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PubMed1986

Actions of angiotensin on area postrema of the rat.

Previous studies have reported that rats drink more saline after area postrema has been removed. The results presented here indicate that prolonged administration of angiotensin II into area postrema of unrestrained rats at 4 pmol/h also caused them to drink more saline. They drank more when angiotensin was released in the anterolateral part of the organ than when it was released anteromedially. Diurnal variation of drinking was not disordered. Dose-response curves showed that rats lacking area postrema drank more saline in response to systemic angiotensin than sham operated animals. The very large 'spontaneous' consumption of saline by rats lacking area postrema was not diminished by saralasin, an angiotensin antagonist. It is concluded that area postrema is a site where systemic angiotensin can act to promote sodium consumption: and that although removing area postrema increases the sensitivity of the drinking response to systemic angiotensin, this enhanced sensitivity is not the cause of the increased sodium consumption.

Angiotensin II↗

PubMed1987

A comparison of GABA- and GAD-like immunoreactivity within the area postrema of the rat and cat.

The immunohistochemical localization of gamma-aminobutyric acid (GABA) was compared to that of glutamate decarboxylase (GAD) in the rat and cat area postrema with the aid of a polyclonal antibody produced in rabbits directed against GABA. In both the rat and cat, dense and very dense accumulations of GABA-like immunoreactive (GABA-LI) varicosities were present throughout the area postrema. GABA-LI cell bodies were present in both species and were evenly distributed throughout the area postrema's extent. However, the rat area postrema contained more GABA-LI cell bodies and varicosities than the cat area postrema. In the cat area postrema, a range of cell sizes were immunostained with the GABA antibody. The GAD antibody, however, failed to reveal cell bodies in the area postrema of the cat, thus indicating that the GABA polyclonal antibody may be a better indicator of GABA-containing somata. Although the mechanism of action of GABA in the area postrema is not understood, it is possible that GABA may play a role in the different functions of the area postrema in emetic and nonemetic species.

Animals↗

PubMed1999

AMPA receptor activation of area postrema neurons.

This study reports on the effects of activation of ionotropic glutamate receptors on area postrema neuron cytosolic calcium concentration ([Ca2+]i). In 140 of 242 area postrema neurons isolated from postnatal rats, application of 100 microM L-glutamate (L-Glu) resulted in a significant increase in [Ca2+]i. The remaining neurons were unaffected. The effects of L-Glu on area postrema [Ca2+]i were dose dependent, with a threshold of response near 1.0 microM and maximal response near 100 microM. To determine if the response of L-Glu in area postrema neurons was due to activation of ionotropic glutamate receptors, the effects of the broad-spectrum ionotropic glutamate receptor antagonist kynurinic acid (Kyn) was determined. Application of 1.0 mM Kyn resulted in a 62.6 +/- 4% inhibition of the L-Glu-evoked response. Application of the selective N-methyl-D-aspartic acid (NMDA) antagonist 2-amino-5-phosphonopentanoic acid had no effect on the response of area postrema neurons to 100 microM L-Glu. In contrast, application of the selective DL-alpha-amino-3-hydroxy-5-methylisoxazole-propionic acid (AMPA)/kainate receptor antagonist 6,7-dinitroquinoxaline (DNQX) effectively blocked the 100 microM L-Glu response. Application of (+/-)-AMPA mimicked the effects observed with L-Glu and was selectively blocked by DNQX. These results suggest that L-Glu activation of area postrema neurons involves activation of AMPA receptors but not NMDA receptors.

2-Amino-5-phosphonovalerate↗

PubMed1994

Food aversion induced by area postrema ablation.

Rats with lesions of the area postrema (APX rats) avoid foods ingested on a regular basis during the period of severe hypophagia immediately following surgery (Tomoyasu & Kenney, 1989). The present work determined whether APX rats would also avoid foods to which they are exposed only after they have recovered from the lesion-induced hypophagia. APX and SHAM-lesion rats were fed a novel food for 8 days beginning at least 1 month after surgery when food intakes (adjusted for body weight) and weight gains of the APX rats had returned to control levels. During 24 h, two-food choice tests, APX rats avoided the food ingested a month after the ablation while avidly ingesting an alternative food, but SHAM rats showed no preference between the foods. There was no indication that this aversion developed by APX rats to foods ingested after recovery from hypophagia is weaker than that developed to foods ingested immediately after the lesion. We conclude that area postrema ablation results in the development of an unconditioned stimulus capable of supporting food-aversion conditioning which remains effective more than 1 month after the ablation. Hence, the relationship between APX-induced food aversion and hypophagia must be indirect and complex. Also, conditioning of food aversions induced by area postrema ablation alone may confound studies of the role of this structure in mediating the development of food aversions after other physiological and/or pharmacological manipulations.

