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 127 records · Page 7Linked to original sources
PubMed1978

[Vascularization and glial structures of the area postrema in sheep (Ovis aries) (author's transl)].

The area postrema of the sheep (Ovis aries) reveals the typical position and structure as seen in the domestic animals. The fetal development of the organ concerning especially the vascularization does not give any reference to a phylogenetic connection with the area postrema of birds. The glial border of the organ ist strikingly marked by the funiculus separans, which seems to be lacking in other domestic animals.

Animals↗
PubMed2000

P2X(2) receptor immunoreactivity in the dorsal vagal complex and area postrema of the rat.

Adenosine 5'-triphosphate (ATP) can function as a fast synaptic transmitter through its actions on ionotropic (P2X) and metabotropic (P2Y) receptors in neuronal tissue. The ionotropic receptors have been classified into seven subtypes (P2X(1)-P2X(7)) by molecular cloning. However, they are difficult to distinguish pharmacologically owing to an absence of specific agonists and antagonists. In this study we used neuroanatomical methods to determine the origin and neurochemical phenotype of the P2X(2) subtype of purinoceptor in the dorsal medulla of the rat. Using immunohistochemistry we observed dense networks of P2X(2) receptor immunoreactive labelled fibres and terminals in the dorsal vagal complex and area postrema, as well as labelled cell bodies in the dorsal vagal nucleus and the area postrema. The P2X(2) receptor was localized presynaptically in vagal afferent fibres and terminals in the nucleus tractus solitarius at the ultrastructural level by combining injections of an anterograde tracer (biotin dextran amine) into the nodose ganglion with pre-embedding immunogold visualization of P2X(2) immunoreactivity. Terminals immunoreactive for the P2X(2) receptor in the nucleus tractus solitarius were found to contain glutamate, but not GABA immunoreactivity by post-embedding immunogold-labelling techniques. In cell bodies in the area postrema, dual immunofluorescence also indicated that P2X(2) receptor immunoreactive cells are glutamatergic but not GABAergic. The P2X(2) receptor was localized to vagal preganglionic neurons in the dorsal vagal nucleus that were identified by prior intraperitoneal injections of the retrograde tracer FluoroGold. No cells immunoreactive for the P2X(2) receptor were observed in the nucleus tractus solitarius. The localization of P2X(2) receptor immunoreactivity presynaptically in vagal afferent terminals indicates that the receptor may be involved in modulating transmitter release from vagal afferent fibres. Furthermore, the presence of the P2X(2) receptor in vagal preganglionic cells and in glutamatergic cells of the area postrema implies that it may, respectively, play a role in regulation of vagal efferent cell activity and modulation of excitatory outputs from the area postrema to other brain regions.

Animals↗
PubMed2004

The distribution of mast cells in the human area postrema.

The topography and phenotype of mast cells in the human area postrema, together with correlation between mast-cell density and microvessel density (MVD), were analysed in 16 brains. Transverse serial sections of formalin-fixed, paraffin-embedded brainstems were stained with toluidine blue and alcian blue/safranin stainings, and with anti-tryptase and anti-CD31 monoclonal antibodies. The mean (+/- SD) numbers of mast cells per section were 1.3 +/- 0.8 and 1.2 +/- 0.7 with toluidine blue and alcian blue/safranin, respectively, whereas anti-tryptase monoclonal antibody showed a mean of 5.1 +/- 2.4 cells. Mast cells were alcian blue- and safranin-positive in 56%, because of the coexistence of low-sulphated (blue-staining) and high-sulphated (red-staining) granules. No significant linear correlation between mast-cell density (4.9 mm(-2)) and MVD (114.5 mm(-2)) was found (r(2) = 0.19, P = 0.09). Mast cells were frequently located close to blood vessels (55%) (33% to venules, 22% to arterioles), indicating that their products play a role in the regulation of blood flow and in vessel permeability in the area postrema. Mast cells were located subependymally in 44% and close to the dorsal aspect of the nucleus of the tractus solitarius in 31%, suggesting a subregional distribution.

Alcian Blue↗
PubMed1991

Efferent metabolic effects of area postrema stimulation in renal hypertensive rats.

