconjugated A chain (rA) as a control. Hypovolemia was induced with subcutaneous colloid injections, and rats then were given either 2 M mannitol, which raises plasma osmolality but lowers plasma sodium, or 1 M NaCl, which raises both. Hypertonic mannitol inhibited saline ingestion in rA-treated control rats but stimulated ingestion in rAOT- and rAANP-treated rats, whereas hypertonic NaCl blunted saline ingestion in rA- and rAOT-treated rats but stimulated ingestion in rAANP-treated rats. Angiotensin II-induced saline intake was similarly potentiated in rAOT- and rAANP-treated rats, indicating that this treatment also activates central inhibitory OT and ANP pathways. These data suggest that central ANP receptors mediate both Na(+)- and osmolality-induced inhibition of NaCl ingestion, whereas central OT receptors primarily mediate osmolality-induced inhibition of NaCl ingestion in rats.

Animals↗
PubMed1995

Dehydration anorexia in decerebrate rats.

Hypertonic saline (HS) administered intraperitoneally reduced the intake of sucrose solution infused intraorally in tube-fed decerebrate rats, as it did in control animals. Similarly, either intraperitoneal or intravenous HS markedly decreased the intake of laboratory chow by neurologically intact control rats. These observations complement recent findings that lesions of putative osmoreceptors in the ventral diencephalon, which eliminate thirst and blunt pituitary secretion of vasopressin and oxytocin in response to HS in rats, have no apparent effect on the HS-induced inhibition of food intake. Taken together they support previous studies indicating an important role for the caudal brainstem in the central control of food intake and suggest that such brainstem control may also include the inhibition of food intake induced by acute hyperosmolality.

Animals↗
PubMed1995

Establishing behavioral and physiological functions of central oxytocin: insights from studies of oxytocin and ingestive behaviors.

Plasma oxytocin (OT) levels are strongly correlated with inhibition of ingestion in many models of stimulated food and NaCl intake in rats, but peripheral administration of OT or OT antagonists has little or no effect on these behaviors. These findings led us to propose that central OT secretion from parvocellular neurons occurring in parallel with pituitary secretion from magnocellular neurons acts to inhibit ingestion of both food and salt. Multiple lines of evidence now support this hypothesis: 1) intracerebroventricular (icv) OT administration inhibits food intake in fasted rats and NaCl intake in hypovolemic rats; 2) icv administration of OT-receptor antagonists significantly blunts the effects of anorexigenic agents on food intake and the action of naloxone to inhibit hypovolemia-induced intake of NaCl, but not water; 3) most treatments that inhibit food and/or NaCl intake stimulate expression of c-fos in parvocellular as well as magnocellular OT neurons, indicating simultaneous activation of both centrally-projecting and pituitary-projecting OT neurons; 4) icv treatment with cytotoxic conjugates of ricin A and OT to disable cells bearing OT receptors leads to a disinhibition of NaCl intake similar to that produced by OT antagonists; 5) administration of ethanol, a well known inhibitor of OT secretion, produces effects on stimulated food and NaCl intake in rats analogous to those produced by OT-antagonists and ricin-OT conjugates. In conjunction with studies demonstrating natriuretic effects of circulating OT, these results therefore support the concept of coordinated central and peripheral OT secretion as a mechanism for regulating body solute homeostasis in rats. These phenomena will be used as a framework to discuss and critically evaluate the criteria that are both necessary and sufficient to firmly establish behavioral and physiological functions of centrally-secreted peptides such as OT.

Animals↗
PubMed1994

Lithium chloride-induced anorexia, but not conditioned taste aversions, in rats with area postrema lesions.

