Biomedical subjects

A J Verberne

Publications and source records attributed to A J Verberne.

At least 19 recordsLinked to original sources

PubMed2001

Regional haemodynamic responses to activation of the medial prefrontal cortex depressor region.

Electrical or chemical stimulation of the medial prefrontal cortex (MPFC) produces depressor and sympathoinhibitory responses. To characterise the MPFC depressor response more fully, we determined the regional haemodynamic changes which occurred in response to stimulation of the MPFC. In halothane-anaesthetised rats, we recorded arterial blood pressure and renal, superior mesenteric, and iliac arterial vascular conductance using miniaturised Doppler flow probes. Electrical stimulation of the MPFC (50-100 microA) was used to map the location of the depressor region. Increases in vascular conductance (or increases in blood flow) were recorded from the renal (+2.3+/-0.5 kHz/mmHgx10(3)), mesenteric (+4.4+/-0.4 kHz/mmHgx10(3)), and iliac (+8.3+/-1.0 kHz/mmHgx10(3)) vascular beds in response to stimulation of the MPFC depressor region coinciding with the ventral infralimbic (IL) and dorsal peduncular (DP) cortical areas. Similar responses were obtained after microinjection of the chemical excitant L-glutamate (n=3, 100 nl, 100 mM), indicating that the responses were due to excitation of cell bodies and not due to axons traversing the area. Administration of the nitric oxide synthesis inhibitor N(G)-nitro-L-arginine methyl ester (L-NAME, 25 micromol/kg, i.v., n=5) significantly reduced the MPFC depressor response (51%, 12.5+/-1.2 to 6.1+/-2.5 mmHg). The increases in conductance in the hindquarter and mesenteric vascular beds were significantly reduced after L-NAME treatment (mesenteric by 77%, iliac by 70%), but there was no significant reduction of renal flow (35%). These observations indicate that the depressor region of the MPFC is localised to ventral regions (IL and DP) and that the depressor response is mediated by increased conductance in the hindquarters and mesenteric vascular beds. Furthermore, the depressor response may be mediated, in part, by release of nitric oxide in these vascular beds.

Animals↗

PubMed2000

Medial prefrontal depressor response: involvement of the rostral and caudal ventrolateral medulla in the rat.

The importance of neurones of the caudal and rostral ventrolateral medulla (CVLM and RVLM, respectively) in mediation of the medial prefrontal cortex depressor response was studied in halothane-anaesthetised rats. Blockade of GABA(A) receptors in the RVLM produced by microinjection of bicuculline (50 nl, 2 mM, n = 6) resulted in reversal of the depressor (-9.5 +/- 1.2 mm Hg) and lumbar sympathetic (-6.5 +/- 5.7 units) responses to pressor (+7.8 +/- 3.5 mm Hg) and sympathoexcitatory (+19.3 +/- 12.5 units) responses and simultaneous blockade of baroreceptor reflex-mediated sympathoinhibition. Baroreflex blockade was reflected by a significant reduction in the gain (slope of the blood pressure vs. lumbar sympathetic nerve discharge regression line) of the reflex. Microinjection of the excitatory amino acid antagonist kynurenic acid (100 nl, 50 mM, n = 6) into the CVLM blocked the baroreflex and significantly reduced the depressor (-9.6 +/- 0.4 to -6.9 +/- 0.6 mm Hg) and lumbar sympathetic (-4.0 +/- 2.1 to 2.9 +/- 1.9 units) responses to medial prefrontal cortex stimulation. These results support the hypothesis that the medial prefrontal cortex depressor response is mediated by a pathway which converges at the level of the RVLM and which is only partly dependent on an excitatory input to caudal ventrolateral medullary neurones.

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PubMed1999

Properties of C1 and other ventrolateral medullary neurones with hypothalamic projections in the rat.

