Neurons in the paraventricular nucleus projecting to the median eminence: a study of their afferent connections from peripheral baroreceptors, and from the A1-catecholaminergic area in the ventrolateral medulla

In male rats anesthetized with urethane-chloralose, extracellular recordings were made from tuberoinfundibular (TI) neurons in the paraventricular nucleus (PVN) identified by antidromic stimulation of the median eminence. Activation of baroreceptors induced by intravenous administration of phenylephrine inhibited approximately two-thirds of the 32 TI-neurons tested. Electrical stimulation of the A1-catecholaminergic area in the ventrolateral medulla produced an excitation in one half of the 28 neurons. Microinjection of L-glutamate (40 nl of 0.5 M solution of pH 7.4-7.6) to the same A1-area evoked an excitation in 7 out of 8 TI-neurons tested. The results show that some TI-neurons in the PVN receive inhibitory synaptic inputs from the baroreceptors and excitatory inputs from neurons in the A1-catecholaminergic area.     

Neurons in the caudal ventrolateral medulla mediate the arterial baroreceptor reflex by inhibiting barosensitive reticulospinal neurons in the rostral ventrolateral medulla in rabbits.

Participation of the caudal ventrolateral medulla in the arterial baroreceptor reflex was examined in urethane-anesthetized, vagotomized and immobilized rabbits whose aortic nerve was cut bilaterally. The extent of the caudal ventrolateral medulla was mapped by decreases in the renal sympathetic nerve activity and arterial pressure following a local microinjection of a neuroexcitatory amino acid, sodium glutamate (0.075-1.5 nmol). It extended between the levels 1.3 mm rostral and 3.0 mm caudal to the obex. An injection of sodium glutamate into the caudal ventrolateral medulla also diminished spontaneous activity of barosensitive reticulospinal neurons in the rostral ventrolateral medulla. In the 'split medulla preparation' in which the medulla was split along the midsagittal plane to disrupt fiber connections associating both sides, a neurotoxic agent, kainic acid, was injected unilaterally into the rostral ventrolateral medulla. This treatment markedly attenuated responses of renal sympathetic nerve activity and arterial pressure induced by a sodium glutamate injection into the ipsilateral caudal ventrolateral medulla, whereas responses to an injection into the contralateral caudal ventrolateral medulla were totally preserved. In four separate experiments, three to five injections of kainic acid were made unilaterally to cover the whole extent of the caudal ventrolateral medulla. The sympathoinhibitory and depressor responses to stimulation of the ipsilateral aortic nerve were then totally abolished. Simultaneously, the cardiac cycle-related rhythmic fluctuation of renal sympathetic nerve activity, which represented activity of the carotid sinus baroreceptor reflex, was attenuated to the noise level. These results, together with our previous electrophysiological demonstration of barosensitive caudal ventrolateral medulla neurons with axonal projections to the rostral ventrolateral medulla, strongly support the hypothesis that neurons in the caudal ventrolateral medulla mediate the arterial baroreceptor-vasomotor reflex through inhibition of barosensitive reticulospinal neurons in the rostral ventrolateral medulla.     

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 neurol 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 μg/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 periph eral administration of CCK, further implicating these ascending catecholaminergic path ways in the neuroendocrine, physiological, and behavioral effects produced by gastric vagal stimulation. © 1995 Wiley-Liss, Inc.     

Fos-determined distribution of neurons activated during the Bezold-Jarisch reflex in the medulla oblongata in conscious rabbits and rats

Experiments were performed in unanaesthetized rabbits and rats to investigate the distribution, within the medulla oblongata, of neurons activated during the Bezold-Jarisch reflex. Repeated intravenous injections of phenylbiguanide evoked depressor and bradycardic responses in both rabbits and rats. Fos-positive neurons were present in the nucleus tractus solitarius and in the caudal ventrolateral medulla oblongata. Double-label tyrosine hydroxylase (TH) immunohistochemical studies in the ventrolateral medulla showed that most Fos-positive neurons in the caudal ventrolateral medulla were TH-negative neurons scattered between A1 noradrenaline cells, in the rabbit and in the rat. Approximately 20% of neurons in the caudal ventrolateral medulla in rabbits, and 50% in rats, were immunoreactive for both Fos and TH. Some Fos-positive, TH-negative neurons in the caudal ventrolateral medullawere retrogradely labelled with cholera toxin B-Gold after injection of this tracer into the sympathoexcitatory region of the rostral ventrolateral medulla. Our data suggests that neurons in the nucleus tractus solitarius, and rostrally projecting TH-negative neurons in the caudal ventrolateral medulla, are part of the pathway by which stimulation of cardiopulmonary receptors inhibits sympathetic vasomotor tone to decrease blood pressure during the Bezold-Jarisch reflex.     