Electrical microstimulation of area postrema in anesthetized normotensive (NR) and renal hypertensive (RHR) rats produced increases of about 53% in rates of glucose metabolism in nucleus tractus solitarii and dorsal motor nucleus of the vagus nerves. However, in nucleus ambiguus, ventrolateral medullary C1 region, locus coeruleus, and lateral parabrachial nucleus, all of which are monosynaptically innervated by area postrema neurons, metabolic responsiveness to postremal stimulation was considerably attenuated in RHR (average increase of 16%) compared to the same structures in NR (average increase of 36%). Disturbances of brainstem neurotransmission or tissue reactivity to postremal pathway activation thus appear to be part of the central pathophysiology of chronic renal hypertension.

Animals↗
PubMed1987

Higher density of 125I-neuropeptide Y receptors in the area postrema of SHR.

125I-Neuropeptide Y (125I-NPY) binding capacities were quantitated in the areas postrema of young (5 weeks) and adult (20 week SHR and compared with age-matched WKY rats using autoradiography. The maximum binding capacity (Bmax) was significantly higher in the area postrema of adult SHR, while no difference was seen at the age of 5 weeks. Our result supports the idea of a functional role for NPY receptors in the central control of blood pressure. NPY receptors in the area postrema may be involved in the perception of circulating NPY resulting in the alteration of the neuronal activity of the nucleus tractus solitarii.

Age Factors↗
PubMed2000

Vasopressin and oxytocin release evoked by NaCl loads are selectively blunted by area postrema lesions.

The present study investigated the effect of area postrema lesions (APX) on stimulated neurohypophysial secretion of vasopressin (VP) and oxytocin (OT) in conscious rats. Blunted increases in plasma levels of both pituitary hormones were observed when rats with APX were infused intravenously with 1 M NaCl solution (2 ml/h for 6 h). In contrast, plasma VP and OT increased normally in rats with APX when equivalent increases in plasma osmolality (but not plasma Na(+)) resulted from intravenous infusion of an equiosmotic solution of 1 M mannitol and 0.5 M NaCl. Furthermore, APX did not affect increases in plasma VP and OT stimulated by plasma volume deficits, nor did APX disrupt OT secretion stimulated by intravenous injection of cholecystokinin. These findings suggest that the area postrema plays an important role in mediating secretion of VP and OT in response to an NaCl load, but not in response to an equiosmotic load that does not cause substantial hypernatremia, and not in response to other stimuli of neurohypophysial hormone secretion. Together with previous reports, these results suggest that APX impairs Na(+) regulation in rats.

Animals↗
PubMed1985

Interactions of vasopressin with the area postrema in arterial baroreflex function in conscious rabbits.

This study compares the effect of arginine-vasopressin with phenylephrine on arterial pressure, heart rate, and renal sympathetic nerve activity in conscious rabbits with and without functional arterial baroreflexes and in rabbits with lesions of the area postrema. In intact rabbits, progressive infusions of arginine-vasopressin result in large decreases in renal sympathetic nerve activity and heart rate for a given increase in blood pressure as compared to progressive infusions of phenylephrine. In sinoaortic-denervated rabbits, the responses of arterial pressure on heart rate and renal sympathetic nerve activity to both arginine-vasopressin and phenylephrine are markedly attenuated, indicating the necessity for afferent baroreceptor activity in this response. This observation indicates that arginine-vasopressin is acting centrally to enhance the baroreflex. A central site of action of circulating vasopressin may be the area postrema, since it is the only circumventricular organ in the hindbrain. Lesioning the region of the area postrema resulted in a normalization of the responses evoked with arginine-vasopressin and phenylephrine. There was no difference in the phenylephrine responses of arterial pressure on renal sympathetic nerve activity or heart rate in area postrema-lesioned animals, compared to control rabbits. Therefore, we conclude that the area postrema or its surrounding tissue is either a site of action of circulating arginine-vasopressin or contains fibers of passage from another site where arginine-vasopressin acts to enhance baroreflex activity.

Animals↗
PubMed1980

The antiaggressive effect of lithium is abolished by area postrema lesion.

Lithium (Li) suppresses intraspecific aggression in rats and other mammals. However, antiaggressive doses of Li have been shown to produce signs of illness and to serve as an unconditioned stimulus for conditioned taste aversions (CTA). Therefore, it is possible that the antiaggressive effects of Li result from Li-induced malaise. Malaise and CTA's produced by some drugs and toxins are mediated by chemoreceptors in the area postrema. In this paper we report [1] that thermal lesion of the area postrema abolishes Li's ability to condition taste aversions and [2] that area postrema lesion abolishes the antiaggressive effect of Li as measured by attack latency in a shock-induced aggression test. Taken together, these findings suggest that some or all of Li's antiaggressive action in rats may result from malaise attributable to Li's action on the area postrema.