Animals↗

PubMed1994

The relationship of efferent projections from the area postrema to vagal motor and brain stem catecholamine-containing cell groups: an axonal transport and immunohistochemical study in the rat.

The area postrema has been implicated as a major station for the processing of visceral sensory information, involved primarily in eliciting rapid homeostatic responses to fluid and nutrient imbalances. Yet the precise relationship of efferent projections from the area postrema to medullary motor and relay nuclei involved in such functions remains unclear. In this study, axonal transport and immunohistochemical techniques were used to investigate the relationship of efferent projections from the area postrema to vagal motor neurons and medullary catecholamine-containing cell groups in the rat. The results may be summarized as follows: (1) The area postrema gives rise to dense inputs to the commissural and medial parts of the nucleus of the solitary tract. Many of these projections are intimately associated with catecholamine-containing neurons in the A2 and C2 cell groups, including a particularly prominent input to a caudally placed cluster of adrenergic neurons (the C2d cell group) in the dorsal aspect of the medial part of the nucleus of the solitary tract. (2) The area postrema provides a dense input to the external lateral part of the parabrachial nucleus. (3) The area postrema does not project significantly to vagal motor neurons in either the dorsal motor nucleus or the nucleus ambiguus, although the possibility for inputs to distal dendrites of dorsal vagal motor neurons cannot be excluded. (4) En route to the parabrachial nucleus, axons of area postrema neurons traverse the regions of the A1, C1 and A5 cell groups, although these fibers make few arborizations, suggesting little functional contact. Together, these results suggest that sensory information received by the area postrema is dispatched to a restricted set of neurons in the commissural, medial, and dorsal parts of the nucleus of the solitary tract, most probably including catecholamine-containing cells in the A2, C2, and C2d cell groups, and to the external lateral portion of the parabrachial nucleus. The targets of area postrema projections are, in turn, in a position to effect adaptive changes in the activities of hypothalamic neurosecretory neurons, vagal motor neurons, and limbic forebrain regions in response to perturbations in fluid and nutrient homeostasis.

Animals↗

PubMed1988

Role of the area postrema in three putative measures of motion sickness in the rat.

After thermal cauterization of the area postrema in rats the absence of conditioned taste aversion to sucrose paired with lithium chloride (0.15 M, 3.3 ml/kg) was used as a pharmacologic/behavioral index of area postrema damage. In a subsequent experiment the effects of area postrema lesions on three measures proposed as species-relevant measures of motion sickness were studied, using off-vertical rotation at 150 degrees/s for either 30 or 90 min. Lesions of area postrema did not alter postrotational suppression of drinking or amount of defecation during motion. The initial acquisition of conditioned taste aversion to a novel cider vinegar solution paired with motion was not affected by lesioning of the area postrema, but these taste aversions extinguished more slowly in lesioned rats than in sham-operates or intact controls. Results are discussed in terms of proposed humoral factors which may induce motion sickness and in light of recent data on the role of the area postrema in similar measures in species possessing the complete emetic reflex.

Animals↗

PubMed1991

Stimulation of area postrema decreases blood flow to choroid plexus.

The goal of this study was to examine effects of stimulation of the area postrema on blood flow to choroid plexus and brain. In chloralose-anesthetized dogs, the area postrema was stimulated electrically, and arterial pressure and blood gases were maintained at control levels. We measured blood flow to brain and choroid plexus of the fourth and lateral ventricles with microspheres. Stimulation of the area postrema at 10 +/- 2 microA (means +/- SE), which was the threshold for changes in arterial pressure and heart rate, decreased blood flow to choroid plexus of the fourth and lateral ventricles by 41 +/- 11 and 51 +/- 6%, respectively (from 349 +/- 38 and 503 +/- 46 ml.min-1.100 g-1, respectively). Stimulation at high amplitudes (67 +/- 5 microA) produced only slightly greater decreases in blood flow to choroid plexus. In contrast, cerebral blood flow did not change during stimulation of the area postrema. After blockade of autonomic ganglia with intravenous chlorisondamine, stimulation of the area postrema had minimal effects on blood flow to choroid plexus. The results indicate that stimulation of the area postrema decreases blood flow to choroid plexus, probably by an autonomic mechanism. We speculate that the area postrema may play a role in regulation of volume in the central nervous system by modulating production of cerebrospinal fluid.