Electrophysiological identification of spinally projecting neurons in the lateral reticular nucleus of the rat

Eighty-four neurons in the caudal ventrolateral medullary reticular formation were antidromically activated by the stimulation of the dorsolateral funiculus in 49 urethane-anesthetized rats. Of 76 neurons, 37 had no spontaneous discharge. Of the neurons that had spontaneous discharges, 80% had firing rates between 0.1 and 15 Hz. The average conduction velocity, determined among 70 neurons, was 15.20 +/- 1.23 m/s, and 87% had conduction velocities within the range of 2-30 m/s. This study further confirms the existence of spinally-projecting neurons in the lateral reticular nucleus (LRN) of the caudal medulla, and some of them are probably responsible for the descending controls of nociception from the LRN.     

Role of medullary excitatory amino acid receptors in mediating the 10-Hz rhythm in sympathetic nerve discharge of cats

We tested the hypothesis that excitatory amino acid (EAA)-mediated transmission plays a role in generating the 10-Hz rhythm in sympathetic nerve discharge (SND) of baroreceptor-denervated, urethane-anesthetized cats. Microinjection of either an N-methyl-d-aspartate (NMDA) or non-NMDA receptor antagonist into any one of three medullary regions (lateral tegmental field, rostral, or caudal ventrolateral medulla) essentially eliminated the 10-Hz rhythm in inferior cardiac SND. We conclude that EAA receptors in the medulla are critical for generation of the 10-Hz rhythm.     

nNOS-containing neurons in the hypothalamus and medulla project to the RVLM

Nitric oxide (NO) within the brain is known to have an important influence on sympathetic nerve activity (SNA). NO is found in the paraventricular nucleus (PVN), caudal ventrolateral medulla (CVLM) and the nucleus tractus solitarius (NTS), regions that project to the rostral ventrolateral medulla (RVLM), an area that is critical in the regulation of SNA. The aim of the present study was to determine whether neurons in the PVN, NTS and CVLM that project to the RVLM contain the neuronal isoform of nitric oxide synthase (nNOS) and are, therefore, capable of producing NO. Under pentobarbitone general anaesthesia, the retrogradely-transported tracer, rhodamine-tagged microspheres, were microinjected into the RVLM of rats (n = 6). Two weeks later, the animals were re-anaesthetised, perfused with para-formaldehyde and the brains were removed. Hypothalamic and medullary sections were processed for nNOS immunohistochemistry and the RVLM-projecting neurons were identified using fluorescence microscopy. We found nNOS-containing neurons were present throughout the PVN, CVLM and NTS and that these were intermingled with neurons that projected to the RVLM. Of the neurons in the PVN and CVLM that projected to the RVLM, approximately 12 +/- 1% and 8 +/- 3%, respectively, contained nNOS. In the NTS only 1 +/- 1% of the neurons were double-labeled. This study highlights anatomical pathways emanating from the PVN and CVLM, in particular, which may contribute to the effects on SNA elicited by NO within the brain.     

Electrophysiological study of paraventricular nucleus neurons projecting to the dorsomedial medulla and their response to baroreceptor stimulation in rats

