Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Area Postrema”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 163 records · Page 9Linked to original sources
PubMed2004

Nicotinic modulation of area postrema neuronal excitability in rat brain slices.

We investigated the functions of nicotinic receptor activation on area postrema neurons by making whole-cell recordings in rat brainstem slices. Excitatory responses to nicotine application were found in approximately 78% (35/45) of all cells tested. Responsive cells included both the cells that display the hyperpolarization-activated cation current (I(h)) and cells that do not display I(h). An inhibitory effect of nicotine was never seen. Current-clamp recordings showed the nicotine-induced depolarization of a cell's membrane potential that could be sufficient to cause spontaneous firing. In voltage-clamp recordings, many cells showed nicotine-induced inward currents (18.3+/-3.2 pA, n=6) that persisted during pharmacological blockade of synaptic transmission (e.g., zero [Ca(2+)](out) and 5 mM [Mg(2+)](out), n=6/8). Other two cells, however, showed increases in the frequency of excitatory postsynaptic currents (EPSCs), which were blocked by CNQX (n=2/8). We analyzed miniature EPSCs (mEPSCs) recorded from cells that showed no inward currents but marked increases in the frequency of mEPSCs (0.8+/-0.2 to 4.8+/-1.7 Hz, n=4) during nicotine application. Nicotine augmented mEPSC amplitude (n=4); however, amplitude distribution was not significantly changed in two of four cells tested. We conclude that nicotinic receptors in the rat area postrema can excite cells via (1) a direct post- and/or extrasynaptic mechanism; and (2) an indirect enhancement of glutamate release.

6-Cyano-7-nitroquinoxaline-2,3-dione↗
PubMed1994

Deoxynivalenol (vomitoxin)-induced conditioned taste aversions in rats are mediated by the chemosensitive area postrema.

The present experiments used a conditioned aversion to a novel saccharin taste to assess the aversive effects of deoxynivalenol (vomitoxin) administration, and to examine the putative mediating role of the chemosensitive area postrema (AP). In experiment 1 adult male rats drank a novel 0.15% saccharin solution followed by injection of deoxynivalenol (n = 7; 0.125 mg/kg, IP) or vehicle (n = 7; propylene glycol, 0.5 ml/kg). In subsequent two-bottle preference tests the rats conditioned with deoxynivalenol displayed significantly (p < 0.01) lower absolute and relative saccharin intake levels in comparison to control rats which exhibited a strong preference for saccharin solution. In experiment 2 adult male rats received area postrema ablations (n = 6) or sham lesions (n = 6). On two conditioning days all rats drank a novel 0.15% saccharin solution followed by injections of deoxynivalenol (0.125 mg/kg, IP). In subsequent two-bottle preference tests the sham-lesioned rats displayed a significant (p < 0.01) aversion to the saccharin stimulus, relative to the area postrema-ablated rats which exhibited a preference for the saccharin solution. Thus, systemic administration of deoxynivalenol, following a novel taste, induced conditioned taste aversions which were mediated by the area postrema.

Animals↗
PubMed1987

Further studies on nicotine-induced emesis: nicotinic mediation in area postrema.

In unanesthetized cats the emetic action of an injection of nicotine into the cerebral ventricle through chronically implanted cannulae was investigated. Nicotine injected in doses of 0.02-1.0 mg produced dose-dependent vomiting, which was abolished after ablation of the area postrema. However, copper sulfate given intragastrically evoked vomiting in cats with an ablated area postrema. The emetic response to intracerebroventricular (ICV) nicotine as well as the vomiting produced by intragastric copper sulfate was depressed or abolished in cats pretreated with ICV reserpine. On the other hand, the emetic response to ICV nicotine and to intragastric copper sulfate was virtually unchanged in cats pretreated with ICV 6-hydroxydopamine and 5,6-dihydroxytryptamine. The duration of vomiting produced by intragastric copper sulfate, but not that of ICV nicotine, was potentiated in cats pretreated with hemicholinium-3. Ganglionic blocking agents, mecamylamine and hexamethonium, injected ICV prevented the vomiting elicited by ICV nicotine. On the other hand, selected anti-muscarinic drugs, alpha and beta adrenergic receptor antagonists, dopamine antagonists, antihistamines and a 5-hydroxytryptamine antagonist all injected into the cerebral ventricle had virtually no effect on the vomiting induced by ICV nicotine. It is postulated that nicotine evokes vomiting by its action on nicotinic receptors within the area postrema but not on catecholaminergic or serotonergic neurones. Finally, acetylcholine could also be involved in the inhibition of the complex mechanisms underlying the central regulation of vomiting.