Aggression↗
PubMed1981

Specific binding and internalization of blood-borne [125I]-iodoinsulin by neurons of the rat area postrema.

The specificity and cellular location of binding sites for blood-borne [125I]iodoinsulin in the area postrema and adjacent paravagal region of the rat brain was determined by means of quantitative light and electron microscope radioautography. In both regions coinjected unlabeled insulin inhibited the binding of [125I]iodoinsulin in a dose-dependent manner, and insulin analogs blocked [125I]iodoinsulin binding in rank order of their known in vitro bioactivity. Electron microscope radioautography of this region showed that insulin specifically bound to neuronal dendrites and cell bodies and that some of the specifically bound radioactivity was internalized and concentrated in a variety of subcellular vacuoles. These observations demonstrate that certain neurons of the area postrema are endowed with the receptive capacity common to all known insulin-sensitive cells. Anatomic considerations suggest that insulin target neurons in the area postrema could mediate insulin feedback on parasympathetic function by relaying information regarding circulating insulin status to central autonomic circuits governing vagal activity. This study represents the first demonstration of a receptor-mediated uptake and concentration of a blood-borne polypeptide hormone by central neurons.

Animals↗
PubMed2002

Electrophysiological properties of the rat area postrema neurons displaying both the transient outward current and the hyperpolarization-activated inward current.

We found coexistence of the transient outward potassium current (I(TO)) and the hyperpolarization-activated inward current (I(H)) in 26 of 82 area postrema neurons tested using the whole-cell patch-clamp technique in rat brain slices. Cells displaying both the I(TO) and the I(H) typically showed "voltage sag" and "rebound potentials" in response to hyperpolarizing current injection and repetitive firing with strong adaptation was seen with depolarizing current injection. When cells were held at membrane potentials more negative than the resting level (e.g., -85mV), the afterhyperpolarization was enhanced. Voltage clamp recordings were performed to examine the characteristics of I(TO) and I(H) in and the contributions of these currents to the electroresponsiveness of area postrema cells. We show, in this study, the voltage-dependent properties of I(H) and I(TO), and how these currents modulate the intrinsic membrane properties of area postrema cells. We discuss the functional significance of the specific subset of area postrema neurons whose cells have both I(H) and I(TO) channels.

Action Potentials↗
PubMed1985

Perfusion-induced oedema does not disrupt perivascular glial sheaths in the rat area postrema: evidence for an inconspicuous type of cell junction?

After perfusion fixation using phosphate-buffered glutaraldehyde, the rat area postrema always contained some portions with lacunar extracellular spaces in the neuropil. This was interpreted as a sign of local oedema due to perfusion-induced extravasation, made possible by the absence of an endothelial blood-brain barrier in the area postrema. All perivascular spaces were delimited from the nervous tissue by a continuous layer of astroglial processes. The cell appositions in these perivascular glial sheaths were not only seen in the regions of the area postrema displaying conventional morphology, but also persisted systematically in those regions containing lacunar extracellular space after fixation. At these sites, the glial sheaths had presumably endured a net outflow of extravasated oedema fluid in vivo. In the neighbouring neuropil at these locations, certain cell appositions with conventional intercellular clefts also persisted. These phenomena might both be interpreted as non-random, functionally important cell contacts with the inconspicuous 'intercellular clefts' containing unstained material. In the case of perivascular glia this might imply a partial restriction of diffusion between blood and brain tissue, allowing certain control or defence functions.

Animals↗
PubMed1990

Metabolic activation of efferent pathways from the rat area postrema.

We used the quantitative [14C]deoxyglucose method and autoradiography to evaluate metabolic activity in 47 individual cerebral structures or subregions that are part of neural pathways emanating from the brain stem circumventricular organ, area postrema. Electrical stimulation of the dorsocentral area postrema in halothane-ventilated rats produced hypotension and increased glucose metabolism by several structures within the ascending trajectories of efferent neural projections from the nucleus. Structures in the caudal medulla oblongata, including three subnuclei of the nucleus of the solitary tract, dorsal motor nucleus of the vagus nerve, and nucleus ambiguus-A1 noradrenergic region, had increases of metabolism during stimulation of 32-62%. Pontine activation occurred specifically in the locus coeruleus and lateral parabrachial nuclei (increases of 24-36%). Magnocellular and parvocellular subdivisions of the hypothalamic paraventricular nucleus, supraoptic and suprachiasmatic nuclei, and median eminence showed increases in metabolism of 22-34%. An 89% elevation of glucose metabolism by the pituitary neural lobe resulted. The findings are evidence for functional activation of specific structures within ascending neural pathways from area postrema to forebrain mechanisms regulating blood pressure and fluid balance.