In male rats anesthetized with urethane, extracellular recordings were made from 415 neurons in the paraventricular nucleus (PVN) and adjacent areas. Of these neurons 64 were excited antidromically by stimulation of the dorsomedial medulla but not by stimulation of the pituitary stalk (first group). Seventy-three neurons were antidromically excited by stimulation of the pituitary stalk but not of the dorsomedial medulla (second group, neurosecretory cells). The other 2 neurons were antidromically excited by stimulation of both the dorsomedial medulla and the pituitary stalk (third group). Latencies of antidromically evoked action potentials by stimulation of the dorsomedial medulla and of the pituitary stalk ranged between 8 and 60 ms (mean +/- S.D., 38.5 +/- 9.8, n = 66) and from 7 to 24 ms (mean +/- S.D., 13.0 +/- 3.6, n = 75), respectively, suggesting unmyelinated fiber projections in both instances. PVN neurons of these 3 groups were found to be dispersed throughout the PVN and no difference in specific locations between the neuron groups existed. Their characteristics, however, were different. The first group of neurons discharged at a slower rate and showed no phasic pattern of firing, while 28% of the second group of neurons ('identified' neurosecretory cells) showed phasic patterns of firing and their rates of discharge were higher than those of the first group of neurons. The two neurons belonging to the third group showed irregular spontaneous discharges. The areas within the dorsomedial medulla stimulation of which evoked antidromic excitation of PVN neurons were located within and adjacent to the nucleus of the tractus solitarius (NTS) and the dorsal motor nucleus of the vagus (DMV). Among PVN neurons which were antidromically excited by stimulation of dorsomedial medulla, 51 cells were examined for their responses to excitation of baroreceptors. An increase in pressure of the 'isolated' carotid sinus excited 2 neurons, and inhibited 7 (14%). On the other hand, 27% (11 out of 41) of neurosecretory cells (second group) were inhibited by baroreceptor stimulation. From these results, it was concluded that essentially separate populations of PVN neurons project to the neurohypophysis and to the NTS, DMV and their vicinities, and that some of the caudally-projecting PVN neurons receive synaptic input from carotid baroreceptor reflex pathway, suggesting the possible involvement of these PVN neurons in central cardiovascular regulation.     

Increased dietary sodium enhances activation of neurons in the medullary cardiovascular pathway during acute sodium loading in the rat

Increased sodium ingestion diminishes baroreflex-induced bradycardia in animals during acute sodium loading. These experiments studied effects of high sodium diet on activation of central nervous system sites associated with baroreflex activation and cardiovascular responses to hypernatremia during systemic sodium administration. Fos-like (Fos-Li) protein immunoreactivity was measured to estimate activation of neurons in the medullary baroreflex pathway (nucleus tractus solitarius (NTS), caudal ventrolateral medulla (CVLM), and rostral ventrolateral medulla (RVLM)), and in the hypothalamic paraventricular (PVN) and supraoptic nuclei (SON) in male Sprague-Dawley rats consuming standard chow and either tap water (TAP) or isotonic saline (ISO) for 2-3 weeks. Fos-Li immunoreactivity in the PVN and SON was similar in rats consuming TAP and ISO infused with 0.6 M NaCl. However, there were significantly more Fos-Li positive cells in NTS and CVLM of animals consuming ISO and infused with 0.6 M NaCl than any other experimental group, while Fos-Li immunoreactivity was similar in the RVLM in all animals. In conclusion, these data demonstrate that activation of neurons in the NTS and CVLM was significantly enhanced by moderate sodium loading in animals consuming high dietary sodium. The increased basal activation of neurons in these medullary sites could account for decreased baroreflex-induced bradycardia observed during ingestion of a high salt diet and acute, moderate sodium loading.     

Response properties of nociceptive neurons in the caudal ventrolateral medulla (CVLM) in monoarthritic and healthy control rats: modulation of responses by the paraventricular nucleus of the hypothalamus (PVN)

We characterized response properties of neurons in the caudal ventrolateral medulla (CVLM), a structure involved in pain modulation. Electrophysiological recordings were performed in pentobarbitone-anesthetized control and monoarthritic rats. Noxious pinch, heat, cold and colorectal distension were used for peripheral test stimulation. To study central modulation of CVLM neurons and role in mediating descending pain regulation from the hypothalamus, glutamate was administered into the paraventricular nucleus of the hypothalamus (PVN). CVLM neurons gave excitatory, inhibitory or no response to noxious test stimulation. Response patterns for part of the neurons varied with submodality of test stimulation; e.g., a cell with an excitatory response to heat could give no or an inhibitory response to cold. Arthritis induced cell type-dependent changes in the spontaneous activity, most prominent of which was increased discharge rate of CVLM cells with an excitatory response to noxious stimulation. Significant arthritis-induced changes were also observed in the magnitudes of the nociceptive responses, among which was an increase in the pinch-induced excitatory response. Glutamate in the PVN of arthritic but not control animals suppressed the excitatory responses of CVLM cells, independent of the submodality of test stimulation and without influence on their spontaneous discharge rates. The results indicate that CVLM neurons give differential responses to noxious stimulation. Arthritis induces changes in response properties of CVLM neurons and in their central regulation by the PVN. These findings are in line with the evidence indicating that the CVLM plays a role in processing of nociceptive signals under inflammatory as well as control conditions.     