1. This study compared (i) the properties of C1 cells with those of neighbouring non-C1 neurones that project to the hypothalamus and (ii) the properties of C1 cells that project to the hypothalamus with those of their medullospinal counterparts. 2. Extracellular recordings were made at three rostrocaudal levels of the ventrolateral medulla (VLM) in alpha-chloralose-anaesthetized, artificially ventilated, paralysed rats. Recorded cells were filled with biotinamide. 3. Level I (0-300 microm behind facial nucleus) contained spontaneously active neurones that were silenced by baro- and cardiopulmonary receptor activation and virtually unaffected by nociceptive stimulation (firing rate altered by < 20 %). These projected either to the cord (type I; 36/39), or to the hypothalamus (type II; 2/39) but rarely to both (1/39). 4. Level II (600-800 microm behind facial nucleus) contained (i) type I neurones (n = 3) (ii) type II neurones (n = 11), (iii) neurones that projected to the hypothalamus and were silenced by baro- and cardiopulmonary receptor activation but activated by strong nociceptive stimulation (type III, n = 2), (iv) non-barosensitive cells activated by weak nociceptive stimulation which projected only to the hypothalamus (type IV, n = 9), (v) cells that projected to the hypothalamus and responded to none of the applied stimuli (type V, n = 7) and (vi) neurones activated by elevating blood pressure which projected neither to the cord nor to the hypothalamus (type VI, n = 4). 5. Level III (1400-1600 microm behind facial motor nucleus) contained all the cell types found at level II except type I. 6. Most of type I and II (17/26) and half of type III cells (4/8) were C1 neurones. Type IV-V were rarely adrenergic (2/12) and type VI were never adrenergic (0/3). 7. All VLM baroinhibited cells project either to the cord or the hypothalamus and virtually all (21/23) C1 cells receive inhibitory inputs from arterial and cardiopulmonary receptors.

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PubMed1999

Medial prefrontal cortex depressor response: role of the solitary tract nucleus in the rat.

The depressor response elicited by unilateral low intensity electrical stimulation of the rat ventral medial prefrontal cortex may be mediated by a connection with the solitary tract nucleus. We tested this hypothesis by (i) examining the influence of medial prefrontal cortex stimulation on the induction of Fos-like immunoreactivity in neurons in the medulla oblongata, and (ii) by testing the effect of inhibition of solitary tract nucleus neurons on the medial prefrontal cortex stimulation-evoked depressor response. Depressor responses (>10 mmHg) were elicited by electrical stimulation of the medial prefrontal cortex every minute for 1 h ('Stimulated' group). Control animals were treated identically but did not receive electrical stimulation ('Unstimulated' group). Neurons exhibiting Fos-like immunoreactivity were abundant at the stimulation site which included the infralimbic area, and dorsal peduncular cortex. Medullary Fos-like immunoreactivity observed in the 'Stimulated' and 'Unstimulated' groups exceeded levels observed in untreated rats and was detected in the rostral, caudal and intermediate areas of the ventrolateral medulla, and the commissural, intermediate, medial and lateral regions of the solitary tract nucleus, as well as the medial vestibular nucleus, and the dorsal motor nucleus of the vagus. The number of neurons displaying Fos-like immunoreactivity in the ipsilateral solitary tract nucleus and caudal ventrolateral medulla of the 'Stimulated' group was found to be significantly elevated compared to the contralateral side (P<0.05), and the 'Unstimulated' group bilaterally. Inhibition of solitary tract nucleus neurons using bilateral injections of the GABA(A) receptor agonist muscimol (44 pmol/25 nl) inhibited the sympathetic vasomotor baroreflex and attenuated the depressor and sympathoinhibitory response to medial prefrontal cortex stimulation by 62% and 65%, respectively. These findings suggest that the projection from the medial prefrontal cortex to the solitary tract nucleus is excitatory and support the hypothesis that the depressor response elicited by medial prefrontal cortex stimulation is mediated, in part, by a cortico-solitary projection which activates the intramedullary baroreflex pathway.

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PubMed1999

Midline medullary depressor responses are mediated by inhibition of RVLM sympathoexcitatory neurons in rats.

Mechanisms underlying the depressor and sympathoinhibitory responses evoked from the caudal medullary raphe (MR) region were investigated in pentobarbital sodium-anesthetized, paralyzed rats. Intermittent electrical stimulation (0.5 Hz, 0.5-ms pulses, 200 microA) of the MR elicited a mixed sympathetic response that consisted of a long-latency sympathoexcitatory (SE) peak (onset = 146 +/- 7 ms) superimposed on an inhibitory phase (onset = 59 +/- 10 ms). Chemical stimulation of the MR (glutamate; Glu) most frequently elicited depressor responses accompanied by inhibition of sympathetic nerve discharge. Occasionally, these responses were preceded by transient pressor and SE responses. We examined the influence of intermittent electrical stimulation (0.5 Hz, 0.5-ms pulses, 25-200 microA) and Glu stimulation of the MR on the discharge of rostral ventrolateral medulla (RVLM) premotor SE neurons. Peristimulus-time histograms of RVLM unit discharge featured a prominent inhibitory phase in response to MR stimulation (onset = 20 +/- 2 ms; duration = 42 +/- 4 ms; n = 12 units). Glu stimulation of the MR reduced blood pressure (-37 +/- 2 mmHg, n = 19) and inhibited the discharge of RVLM SE neurons (15 of 19 neurons). Depressor and sympathoinhibitory responses elicited by chemical and electrical stimulation of the MR region are mediated by inhibition of RVLM premotor SE neurons and withdrawal of sympathetic vasomotor discharge.