Animals↗

PubMed1986

Insulin excites neurons of the area postrema and causes emesis.

Responses of neurons of the canine area postrema were recorded to ionophoretic application of insulin, apomorphine, leucine-enkephalin and glutamate. Each excited the neurons directly in a dose-dependent fashion. Like apomorphine and leucine enkephalin, which are known to induce emesis by activation of area postrema neurons, insulin given systemically induced emesis in intact dogs but not in animals with area postrema ablations. These results provide further support for a critical role of the area postrema in triggering the emetic reflex, and are the first definitive demonstration of a direct excitatory action of insulin on mammalian neurons.

Animals↗

PubMed1988

Electrical intracerebral stimulation of the area postrema on taste aversion learning.

The structural characteristics of the area postrema, its anatomical connections, participation in the detection of emesis-provoking substances and the effects of area postrema lesions on taste aversion learning acquisition, are all factors which speak in favor of a role as a chemoreceptor zone involved in the detection of aversive agents which act as effective inducers of taste aversion learning. The feasibility of substituting electrical intracerebral stimulation of the area postrema for the aversive stimulus was investigated in a taste aversion learning paradigm. In Expt. 1, 0.1-ms rectangular pulses of 50 Hz, delivered intermittently or continuously for 4 h after a 15-min delay following ingestion of the gustatory stimulus, produced reliable learning. Expt. 2 showed the learning thus induced to reflect all the characteristics features attributed to taste aversion learning: one-trial learning, long interstimulus delay and cue-consequence specificity. These results suggest that the area postrema could participate in the detection of the aversive consequences of particular taste aversion learning-inducing agents.

Animals↗

PubMed1998

Effects of glutamate-induced excitotoxicity on calretinin-expressing neuron populations in the area postrema of the rat.

We mapped the distribution of calretinin-immunoreactive neuron populations in a circumventricular organ of the rat, the area postrema, and investigated their sensitivity to excitotoxic stimuli mediated by subcutaneously administered monosodium glutamate. We were specifically interested to ascertain whether the presence of calretinin can, per se, confer an in vivo intrinsic resistance for area postrema neurons to glutamate excitotoxicity. We found that dense populations of calretinin-positive neurons displayed a subregional compartmentation in coronal sections of the area postrema along its rostrocaudal axis. We demonstrated that calretinin-positive neurons differ in their sensitivities to monosodium glutamate depending on their position within the area postrema. Neurons in the caudal area postrema were the most sensitive ones, while those in the rostral area postrema were spared of degeneration. We conclude that calretinin-positive neurons in the area postrema are not uniformly protected against glutamate excitotoxicity. It is possible that differences in the local concentrations of monosodium glutamate due to regional heterogeneities in density and permeability of the capillary bed rather than neuronal expression of calretinin account for the observed effects.

Animals↗

PubMed1991

Effects of area postrema stimulation on neurons of the nucleus of the solitary tract.

Previous studies have suggested that neurons of the area postrema may modulate cardiovascular function through an interaction at the level of the nucleus of the solitary tract (NTS). Using an in vitro brain slice preparation of the rabbit medulla, the present study investigated the electrophysiological and pharmacological effects of area postrema stimulation on NTS neuronal activity. In the majority of neurons tested (85.7%), electrical stimulation of the area postrema consistently produced either single or multiple action potentials in NTS neurons. Latency values for neurons showing single spike responses to area postrema stimulation ranged from 3.0 to 17.0 ms with an average latency of 9.3 +/- 4.3 ms. The average threshold for area postrema activation of these nonspontaneously active NTS neurons was 99.8 +/- 12 microA with a stimulus threshold range between 15 and 200 microA (n = 53). Perfusion of the slice with phentolamine (1.0 microM) or yohimbine (200 nM) blocked the area postrema-evoked action potentials, whereas perfusion of the slice with prazosin (200 nM) had no effect. These findings suggest that area postrema neurons do modulate NTS neuronal activity and that this modulation results in an increase in NTS neuronal activation.