Baroreflex dependent and independent roles of the caudal ventrolateral medulla in cardiovascular regulation

The caudal ventrolateral medulla (CVLM) plays a critical role in cardiovascular regulation. Convincing data now support the hypothesis that inhibition of sympathoexcitatory neurons in the rostral ventrolateral medulla (RVLM) by CVLM neurons constitutes the necessary inhibitory link in baroreceptor reflex mediated control of sympathetic vasomotor outflow. Inhibition or destruction of the CVLM produces severe acute hypertension, consistent with blockade of baroreceptor reflexes and withdrawal of inhibition of RVLM sympathoexcitatory neurons. However, other data indicate that the CVLM also tonically inhibits RVLM sympathoexcitatory neurons in a manner not driven by baroreceptor input. In some studies, inhibition of the CVLM results in an increase in arterial pressure (AP) without inhibiting baroreceptor reflexes, possibly reflecting baroreceptor-independent and baroreceptor-dependent sub-regions of the CVLM. Furthermore, in baroreceptor-denervated rats, inhibition of the CVLM still leads to large increases in AP. In addition, in spontaneously hypertensive rats (SHR) central processing of baroreceptor reflexes appears normal but CVLM-mediated inhibition of the RVLM seems to be attenuated, suggesting that it is specifically a baroreceptor-independent mechanism of cardiovascular regulation in SHR that is altered. Taken together, these findings support an important, tonic, baroreceptor-independent inhibition of RVLM sympathoexcitatory neurons exerted by the CVLM.     

Electrophysiological properties of spinally-projecting A5 noradrenergic neurons

Spinally-projecting A5 neurons were studied with anatomical and electrophysiological techniques in the rat. A detailed study of the number and distribution of spinally-projecting catecholaminergic (CA) and non-catecholaminergic neurons present in a defined area of ventrolateral pontine reticular formation was performed using a sequential technique for the detection of CA fluorescence and retrogradely transported HRP. Using control animals and rats with 6-hydroxydopamine-induced lesions of spinal CA axons, it was concluded that up to 93% of all noradrenergic (NE) neurons present in the area investigated send an axonal process to the thoracic spinal cord and that NE neurons constitute at least 90% of all spinally-projecting neurons present in the same area. Single unit recordings of spinally-projecting neurons were obtained in the same area of the reticular formation in urethane-anesthetized, paralyzed and respirated rats. Based on the above-mentioned anatomical data, antidromic activation from thoracic spinal cord provided a necessary and sufficient criterion for the identification of A5 NE cells. These neurons had a conduction velocity of 2.5 m/s, a discharge rate of up to 4 spikes/s and all were inhibited by i.v. clonidine or desmethylimipramine (DMI). The inhibition produced by the latter drugs was always reversed by the alpha-2 adrenergic antagonists piperoxan or yohimbine. Antidromic (AD)-activation was followed by a period of inhibition whose duration was increased by raising the intensity of the stimulus or by administration of the NE-uptake inhibitor DMI. The effect of the latter was reversed by administration of the alpha-2 antagonist piperoxan.     

Clonidine diminishes c-jun gene expression in the cardiovascular sensitive areas of the rat brainstem

The present study investigated the effect of clonidine on the basal and inducible c-jun and c-fos mRNA expression in the nucleus tractus solitarius (middle, mNTS, and rostral, rNTS) and the rostral ventrolateral medulla (caudal, cRVLM, and rostral, rRVLM). Conscious rats received saline, clonidine (30 microg/kg, i.v.), saline plus sodium nitroprusside (NP), or clonidine plus NP. Under basal conditions (saline-infused rats), c-jun mRNA was expressed in the mNTS and rRVLM but not in the rNTS or cRVLM whereas c-fos mRNA was not detectable. Clonidine attenuated the increases in c-fos in the mNTS and cRVLM and c-jun gene expression in the mNTS and rRVLM caused by NP-evoked hypotension and also reduced the basal expression of c-jun mRNA in the mNTS and rRVLM. These findings establish a causal link between clonidine inhibition of c-fos expression in brainstem and its hypotensive action, and provide the first evidence that clonidine attenuates the expression of the closely linked c-jun gene in neurons implicated in centrally mediated hypotension.     

Negative chronotropism of the heart is inhibited with lesions of the caudal medulla in the rat

Neurons in the ventrolateral medulla are essential for cardiorespiratory regulation. It has been suggested that neurons in the caudal ventrolateral medulla are responsible for the negative chronotropic effect of the heart, at least in carnivores, because injection of glutamate into this area decreases heart rate significantly. In the present study, we monitored heart rate both before and after injections of the excitotoxin ibotenic acid into the most caudal part of the ventrolateral medulla in rats. We found that resting heart rate increased significantly by more than 53% (P<0.0001) after the ibotenic acid injections. This result suggests that neurons located in the caudal ventrolateral medulla are responsible for the negative chronotropic effect of the heart in the rat, especially its most caudal part.     