Acetylcholine↗
PubMed1988

Development of the subfornical organ and area postrema of the male albino mouse. Karyometric effect of neonatal and prepuberal castration.

We have studied the karyometric development of the nuclei of the ependymal cells and neurons of the subfornical organ and the area postrema in the male albino mouse from the 5th to the 190th postnatal day. We have found similar patterns of development in both although the area postrema showed more significant postnatal oscillations than those of the subfornical organ, suggesting a more intimate chronological relationship to gonadal development. We have furthermore analyzed the development in two experimental groups: in the one animals were castrated at birth, in the other, castration was made on the 20th postnatal day. We have found that neonatal castration produced a significant decrease of nuclear sizes; this was more evident in the subfornical organ than in the area postrema in earlier stages of development while the response was similar in both at peripuberal ages. The response to prepuberal castration was similar in both organs.

Aging↗
PubMed1986

Dimethylphenylpiperazinium-induced vomiting: nicotinic mediation in area postrema.

In unanesthetized cats the emetic action of dimethylphenylpiperazinium (DMPP) was investigated, after it was injected into the cerebral ventricles through chronically implanted cannulae. DMPP injected in 0.2-2.0 mg doses into the cerebral ventricle produced dose-dependent vomiting, which was abolished after ablation of area postrema. However, copper sulfate given intragastrically evoked vomiting in cats with an ablated area postrema. Further, the emetic response to ICV DMPP and to intragastric copper sulfate was depressed or abolished in cats pretreated with ICV reserpine. The emetic response to ICV DMPP, but not that caused by intragastric copper sulfate, was potentiated in cats pretreated with ICV 5,6-dihydroxytryptamine. Ganglionic blocking agents, mecamylamine and hexamethonium, injected ICV prevented the vomiting elicited by ICV DMPP. On the other hand, selected anti-muscarinic drugs, alpha and beta adrenergic antagonists, dopamine antagonists, antihistamines and a 5-hydroxytryptamine (5-HT) antagonist all injected into the cerebral ventricles had virtually no effect on the vomiting induced by DMPP. It is postulated that DMPP evokes vomiting by its action on nicotinic receptors of nerve cells within the area postrema but not on catecholaminergic, serotonergic, or cholinergic receptors. Finally, 5-HT and acetylcholine could also be involved in the inhibition of the complex mechanisms underlying the central regulation of vomiting.

Adrenergic alpha-Antagonists↗
PubMed1995

The role of alpha-adrenergic mechanisms within the area postrema in dopamine-induced emesis.

Intracerebroventricular injection of dopamine (0.5-4.0 mg) produced dose-dependent and short-lasting emesis (1-8 min) in cats, which was abolished after ablation of the area postrema. Relatively selective alpha 2-adrenoceptor antagonists (yohimbine and idazoxan) and a mixed alpha 1- and alpha 2-adrenoceptor antagonist (tolazoline), but not a non-selective alpha 1-adrenoceptor antagonist (prazosin), injected intracerebroventricularly inhibited the emesis induced by intracerebroventricular dopamine. However, dopamine receptor antagonists (chlorpromazine, droperidol, spiperone, domperidone, triflupromazine, sulpiride and metoclopramide), an antimuscarinic drug (atropine), a ganglionic blocking agent (mecamylamine), an opioid receptor antagonist (naloxone) and a 5-HT receptor antagonist (methysergide), all injected intracerebroventricularly, had no significant effect on emesis evoked by intracerebroventricular dopamine. The emetic response to intracerebroventricular dopamine was attenuated in cats pretreated with intracerebroventricular reserpine, 6-hydroxydopamine, alpha-methyl-p-tyrosine and hemicholinium-3. It is postulated that dopamine-induced emesis is mediated through the release of noradrenaline acting at alpha 2-adrenoceptors and that it depends on the integrity of monoaminergic and possibly cholinergic structures within the area postrema. It appears, therefore, that the emetic effect of intracerebroventricular dopamine is mediated by adrenergic rather than dopaminergic mechanisms in the area postrema, at least in the cat.

Adrenergic alpha-Antagonists↗
PubMed1985

Inhibition of the response to pain by the action of serotonin and carbachol topically applied to the area postrema of conscious guinea pigs.