Area postrema (AP) lesions were produced by vacuum aspiration in adult male Sprague-Dawley rats. Consistent with previous findings, when water-deprived rats were allowed to drink novel flavored fluids immediately before treatment with LiCl (3 mEq/kg, i.p.), sham-operated and non-operated control rats demonstrated a pronounced aversion to the fluids whereas rats with AP lesions did not decrease fluid consumption significantly. However, in a 30-min test period after overnight food deprivation, rats with AP lesions reduced food intake significantly and to an equivalent degree as control animals when pretreated with LiCl (3 mEq/kg, i.p. or i.v.). These and other results are consistent with the traditional view that AP mediates the sensation of nausea produced by LiCl treatment (hence the loss of conditioned taste aversions after AP lesions), but suggest that neither nausea nor AP is necessary for the marked disinclination to eat that is induced in rats by acute administration of LiCl.

Analysis of Variance↗
PubMed1994

Exogenous cholecystokinin activates cFos expression in medullary but not hypothalamic neurons in neonatal rats.

The central distribution of neurons activated to express cFos immunoreactivity in response to peripheral administration of cholecystokinin octapeptide (CCK) was examined in 2-day-old rats. Similar to previous results in adult rats, neurons in specific subregions of the area postrema and nucleus of the solitary tract (NST) expressed cFos after CCK treatment. However, in marked contrast to results in adult rats, CCK treatment in neonates did not stimulate cFos expression in hypothalamic neurons or in other forebrain areas, and did not increase plasma oxytocin levels. These results suggest that vagal sensory activation of intrinsic brainstem circuits may be sufficient for the known inhibitory effects of exogenous CCK on gastric motility and feeding in neonatal rats. The prominent forebrain activation produced by CCK administration in adult rats likely reflects later maturation of direct and relayed ascending neural projections from the NST.

Aging↗
PubMed1994

Compound complementarities in the study of motivated behavior.

In his classic article, Stellar (1954) proposed that diverse motivated behaviors reflected the activity of excitatory and inhibitory centers in the hypothalamus. His specific and testable ideas provided the theoretical focus for a great deal of fruitful research on the biological bases of behavior for 2 decades. Subsequently, new findings and technical developments again changed the perspective and experimental approaches in behavioral neuroscience. The authors suggest that the modern emphasis on the anatomy and chemical function of neuronal systems has come at the expense of understanding the subcomponents of behavior and the hierarchical levels of integration involved in transforming reflexes into operant acts. Increased attention in the future to the infrastructure of the behaviors being elucidated, when combined with reductionistic studies of neurons, will fulfill the potential contribution to behavioral neuroscience that is implicit in Stellar's article.

Animals↗
PubMed1994

Acute effects of ethanol on ingestive behavior in rats.

The effects of acute ethanol administration on the ingestion of NaCl and food were assessed in adult rats subjected to 1-hr drinking and feeding tests 30 min after intraperitoneal administration of ethanol. Ethanol pretreatment did not induce spontaneous NaCl ingestion, but significantly potentiated angiotensin II-stimulated salt appetite, but not water intake, in a dose-dependent manner. Similarly, ethanol pretreatment significantly potentiated neuropeptide Y-stimulated food intake in nonfasted rats, but did not, by itself, cause spontaneous food ingestion. Ethanol pretreatment also significantly blunted pituitary secretion of oxytocin in response to multiple excitatory stimuli. Finally, administration of oxytocin intracerebroventricularly prevented the ethanol-induced potentiation of salt appetite elicited by angiotensin II. In view of our previous findings that central oxytocin secretion inhibits both NaCl and food intake, we propose that ethanol potentiates the ingestion of various solutes in rats, in part, by inhibiting brain-projecting oxytocinergic pathways concurrently with its well-known effects to inhibit pituitary oxytocin secretion.

Alcoholic Intoxication↗
PubMed1994

Chronic nucleus tractus solitarius lesions do not prevent hypovolemia-induced vasopressin secretion in rats.