Animals↗
PubMed2006

Inhibitory synaptic transmission in area postrema neurons of the rat showing robust presynaptic facilitation mediated by nicotinic ACh receptors.

Inhibitory synaptic transmission and its modulation in neurons of the area postrema (AP), one of autonomic nuclei in the medulla, were studied using whole-cell patch-electrodes applied to slices from rats on postnatal days 10-24. When glycine (100 microM) or GABA (10 microM) was applied to AP neurons from a "Y tube", large outward currents that showed reversal potential of - 67 mV (approximate Cl- equilibrium potential estimated) were induced. At a holding potential of - 10 mV, application of high K+ to the AP neurons evoked massive inhibitory postsynaptic currents (IPSCs) in the neurons. Most of the evoked synaptic currents were blocked by bicuculline, while the remaining currents were sensitive to strychnine, indicating that the major inhibitory transmission in the area postrema was GABAergic. When nicotine (5-100 microM) was applied to AP neurons, robust IPSCs having GABAergic identity were evoked. Even in the presence of tetrodotoxin, nicotine could induce GABAergic IPSCs, most of which, however, disappeared in the presence of 5 mM Mg2+. Presynaptic facilitation was also induced by other nicotinic agonists, including cytisine, 1,1-dimethyl-4-phenyl-piperazinium iodide, ACh and choline. The nicotine-induced presynaptic facilitation was inhibited by mecamylamine and slightly inhibited by dihydro-beta-erythroidine or alpha-Bungarotoxin. These results indicate that nicotinic receptors are expressed at GABAergic presynaptic terminals in the area postrema and induce Ca2+ influx to trigger vesicular release. The major nicotinic receptors involved are thought to be heteromeric subtypes such as alpha3beta4 receptors, which may regulate inhibitory transmission potently responding to endogenous or exogenous nicotinic agents appeared in this area.

Animals↗
PubMed1973

Cellular localization of the uptake of 5-hydroxytryptamine in the area postrema of the rabbit after injection into a lateral ventricle.

1. The cellular localization of 5-hydroxytryptamine (5-HT) was investigated in the area postrema of the rabbit after intraventricular injection under different experimental conditions.2. 5-HT was found to be accumulated in different parts in and near to the area postrema, e.g. in glial cells, dorsal surface of the area postrema and ependyma of the central canal.3. The concentrations of 5-HT and 5-hydroxy indol-3-yl acetic acid (5-HIAA) were measured in different parts of the brain and CSF in control and in 5-HT treated animals with and without pargyline pretreatment. Intraventricular injection of 5-HT increased the concentration of 5-HT and 5-HIAA in the brain and in the CSF; pretreatment with pargyline further increased the concentrations of 5-HT but decreased the concentration of 5-HIAA.

Animals↗
PubMed2004

Activation of presynaptic 5-HT3 receptors facilitates glutamatergic synaptic inputs to area postrema neurons in rat brain slices.

Whole-cell voltage-clamp recordings were performed to investigate the serotonergic modulation of neurotransmitter release onto rat area postrema neurons in vitro. The bath application of serotonin (5-HT; 50 microM) or phenylbiguanide (PBA; 50 microM), a potent 5-HT3 receptor agonist, increased the frequency of spontaneous excitatory postsynaptic currents (sEPSCs) or miniature EPSCs (mEPSCs) in 35 of 83 neurons (42%). These increases occurred in all electrophysiological cell classes. No cells exhibited a decrease in EPSC frequency. The majority of responding cells showed no inward currents during the application of serotonergic agonists (n = 34/35). However, the amplitude of mEPSCs was increased in 11/11 cells with 5-HT or 3/11 cells with PBA. ICS-205,930, a potent 5-HT3 receptor antagonist, markedly suppressed the 5-HT-induced facilitation of sEPSCs (n = 5) or mEPSCs (n = 5). An increase in the frequency of mEPSCs after PBA exposure was found, even with media containing Cd2+ (50 microM) or zero Ca2+. mEPSCs and evoked EPSCs were completely blocked in media containing the non-NMDA ionotropic receptor antagonist, CNQX (10 microM), indicating that EPSCs were glutamate events. These results suggest that glutamate release is increased in the area postrema by presynaptic 5-HT3 receptor activation. Furthermore, we present evidence that 5-HT3 receptor activation may be able to directly release glutamate from terminals, bypassing a requirement for voltage-dependent calcium entry into terminals. Such a mechanism may contribute to the chemosensitive function of area postrema neurons.