The amplitude of vocalization and the motor defense response evoked by painful electrical stimulation were recorded in unanesthetized guinea pigs submitted to topical application of 1.0 microgram/microliter carbachol to the area postrema. Carbachol was found to have an analgesic effect. A similar application of 3.0 micrograms/microliter 5-hydroxytryptamine (5-HT) also had an analgesic effect, whose duration, however, was only half that of carbachol and whose intensity was lower, although the latency of the response was 2 seconds for both drugs. When 100 micrograms/microliter lysergic acid was applied to the area postrema the results did not differ significantly from control values, with only a small tendency toward hyperalgesia being observed. The present results, taken together with those obtained with noradrenalin in a previous study, suggest that the rich endowment of neurotransmitters in the area postrema may indicate a polyvalent analgesic mechanism able to provide a finer regulation of analgesia.

Analgesia↗
PubMedDate not supplied

Effects of area postrema lesions on taste aversions produced by treatment with WR-2721 in the rat.

The conditioned taste aversion procedure was used to further assess some behavioral effects of treatment with the putative radioprotectant WR-2721 and the role of the area postrema in mediating the behavioral effects of treatment. Treatment with 40, 150 or 300 mg/kg WR-2721 produced dose-dependent changes in sucrose intake in both control rats and rats with area postrema lesions. The effectiveness of the lesion in disrupting the acquisition of an aversion varied as a function of the dose administered, with the lesions producing the greatest disruption of aversion learning at the lowest dose and little disruption at the highest dose tested. At all dose levels, sucrose intake was greater for the rats with area postrema lesions than for the sham-operated control rats. Treatment with WR-2721 also produced significant decreases in total fluid intake, particularly at the higher dose levels. The results are discussed as indicating that treatment with WR-2721 produces highly toxic effects on behavior and that the use of the compound as a radioprotectant for radiotherapy requires additional assessment of its effects on brain function and behavior.

Amifostine↗
PubMed1992

Area postrema mediation of physiological and behavioral effects of lithium chloride in the rat.

The area postrema (AP), a chemoreceptor trigger zone for nausea and vomiting, has been implicated in taste aversion conditioning with LiCl. In addition to taste aversion acquisition, the present studies indicate that a number of other responses to LiCl administration are eliminated by lesions of the AP. These include a behavioral response, 'lying-on-belly' as well as two physiological responses, delayed stomach emptying and hypothermia. These findings suggest that the area postrema is critically involved in the detection of LiCl and in a wide range of responses to this toxin. They also provide strong evidence that the failure to acquire conditioned taste aversions to LiCl-paired flavors after AP lesions can be attributed to the absence of a significant 'illness' response in lesioned animals.

Animals↗
PubMed1999

Role of AT1 receptors in area postrema on baroreceptor reflex in spontaneously hypertensive rats.

Intravenous injection of angiotensin II type 1 (AT1) receptor antagonist improves the baroreceptor reflex gain in spontaneously hypertensive rats (SHRs). To investigate the role of area postrema in the modulation of the baroreflex control by AT1 receptor, the effects of intravenous injection of CV-11974 (AT1 receptor antagonist) on the baroreflex control of renal sympathetic nerve activity (RSNA) and heart rate (HR) were examined in sham and area postrema-lesioned SHRs. The baseline mean arterial pressure was similar in both groups. However, baseline heart rate was significantly lower (p < 0.01) in area postrema-lesioned SHR than in sham-lesioned SHR, 307 +/- 11 and 365 +/- 10 beats/min (bpm), respectively. Intravenous CV-11974 (0.05 mg/kg) significantly decreased mean arterial pressure; however, it did not change HR and RSNA in either group. Reflex changes in RSNA and HR were elicited by intravenous infusion of either phenylephrine or sodium nitroprusside before and after intravenous injection of CV-11974. Intravenous CV-11974 increased baroreflex control of RSNA (Gmax; -1.57 +/- 0.08 vs. -1.92 +/- 0.12%/mmHg, p < 0.05) and HR (Gmax; -0.54 +/- 0.12 vs. 1.25 +/- 0.24 bpm/mmHg, p < 0.05) in sham-lesioned SHRs. However, intravenous CV-11974 failed to alter the baroreflex sensitivities in area postrema-lesioned SHRs. These results suggest that the area postrema does not play a crucial role in maintenance of high blood pressure in adult SHRs, and that the improvement of baroreflex control of RSNA and HR by intravenous CV-11974 is mediated via the area postrema in SHRs.

Angiotensin Receptor Antagonists↗
PubMed2004

Membrane-transport systems in the fenestrated capillaries of the area postrema in rat and calf.