The present study examined the hypothesis that hypovolemia stimulates vasopressin (VP) secretion by removing tonic inhibitory baroreceptor input. Serial hemorrhage (4 samples of 2 ml/300 g body wt taken every 10 min) increased plasma VP levels in conscious rats devoid of cardiac and arterial baroreceptor reflex responses due to chronic bilateral lesions of nucleus tractus solitarius (NTS). The VP response to hemorrhage was similar to that seen in control rats and chronic sinoaortic-denervated (SAD) rats. After subcutaneous injection of 30% polyethylene glycol, NTS-lesioned rats, SAD rats, and control rats had elevated VP levels that correlated with the induced depletion of plasma volume. Additionally, in alpha-chloralose-anesthetized control rats, chronic SAD rats, and chronic NTS-lesioned rats, bilateral vagotomy had minimal effects on basal VP levels, and vagotomy in chronic NTS-lesioned rats did not prevent hemorrhage-evoked increases in VP secretion. These results do not support the idea that hemorrhage-induced VP secretion occurs through reduction in tonic inhibitory baroreceptor input. Instead, neither cardiac nor arterial baroreceptor input appears to be necessary for hypovolemia-induced VP secretion in rats.

Animals↗
PubMed1994

Sodium deprivation blunts hypovolemia-induced pituitary secretion of vasopressin and oxytocin in rats.

The present investigations determined the effects of dietary sodium deprivation on the neurohypophysial secretion of arginine vasopressin (AVP) and oxytocin (OT) by rats in response to nonhypotensive hypovolemia induced by subcutaneous injection of 30% polyethylene glycol solution. In rats fed either standard sodium-rich laboratory chow or sodium-deficient diet for 8 days, AVP secretion increased gradually in proportion to plasma volume deficits up to 22-28% while pituitary secretion of OT was not stimulated. However, when hypovolemia was more pronounced, secretion of both hormones was marked in rats fed standard chow, whereas rats fed sodium-deficient diet were significantly less responsive. These effects did not reflect a general insensitivity of the neurohypophysial system because sodium-deprived and chow-fed rats secreted AVP and OT equivalently in response to intravenous infusion of 1.5 M NaCl solution. Nor did they reflect a general insensitivity to hypovolemia because sodium-deprived rats drank substantial, above-normal volumes of water after colloid treatment. Instead, the results appear to reflect a specific inhibition of stimulatory baroreceptor inputs to AVP and OT neurons during dietary sodium deprivation in rats.

Animals↗
PubMed1994

Inhibitory effects of estrogen on stimulated salt appetite in rats.

Adult male rats consumed 50-150% more 0.5 M NaCl solution than females did during a 7-hr drinking test when robust salt appetite was elicited by dietary sodium deprivation for 8 days, daily injections of deoxycorticosterone, or adrenalectomy followed by 2 days of sodium deprivation. In contrast, male rats drank much less saline after systemic treatment with the natriuretic agent furosemide, adrenalectomy followed by 1 day of sodium deprivation, or sc treatment with colloid solution after 2 days of sodium deprivation, and female rats drank comparably small volumes. Conversely, 30-day-old prepubescent male and female rats showed equally robust salt appetites after 8 days of sodium deprivation. These and other findings support an inhibitory role of estrogen on salt appetite in rats, which appears to occur only when the appetite is especially pronounced.

Animals↗
PubMed1993

Distribution and neurochemical phenotypes of caudal medullary neurons activated to express cFos following peripheral administration of cholecystokinin.