6-Cyano-7-nitroquinoxaline-2,3-dione↗
PubMed1987

Interaction of vasopressin with area postrema during volume expansion.

Effects of arginine vasopressin (AVP) on inhibition of renal sympathetic nerve activity (RSNA) during activation of cardiopulmonary reflexes by volume expansion were examined in conscious sinoaortic-denervated rabbits. The role of the area postrema in mediating these effects was also evaluated in rabbits subjected to area postrema lesion. Animals were subjected to 12% volume expansion with whole blood alone or during infusion of AVP (0.6 mU . kg-1 . min-1). Volume expansion in area postrema-intact animals caused a progressive reflex inhibition of RSNA (maximum = -36.5 +/- 3.3% delta RSNA). Vasopressin infusion did not significantly alter resting arterial pressure, right atrial pressure, heart rate, or RSNA. However, maximum inhibition of RSNA during volume expansion (-62.6 +/- 3.2% delta RSNA) was significantly augmented during AVP infusion, and the augmentation was reversed by a specific vascular (V1) AVP receptor antagonist. Vagotomy eliminated RSNA responses to volume expansion with or without AVP. In area postrema-lesioned animals, the RSNA response to volume expansion was similar to that of intact animals (-31.8 +/- 2.3% delta RSNA). However, AVP did not augment the RSNA response to volume expansion in lesioned animals (-30.4 +/- 2.5% delta RSNA). Thus exogenous AVP augmented cardiopulmonary reflex-mediated inhibition of RSNA due to volume expansion. This effect appeared to be mediated by the V1 AVP receptor and to require the presence of an intact area postrema.

Animals↗
PubMed2006

ANG II-induced hypertension and the role of the area postrema during normal and increased dietary salt.

It has been shown that the area postrema (AP) plays a role in the development of certain types of chronic angiotensin II (ANG II)-induced hypertension in the rat but is not of great importance in the salt sensitivity of arterial pressure. It has recently been proposed, however, that elevated sodium levels may exacerbate the hypertensive effects of ANG II, which by itself dramatically affects salt sensitivity, by acting at sodium-sensing neurons in certain circumventricular organs of the brain. Thus the interactions of ANG II, sodium, and the central nervous system remain to be fully understood. The purpose of this study was to examine the role of the AP in ANG II-induced hypertension during periods of normal and elevated dietary salt. We hypothesized that an intact AP was necessary for the full development of hypertension under chronic ANG II infusion and that its role would be pronounced during periods of increased dietary sodium. To test this, male Sprague-Dawley rats underwent ablation of the area postrema (APx, n = 6) or sham operation (sham, n = 6). After 3 wk of recovery, rats were instrumented with radiotelemetry transducers for constant blood pressure and heart rate monitoring and venous catheters for vehicle infusion. After a 3-day control period of 0.9% saline infusion (7 ml/day) and 0.4% dietary sodium, a 10-day period of ANG II infusion (10 ng.kg(-1).min(-1)) was begun, immediately followed by a second 10-day period during which rats were fed a 4.0% sodium diet. By day 6 of ANG II infusion, mean arterial pressure (MAP) in APx rats had increased to 139 +/- 4 mmHg, whereas MAP in sham rats had increased to 126 +/- 3 mmHg. This difference was found to be significant and continued through day 1 of the high-salt period, after which MAP of the two groups had risen to similar levels. On day 9 of high salt, MAP was again observed to be significantly higher (162 +/- 1 mmHg) in APx rats when compared with sham rats (147 +/- 4 mmHg.) These results do not support the hypothesis that the AP is necessary for the full development of ANG II-induced hypertension at normal or elevated levels of dietary sodium.

Angiotensin II↗
PubMed1984

Area postrema: site where cholecystokinin acts to decrease food intake.

Administration of cholecystokinin (CCK) reduces food intake in rats. This effect of CCK was attenuated in rats with thermal lesions of the area postrema. This result was specific to CCK, as area postrema lesions had no effect on the reduction in food intake produced by amphetamine. The effect of the lesions was not due to changes in taste sensation as the lesioned rats showed no deficits in morphine induced conditioned taste aversions. Thus, the area postrema may be the major site where CCK acts to decrease food intake.

Analysis of Variance↗