Hypothalamic and brainstem sources of pituitary adenylate cyclase-activating polypeptide nerve fibers innervating the hypothalamic paraventricular nucleus in the rat

The hypothalamic paraventricular nucleus (PVN) coordinates major neuroendocrine and behavioral mechanisms, particularly responses to homeostatic challenges. Parvocellular and magnocellular PVN neurons are richly innervated by pituitary adenylate cyclase-activating polypeptide (PACAP) axons. Our recent functional observations have also suggested that PACAP may be an excitatory neuropeptide at the level of the PVN. Nevertheless, the exact localization of PACAP-producing neurons that project to the PVN is not understood. The present study examined the specific contribution of various brain areas sending PACAP innervation to the rat PVN by using iontophoretic microinjections of the retrograde neuroanatomical tracer cholera toxin B subunit (CTb). Retrograde transport was evaluated from hypothalamic and brainstem sections by using multiple labeling immunofluorescence for CTb and PACAP. PACAP-containing cell groups were found to be retrogradely labeled from the PVN in the median preoptic nucleus; preoptic and lateral hypothalamic areas; arcuate, dorsomedial, ventromedial, and supramammillary nuclei; ventrolateral midbrain periaqueductal gray; rostral and midlevel ventrolateral medulla, including the C1 catecholamine cell group; nucleus of the solitary tract; and dorsal motor nucleus of vagus. Minor PACAP projections with scattered double-labeled neurons originated from the parabrachial nucleus, pericoeruleus area, and caudal regions of the nucleus of the solitary tract and ventrolateral medulla. These observations indicate a multisite origin of PACAP innervation to the PVN and provide a strong chemical neuroanatomical foundation for interaction between PACAP and its potential target neurons in the PVN, such as parvocellular CRH neurons, controlling physiologic responses to stressful challenges and other neuroendocrine or preautonomic PVN neurons.     

Characteristics of caudal ventrolateral medullary neurons antidromically activated from rostral ventrolateral medulla in the rabbit.

We made extracellular recordings from 107 spontaneously active neurons in the caudal ventrolateral medulla, after identifying the cells by antidromically activating them from the rostral ventrolateral medulla, in urethane-anesthetized rabbits. We tested the response of these neurons to inputs from baroreceptors and chemoreceptors. The median conduction velocity for antidromically activated neurons was 0.84 m/s. Raising blood pressure with intravenous noradrenaline excited 22% of 96 neurons tested, inhibited 61%, and had no effect on the remaining 17%. The spontaneous discharge rate of neurons excited by an increase in blood pressure was 1.6 +/- 0.3 spikes/s, lower than the discharge rate of neurons inhibited by this procedure (4.9 +/- 0.5 spikes/s). Excitation of chemoreceptors by hypoxia increased the discharge rate of 14/16 neurons tested in the group excited by baroreceptor inputs. In the group inhibited by baroreceptor inputs 21/35 neurons tested were excited and 12/35 neurons were inhibited by chemoreceptor inputs. Neurons excited by an increase in blood pressure were located in the previously defined caudal vasodepressor region and in a region just rostral to the obex, intermediate between the vasodepressor region and the rostral sympathoexcitatory region. These neurons may form part of the central inhibitory link in the baroreceptor-vasomotor pathway. Other antidromically activated neurons in the vasodepressor region may be inhibitory vasomotor cells with a function relatively independent of baroreceptor inputs, or they may be A1 catecholamine neurons, with axons passing through the rostral medulla en route to the forebrain.     