Immunocytochemical localization of the protein product of the proto-oncogene c-fos allows anatomical identification of physiologically activated neurons. The present study examined the subnuclear distribution of cFos protein in the rat caudal medulla following peripheral administration of cholecystokinin octapeptide, which reduces feeding and gastric motility by a vagally mediated mechanism. To begin phenotypic characterization of neurons activated to express cFos following cholecystokinin treatment, double-labeling techniques were used to identify vagal motor neurons and neurons immunoreactive for tyrosine hydroxylase, neuropeptide Y, and neurotensin. Activated cells were most prevalent in the subnucleus medialis of the nucleus of the solitary tract, less prevalent in the subnucleus commissuralis, and virtually absent in the subnuclei centralis and gelatinosus. Many activated cells occupied the caudal area postrema; some of these were catecholaminergic. In contrast, activated cells were sparse within the medial rostral area postrema. Other activated cells occupied the dorso- and ventrolateral medulla and the midline raphe nuclei. Retrograde labeling of vagal motor neurons confirmed that very few were activated. Those that were activated occupied the caudal dorsal motor nucleus. In the dorsomedial medulla, 51% of catecholaminergic neurons and 39% of neurons positive for neuropeptide Y were activated, but no neurotensin-positive neurons were activated. In the ventrolateral medulla, 25% of catecholaminergic neurons and 27% of neuropeptide Y-positive neurons were activated. By characterizing the subnuclear distribution and chemical phenotypes of neurons activated by exogenous cholecystokinin, these data contribute to elucidation of the neural circuits mediating the behavioral, physiological, and neuroendocrine effects produced by this peptide.

Animals↗
PubMed1993

Central oxytocin inhibition of salt appetite in rats: evidence for differential sensing of plasma sodium and osmolality.

Sodium chloride ingestion is stimulated during conditions of sodium deficiency to maintain body fluid and electrolyte balance. Recent studies have indicated that salt appetite in rats is often inversely related to peripheral and central secretion of the hormone oxytocin (OT). We studied the potential role of central OT on salt and water ingestion by treating rats intracerebroventricularly with OT conjugated to the A chain of the plant cytotoxin ricin (rAOT) to produce a chronic selective inactivation of brain cells containing OT-receptive elements. The rats treated with rAOT and control rats treated with the ricin A chain alone were given 5-hr two-bottle (water and 0.5 M NaCl) drinking tests 30 min after they were made hyperosmolar by injections of hypertonic (2M) mannitol solution, which elevated plasma osmolality but reduced plasma Na+ concentration. In the control rats only water intake was stimulated in response to the induced hyperosmolality, but in the rAOT-treated rats hypertonic mannitol caused a robust salt appetite as well as thirst. Analogous results were obtained in rats treated with two different OT-receptor antagonists prior to induction of hyperosmolality with mannitol. In contrast to these results, when hyperosmolality was induced by administration of equivalently hypertonic (1M) NaCl, which elevated both plasma osmolality and plasma Na+ concentration, only water intake but not salt intake was stimulated in both control and OT-receptor antagonist-treated rats. When salt appetite was stimulated by the physiological stimulus of polyethylene glycol-induced hypovolemia, hypertonic mannitol similarly inhibited salt ingestion in control animals but not in rAOT-treated rats, whereas hypertonic NaCl inhibited subsequent salt ingestion in both groups. These results suggest that salt appetite is regulated by both Na(+)- and osmolality-sensing mechanisms in rats. In addition, they indicate that central OT likely mediates a significant component of osmolality-related inhibition of salt appetite but does not appear to be essential for Na(+)-related inhibition of this important homeostatic behavior.

Animals↗
PubMed1993

Cold-induced increases in phenylethanolamine N-methyltransferase (PNMT) mRNA are mediated by non-cholinergic mechanisms in the rat adrenal gland.