The capillaries of the area postrema (AP) lack the morphological peculiarity of the blood-brain barrier (BBB), and the AP neurons are considered located outside the BBB. Using the immunofluorescent method, we have investigated the expression of membrane transport systems that are instrumental to the BBB function, such as caveolin-1, -2, P-glycoprotein, and glut-4, in the capillary endothelium of the rat and calf AP. The expression of these molecules was verified after fibronectin immunostaining of the microvessels. Both in the rat and calf, caveolin-1, -2, and P-glycoprotein were expressed in the AP capillaries. A quantitative analysis revealed that the proportion of the capillary profiles expressing these transport systems was very close to 100% of the fibronectin immunolabelled profiles. On the contrary, none of the AP capillaries showed glut-4 immunoreactivity. The present investigation demonstrates that the endothelial layer of the AP capillaries, in spite of the paracellular passage of polar molecules through the leaky tight junctions and fenestrations, could be an active interface which is able to control the entry of a wide range of blood-borne compounds into the brain by means of specific mechanisms, including an efflux pump.

ATP Binding Cassette Transporter, Subfamily B, Mem↗
PubMed2000

Observation of the ultrastructure and synaptic relationships of angiotensin II-like immunoreactive neurons in the rat area postrema.

The ultrastructure and synaptic relationships of the angiotensin II-containing neurons in the area postrema of the rat were studied by immunocytochemistry using the avidin-biotin-complex-DAB method, and also using silver-gold intensification following the DAB reaction. At the light microscopic level, the angiotensin II-like immunoreactive neurons were observed within the area postrema, especially in the upper region. At the electron microscopic level, the angiotensin II-like immunoreactive cell bodies were observed as having a round, unindented nucleus. The nuclei of these neurons were not immunostained. The angiotensin II-like immunoreactive axon terminals often contained a few dense core vesicles in addition to many small clear synaptic vesicles. Numerous axon terminals were found to make synapses on immunonegative dendrites; they were also found to make synapses on angiotensin II-like immunoreactive dendrites. Many angiotensin II-like immunoreactive dendrites received synapses from immunonegative axon terminals. Although angiotensin II-like immunoreactive cell bodies were sometimes postsynaptic to immunoreactive axon terminals, they did not receive synapses from immunonegative axon terminals. These results provide solid morphological evidence of AP endogenous angiotensin II and confirm that in spite of circulating angiotensin II, the local neurons in the AP may also play an important role in angiotensin II-induced cardiovascular regulation.

Angiotensin II↗
PubMed1986

Excitation of neurons in the canine area postrema by prostaglandins.

The effects of prostaglandins on electrical activity of neurons in the canine area postrema were studied using the techniques of extracellular recording with iontophoresis. Excitatory responses were obtained upon application of prostaglandins A1, B1, B2, E1, F1 alpha, and F2 alpha in between 24 and 50% of the cells studied. The excitation was very similar in pattern to that observed to apomorphine, biogenic amines, and several neuropeptides in that it had a relatively long latency, low maimal frequency, and prolonged duration. Since the area postrema is known to play a central receptive role in initiating emesis to circulating toxins, these results suggest that prostaglandins may play a role in the initiation of some forms of emesis.

Animals↗
PubMed1984

Area postrema lesions cause overconsumption of palatable foods but not calories.

Rats with lesions of the area postrema and immediately adjacent solitary nucleus consume greater amounts of highly palatable food during short exposures than do control rats. When a highly palatable substance (cookies or glucose solutions) is available continuously along with laboratory chow, lesioned rats exhibit average 24 hour calorie intakes which are not different from those of control rats. Nevertheless, the lesioned animals ingest a significantly greater proportion of total calories as the highly palatable substances than do control rats. The data suggest that lesions involving the area postrema and adjacent nucleus of the solitary tract enhance intake of highly palatable food without causing overconsumption of calories.

Animals↗
PubMed1980

The role of endogenous opiates in the area postrema pressor pathway.

1. Intra-vertebral artery-administered angiotensin II acts at the area postrema to facilitate central sympathetic vasomotor activity. Recent evidence suggests a possible role of the opiate system in the mechanism of action of angiotensin II at the level of the brain stem. 2. In these experiments, we show that the morphine antagonist naloxone reduces significantly the magnitude of the pressor response to vertebral artery-infused angiotensin II. 3. Morphine, in contrast, doubled the peak of the vertebral response to identical doses of the peptide. Neither naloxone nor morphine affected the pressor responses to intravenously administered angiotensin II. 4. The data suggest that the endogenous opiate system in the medulla modulates the cardiovascular effects of angiotensin II at the level of the area postrema.