Collateral axonal projections from the A1 noradrenergic cell group to the paraventricular nucleus and bed nucleus of the stria terminalis in the rat

The A1 noradrenergic cell group in the caudal ventrolateral medullary reticular formation of the rat sends efferent projections to a number of regions in the basal forebrain and hypothalamus, but the extent to which these projections represent collateral branches of individual axons is not known. Immunohistochemical labeling of medullary neurons containing the catecholamine biosynthetic enzymes tyrosine hydroxylase, dopamine beta-hydroxylase, and phenylethanolamine N-methyltransferase was used to reveal the anatomical location of A1 noradrenergic neurons within the ventrolateral medulla. Subsequently, the retrograde fluorescence double-labeling technique was employed to investigate the collateralization of ascending A1 efferent axons. The subcommissural bed nucleus of the stria terminalis (BST) was injected with rhodamine-fluorescent latex microspheres and the ipsilateral left paraventricular nucleus of the hypothalamus (PVN) was injected with Fast blue. Within the ventrolateral medulla, single- and double-labeled neurons were identified in a distribution corresponding to that demonstrated for A1 noradrenergic perikarya. The results indicate that some ascending axons from cells within the A1 region collateralize to effect a simultaneous innervation of the BST and PVN. The innervation of multiple efferent targets by single neurons within the A1 region may have important implications with respect to A1's postulated role in central cardiovascular regulation.     

Central integration of the Bezold-Jarish reflex in the cat

The medullary structures involved in the central Bezold-Jarisch reflex pathway were studied by recording unit activity of sympatho-excitatory (SE) or inhibitory (SI) cardiovascular neurons in pentobarbital-anesthetized cats. The neurons were selected based upon their spontaneous activity and upon their sensitivity to baroreceptor reflex activation by

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-phenylephrine. The Bezold-Jarisch reflex was induced by i.v. injection of chlorophenylbiguanide 10 μg/kg which produced a short-lasting decrease in blood pressure, heart rate and renal nerve activity. 76 neurons were studied. In 10 out of 12 SE neurons of the rostral ventrolateral medulla the activity was inhibited by chlorophenylbiguanide whereas in 10 out of 11 SI neurons and 6 out of 6 baroreflex-insensitive cells of the caudal ventrolateral medulla it was activated. The others cells were insensitive. Three types of neurons: excitatory, inhibitory or non-barosensitive, were recorded in the lateral tegmental field (27 cells) and the medullary raphe (20 cells). These neurons were either activated, inhibited or insensitive to Bezold-Jarisch reflex activation. Microinjection of the glutamate receptor antagonist kynurenic acid (2.5 nmol/site) or the GABAergic agonist muscimol (1 nmol/site) into the nucleus tractus solitarii abolished the effects of both

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-phenylephrine and chlorophenyl-biguanide on heart rate and renal nerve activity. These results indicate that the cardiovascular neurons (sympatho-excitatory and sympatho-inhibitory) located in the medullary areas, involved in cardiovascular and baroreflex mechanisms, are implicated in the central Bezold-Jarisch reflex pathway.     

Connections of the hypothalamic paraventricular necleus with the neurohypophysis, median eminence, amygdala, lateral septum and midbrain periaqueductal gray: An electrophysiological study in the rat

Extracellular recordings were obtained from 555 paraventricular (PVN) nucleus neurons in pentobarbital-anesthetized male rats. Cells were examined for their spontaneous activity patterns and response to single 1-Hz electrical stimulation of the neurohypophysis, median eminence, amygdala, lateral septum (LS) and midbrain periaqueductal gray (PAG).Neurohypophyseal stimulation evokedantidromic activation from 109 neurons. Among spontaneouly active neurohypophyseal neurons, evidence of a recurrent inhibitory pathway usually required pituitary stimulus intensities twice threshold for antidromic activation. Orthodromic excitatory or inhibitory responses followed amygdala and LS stimulation, but not PAG stimulation. The amygdala influence was predominantly inhibitory to ‘phasic’ (putative vasopressin-secreting) PVN neurohypophyseal neurons. Neurohypophyseal stimulation evokedorthodromic responses from 124 PVN cells; some of these neurons were also responsive to stimulation in other sites.Median eminence stimulation evoked antidromic responses from 37 PVN neurons; some of these cells also displayed phasic activity but not evidence for recurrent inhibition. Twelve cells in this group were also activated antidromically from both the median eminence and the neurohypophysis; collision tests suggest that the median eminence innervation may be an axon collateral of a neurohypophyseal pathway. Amygdala stimulation was inhibitory to some cells in this category.Amygdala, LS and PAG stimulation evoked antidromic activation from a small number of PVN cells, but none of these cells appeared to innervate more than one area, including the neurohypophysis, and none displayed phasic activity. Orthodromic responses were recorded among other PVN neurons after stimulation in these sites; however, PAG stimulation was the least effective stimulation area.These observations provide additional electrophysiological data that confirm efferent PVN connections to all areas tested, afferent connections from amygdala and LS but not PAG, and the possibility for coordinated activity among PVN neurons through local recurrent or common afferent connections.