Previously, we reported that cold stress induces a rapid increase in adrenomedullary PNMT mRNA levels, followed by concomitant increases in PNMT immunoreactivity (10). In the present study, the extracellular signals mediating this adaptive response to stress were investigated using northern analysis and RNA slot-blot hybridization. Although adrenal denervation significantly diminished cold-induced increments in adrenomedullary PNMT mRNA levels, it did not completely abolish the cold stress response. In contrast to these results, splanchnectomy completely inhibited cold-induced increments in TH mRNAs in the same tissue samples. These findings indicate that the effects of cold exposure on PNMT mRNA levels are mediated by both neural and non-neural mechanisms, and that adrenal PNMT and TH are differentially regulated in response to cold stress. Surprisingly, the neural component of the PNMT stress response could not be attenuated by peripheral administration of chlorisondamine, a powerful nicotinic ganglionic blocking agent. In contrast, chlorisondamine was effective in inhibiting sympathetic neural activity, as judged by the drug's ability to completely block increases in blood pressure, heart rate, and plasma catecholamines resulting from spinal cord stimulation in pithed rats. The administration of atropine, a muscarinic receptor antagonist, also failed to inhibit cold-induced alterations in adrenal PNMT mRNA. These results suggest that the trans-synaptic induction of adrenal PNMT mRNA involves a non-cholinergic component, and that cold-induced increases in PNMT mRNA are not coupled to acetylcholine-mediated adrenal catecholamine release.

Adrenal Glands↗
PubMed1992

Gastric motility in conscious rats given oxytocin and an oxytocin antagonist centrally.

Previous experiments have shown that gastric motility is inhibited by microinjection of oxytocin (OT) into the dorsal motor nucleus of the vagus (DMN) in anesthetized rats, and that the inhibition of gastric motility after electrical stimulation of the hypothalamic paraventricular nucleus (PVN) is blocked by microinjection of an OT receptor antagonist directly into the DMN. As an extension of these observations, the present series of studies demonstrate that gastric motility in unanesthetized, freely moving rats was reduced both by intracerebroventricular (i.c.v.) administration of OT and by electrical stimulation of the PVN, and that both of these inhibitory effects were blocked by i.c.v. administration of an OT antagonist. Moreover, an OT antagonist administered i.c.v. alone caused an increase in baseline gastric motility. However, pretreatment with the same OT antagonist i.c.v. did not block the inhibitory effects of systemic LiCl or cholecystokinin on gastric motility in conscious rats. These results suggest that oxytocinergic neurons exert a tonic inhibitory effect on gastric motility in rats, but that the inhibitory effects of LiCl and cholecystokinin on gastric motility are not primarily mediated by parvocellular OT-containing neurons projecting from the PVN to the DMN.

Angiotensin Receptor Antagonists↗
PubMed1992

Cholecystokinin induces c-fos expression in hypothalamic oxytocinergic neurons projecting to the dorsal vagal complex.

Systemic administration of cholecystokinin (CCK) decreases gastric motility and stimulates pituitary secretion of oxytocin (OT). Although peripheral OT does not affect gastric function, increasing evidence suggests that central OT secretion acting within the dorsal vagal complex (DVC) can alter gastric motility. To evaluate whether systemically administered CCK is capable of activating oxytocinergic neurons projecting to the DVC, we utilized fluorogold retrograde labeling from the DVC in combination with c-fos and OT immunocytochemical staining to quantitatively analyze paraventricular nucleus (PVN) neurons of rats following injection of CCK at a dose known to cause maximal pituitary OT secretion (100 micrograms/kg i.p.). Our results showed that 2320 +/- 63 PVN neurons were retrogradely labeled from the DVC; 146 +/- 21 (6.3%) of these contained OT, and these cells were predominantly located in the medial parvocellular subdivision of the PVN. Of all retrogradely labeled cells, 671 +/- 112 (28.9%) expressed c-fos after CCK stimulation, and 68 +/- 14 of these (10.1%) contained OT. Approximately 50% of the OT-containing neurons retrogradely labeled from the DVC stained positively for c-fos. Many magnocellular OT neurons in the PVN that were not retrogradely labeled from the DVC also expressed c-fos after CCK stimulation. These results demonstrate that parvocellular OT neurons projecting to the DVC are co-activated along with magnocellular OT neurons projecting to the pituitary following administration of a large dose of CCK, and lend support to a possible functional role for OT as a central neurotransmitter that modulates vagal efferent traffic to the gastrointestinal tract.

Animals↗