Afferent Pathways↗

PubMed1991

GABA-mediated inhibition of medullary vasomotor neurones by area postrema stimulation in rats.

1. The cardiovascular responses, together with the effects on medullary sympathoexcitatory (vasomotor) neurones of the rostral ventrolateral medulla, of area postrema stimulation have been studied in vivo. 2. Electrical (10 Hz) or chemical stimulation using microinjections of L-glutamate of the area postrema produced a vasodepressor response and an inhibition of the medullary sympathoexcitatory neurones in the nucleus reticularis rostroventrolateralis (RVL), while similar stimulation in the adjacent nucleus tractus solitarii (NTS) caused increases in arterial pressure. 3. Single-pulse stimulation of the area postrema revealed at least three influences on the activity of RVL vasomotor neurones, one being excitatory and two inhibitory. 4. The inhibitions evoked in the medullary vasomotor neurones on area postrema stimulation were blocked by ionophoretic application of bicuculline, a GABAA receptor antagonist, without altering the excitatory input to the same neurones. Bilateral microinjections of bicuculline into the RVL in regions where the vasomotor neurones had been identified totally eliminated the vasodepression due to area postrema stimulation. 5. These data support a role for the area postrema in cardiovascular control. It is concluded that the area postrema exerts its action on cardiovascular control in part via GABAergic inhibition of the 'vasomotor' neurones in the nucleus reticularis rostroventrolateralis.

Action Potentials↗

PubMed1994

The area postrema and vomiting.

The area postrema (AP) has been implicated as a chemoreceptor trigger zone for vomiting (emesis) for over 40 years. The AP is located on the dorsal surface of the medulla oblongata at the caudal end of the fourth ventricle. It is one of the so-called circumventricular organs that serve as an interface between the brain parenchyma and the cerebrospinal fluid (CSF)-containing ventricles. The AP lacks a specific blood-brain diffusion barrier to large polar molecules (i.e., a "blood-brain barrier") and is thus anatomically positioned to detect emetic toxins in the blood as well as in the CSF. The AP along with the nucleus of the solitary tract (NTS) and the dorsal motor nucleus of the vagus makes up the so-called dorsal vagal complex, which is the major termination site of vagal afferent nerve fibers. Lesions of the AP prevent vomiting in response to most, but not all, emetic drugs. However, the AP is not essential for vomiting induced by motion or by activation of vagal nerve afferents. The role of the AP in radiation-induced vomiting remains controversial. Electrophysiological studies have reported that neurons in the AP increase their firing in response to emetic drugs. Similarly, studies using the 2-deoxyglucose uptake and c-fos expression techniques have shown that the AP is excited by systemic administration of emetic drugs. Activation of the AP probably leads to nausea and vomiting through its projection to the neighboring NTS. The NTS may serve as the beginning of a final common pathway by which different emetic inputs trigger vomiting.

Animals↗

PubMed1991

Electrophysiological evidence of baroreceptor input to area postrema.

Subpopulations of rat area postrema (AP) and nucleus tractus solitarius (NTS) neurons exist that are responsive to changes in blood pressure. The hypothesis that these effects may be mediated by afferent baroreceptor input was examined. Orthodromic responses of AP and NTS neurons to aortic depressor nerve (ADN) stimulation were observed. Sixty-three percent of AP neurons were affected by ADN stimulation, with most exhibiting short-duration excitatory responses (latency, 27 +/- 1 ms; duration, 11 +/- 1 ms). Fifty-five percent of NTS neurons were influenced by ADN stimulation, although effects in this region were more heterogeneous (24% of neurons excited, 31% inhibited). Thus, in the rat, apparently both AP and NTS neurons receive afferent barosensory information.

Afferent Pathways↗

PubMed1992

Atrial natriuretic factor binding sites in rat area postrema: autoradiographic study.