Angiotensin II↗
PubMed1996

Role of area postrema in transgene hypertension.

Transgenic [Tg(+)] rats carrying the mouse Ren-2d gene [(mRen-2d)27] are a newly established monogenetic form of experimental hypertension. To determine whether the area postrema contributes to the development of hypertension in mRen-2 Tg(+) rats, this circumventricular organ in the fourth ventricle was removed from 5-week-old Tg(+) rats. From weeks 4 through 9, systolic blood pressure was measured weekly by tail-cuff plethysmography in area postrema-lesioned and sham-lesioned Tg(+) rats. Although systolic blood pressure rose markedly in sham-lesioned Tg(+) rats, the increase in systolic blood pressure was significantly attenuated in area postrema-lesioned Tg(+) rats. At 9 weeks of age, a femoral artery was cannulated for the measurement of arterial pressure in awake rats. Mean arterial pressure (MAP) in area postrema-lesioned Tg(+) rats was significantly (P < .01) lower than that in sham-lesioned rats: 171 +/- 7 and 132.+/- 5 mm Hg, respectively. Baroreceptor reflex was evaluated by intravenous infusion of sodium nitroprusside. There was no significant difference in baroreceptor reflex sensitivity between the two groups. Intravenous pentolinium (5 mg/kg), used to produce sympathetic ganglionic block, caused significant decreases in MAP in both groups. However, the reduction of MAP in the sham-lesioned group was significantly (P < .05) greater than that in the area postrema-lesioned group: -73 +/- 4 and -48 +/- 6 mm Hg, respectively. The ratio of left ventricular weight to body weight in sham-lesioned Tg(+) rats was significantly larger than that of area postrema-lesioned rats. These results suggest that ablation of the area postrema markedly attenuates the development of hypertension in mRen-2d Tg(+) rats, and this attenuation may be attributed to decrease in sympathetic outflow.

Animals↗
PubMed1996

Glucagon-like peptide I receptors in the subfornical organ and the area postrema are accessible to circulating glucagon-like peptide I.

The intestinal incretin hormone glucagon-like peptide I (GLP-I) inhibits gastric motility and secretion in normal, but not in vagotomized subjects, pointing to a centrally mediated effect. Therefore, our aim was to study the availability of rat brain GLP-I receptors to peripherally injected 125I-labeled GLP-I. The specificity of the binding was tested by co-injection of excess amounts of unlabeled GLP-I. Using light microscopical autoradiography of rat brain sections, we found specific 125I-GLP-I binding exclusively in the subfornical organ and the area postrema. This binding was abolished when an excess amount of unlabeled GLP-I was co-injected with the labeled GLP-I. We conclude that cells in the subfornical organ and the area postrema could be responsive to blood-borne GLP-I. The observed binding of peripherally administered GLP-I to the subfornical organ and the area postrema, which both have close neuroanatomical connections with hypothalamic areas involved in water and appetite homeostasis, is consistent with the potential roles of circulating GLP-I in the central regulation of appetite and autonomic functions.

Animals↗
PubMed1986

The functional and structural borders between the CSF- and blood-dominated milieus in the choroid plexuses and the area postrema of the rat.

In the borderline area between the hemal milieu of the choroid plexuses (PC) and the interstitial cerebrospinal-fluid (CSF) compartment, ground substances displaying increased amounts of basal lamina-like material and containing negatively charged sulfated glycosaminoglycans appear to be endowed with selective properties. They may function as a sieve or filtration barrier gradually controlling the passage of substances between the two milieus, depending on their charge and molecular weight. Special structural features and functional properties of ependymal cells are associated with such bordering structures. These ependymal cells are transitional elements between choroid epithelium and ciliated ependymal cells. As judged from experiments with horseradish peroxidase and conventional electron microscopy, occluding junctions at the basal pole of these cells prevent a rapid alteration in the milieu conditions, enabling gradual change from hemal to CSF composition near the bases of these transitional ependymal cells. The borderline structures between the hemal milieu of the PC and the area postrema are established by leptomeningeal cells which face a hemal milieu, are endowed with conspicuous tight junctions, and produce a flocculent substance, the light-microscopic equivalent of which is PAS positive. These structures probably establish an effective barrier between the two milieus of different composition. The functional characteristics and the morphology of the meningeal cells facing the hemal milieu of neurohemal regions resemble closely the neurothelial cells, which are interposed between the CSF milieu and the hemal milieu in the dura mater. The present results suggest that the location between the hemal and the CSF milieu is decisive for the transformation of leptomeningeal cells into "neurothelial" elements.

Animals↗