The area postrema (AP) is a brain stem circumventricular organ implicated, among other functions, in central cardiovascular (CV) regulation. Competition binding analysis performed by quantitative in vitro autoradiography demonstrated specific, high-affinity (Kd, 0.32 +/- 0.11 nM), low-capacity (Bmax, 57.5 +/- 10.9 fmol/mg protein) atrial natriuretic factor (ANF) binding sites in the AP. C-ANF [des-(Gln116-Gly120)ANF-(Arg102-Cys121)-NH2] and ANF-(Phe106-Ile113)-NH2 (two ligands endowed with selectivity for the ANF-C receptor), as well as C-type natriuretic peptide (CNP), did not compete noticeably at pathophysiological concentrations for 125I-ANF binding. 125I-[Tyr0]CNP bound to the AP to a much lower extent than 125I-ANF. Electron microscopic autoradiography in vivo disclosed that 125I-ANF was preferentially bound to axon, dendrite, and astrocyte plasmalemma. These studies demonstrate that the AP contains natriuretic peptide binding sites with pharmacological characteristics of the ANF-A and ANF-B but not of the ANF-C receptor subtype. In the AP, ANF interacts with those sites resembling ANF-A receptors. Cellular localization of these binding sites may relate to their possible involvement in the centrally mediated salt and water regulation and/or CV effects of circulating ANF.

Animals↗

PubMed2001

The role of the dura in conditioned taste avoidance induced by cooling the area postrema of male rats.

Experiments were designed to assess the contribution of the dura mater to the formation of conditioned taste avoidance induced by cooling the area postrema. The results of the first experiment verified that the temperature of the dura showed a temperature gradient at various distances from the tip of the cold probe. In the second and third experiments, a circle of dura was cut away so that different amounts of the area postrema could be cooled without cooling the overlying dura. Cooling the dura plus the area postrema did not produce a stronger avoidance than just cooling the area postrema. In the fourth experiment, the cerebellar cortex was cooled with and without cooling the dura. Cooling the cerebellar cortex produced conditioned taste avoidance, and cooling the dura plus the cerebellar cortex did not produce a stronger avoidance. Taken together, these results suggest that cooling the dura mater does not contribute to the conditioned taste avoidance induced by cooling the area postrema. The results of the fifth experiment showed that cooling the area postrema produced a stronger conditioned taste avoidance than cooling the cerebellar cortex. It is suggested that the avoidance induced by cooling both of these structures is the result of physiological changes occurring when neurons in these structures are inactivated and when the subdural meninges are cooled. Furthermore, these changes are more severe when the area postrema is cooled.

Animals↗

PubMed1983

Area postrema lesions in rats enhance the magnitude of body rotation-induced conditioned taste aversions.

The role of the area postrema, a circumventricular organ located on the dorsal medulla in the fourth ventricle, in body rotation-induced conditioned taste aversions was examined in male hooded rats. One group of rats received lesions of the area postrema, another group was given sham lesions, and two other groups received no surgery. Three groups of rats, those with area postrema lesions, those with sham lesions, and one unoperated group, were given pairings of 1-hr access to a 0.1% sodium saccharin solution with 30 min of body rotation at 70 rpm (on a schedule of 15-sec on--5-sec off). A fourth group of unoperated rats was given pairings of access to the saccharin solution with 30 min of sham rotation. The three rotated groups all developed a taste aversion to the saccharin solution whereas the sham-rotated group did not. The group with lesions of the area postrema exhibited a greater aversion to the saccharin taste than the other two rotated groups. In a second phase of the experiment all rats were given pairing of 1-hr access to chocolate milk with injections of scopolamine methyl nitrate (1 mg/kg). The area postrema-lesioned group failed to exhibit a taste aversion to the chocolate milk whereas the other groups all showed very strong aversions. It was concluded that area postrema lesions abolish taste aversions induced by blood-borne toxins such as scopolamine methyl nitrate, but enhance taste aversions induced by motion sickness. Some speculations concerning the enhanced taste aversions induced by motion sickness in area postrema lesioned rats, are provided.

Animals↗

PubMed1984

Recall of a previously acquired conditioned taste aversion in rats following lesions of the area postrema.

A conditioned taste aversion was produced by pairing a novel sucrose solution with either 3 mEq lithium chloride or with 100 rad gamma radiation in rats with the area postrema intact. Lesions of the area postrema were then made in half of the rats exposed to each treatment and in rats that were not treated with the unconditioned stimulus. When tested for a conditioned taste aversion, all treated rats showed a significant aversion to the sucrose solution compared to the untreated control rats. There were no significant differences between rats with area postrema lesions and those with the area postrema intact, indicating that the lesions had no effect on the recall of the previously acquired aversion. The results are interpreted as being consistent with the hypothesis that the role of the area postrema in taste aversion learning is to monitor blood and cerebrospinal fluid for potential toxins and to transmit that information to the central nervous system.

Analysis of Variance↗