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PubMed1998

Cortical modulation of the cardiovascular system.

Cortical modulation of central cardiovascular control mechanisms has been recognized for many decades. However, it is only recently that the mechanisms underlying cortical influences on circulatory function have been systematically examined. This review considers the view that certain regions of the cerebral cortex, including the medial prefrontal cortex (MPFC) and insular cortex (IC), participate in specific aspects of central circulatory control. Anatomical investigations indicate that these cortical areas are connected with hypothalamic, midbrain, pontine and medullary brain regions involved in cardiovascular control. Lesions of the MPFC and IC have demonstrated modulation of the activity of cardiovascular reflexes such as the baroreceptor heart rate reflex and involvement in conditioned cardiovascular responses. Electrophysiological studies have provided evidence that cortical regions are able to influence premotor sympathoexcitatory vasomotor neurons within the rostral ventrolateral medulla and subsequently alter sympathetic vasomotor tone. Cortical regions such as the IC receive visceral sensory information arising from baroreceptors and chemoreceptors within the cardiovascular system. In contrast, the MPFC receives afferents predominantly from limbic sources, although its outputs include structures associated with central sympathetic vasomotor control. Cortical modulation of circulatory function has been demonstrated in man and may underlie the cardiovascular components of a number of conditions. It is suggested that cortical areas involved in visceral sensory or visceral motor processes associated with circulatory function may be involved in generation of patterns of cardiovascular responses specific for certain behaviours.

Afferent Pathways↗

PubMed1997

Cuneiform nucleus stimulation-induced sympathoexcitation: role of adrenoceptors, excitatory amino acid and serotonin receptors in rat spinal cord.

Stimulation of the midbrain cuneiform nucleus has previously been shown to produce increases in arterial blood pressure and lumbar sympathetic nerve activity. While this sympathoexcitatory effect is, in part, due to excitation of premotor sympathoexcitatory neurons in the rostral ventrolateral medulla, the specific spinal neurotransmitter systems recruited by cuneiform nucleus stimulation remains to be elucidated. In this study, mean arterial pressure, resting and cuneiform nucleus stimulation-evoked lumbar sympathetic nerve activity were analysed following intrathecal injections of an excitatory amino acid antagonist (kynurenic acid), alpha1-adrenoceptor antagonist (prazosin) and a serotonin receptor antagonist (methiothepin) in anesthetized, paralysed male Sprague-Dawley rats. Mean arterial pressure and resting sympathetic nerve discharge were decreased by all treatments (n = 6/group) compared to the vehicle control group. Intermittent electrical stimulation of the cuneiform nucleus produced a bimodal sympathoexcitatory response, of which the short latency peak was significantly attenuated (43% reduction) by intrathecal kynurenate whereas the long latency peak was reduced by intrathecal prazosin (decrease of 21%) and methiothepin (38% attenuation). These results are consistent with the significant roles of excitatory amino acid, alpha1-adrenergic and serotonin receptors in modulating the activity of sympathetic vasomotor preganglionic neurons supplying the lumbar sympathetic nerve trunk, and suggest the existence of at least three neuronal groups and/or pathways associated with the sympathoexcitatory response to cuneiform nucleus stimulation.

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PubMed1997

Neuronal activation in the forebrain following electrical stimulation of the cuneiform nucleus in the rat: hypothalamic expression of c-fos and NGFI-A messenger RNA.

Forebrain neuronal connections associated with the cardiovascular response to unilateral, low-intensity, electrical stimulation of the mesencephalic cuneiform nucleus were examined in the halothane-anesthetized and paralysed rat by in situ hybridization histochemistry using specific 35S-labelled oligonucleotides for detection of c-fos and nerve growth factor inducible-A gene (NGFI-A) messenger RNAs. Stimulation of the cuneiform nucleus led to increases in mean arterial pressure and heart rate, whereas no cardiovascular response was observed in animals stimulated in the inferior colliculus or in sham-operated animals [see concurrent mid- and hindbrain study [Lam W. et al. (1996) Neuroscience 71, 193-211]. Cuneiform nucleus stimulation was associated with increased c-fos and NGFI-A messenger RNA levels bilaterally in the ventromedial, dorsomedial and lateroanterior hypothalamic nuclei, lateral and anterior hypothalamic areas, and ipsilaterally in the medial amygdaloid nucleus, at levels significantly greater than those in inferior colliculus-stimulated, sham-operated and naive, unoperated animals. C-fos, but not NGFI-A, messenger RNA expression was increased bilaterally in the piriform cortex and subparafascicular thalamic nucleus. These results are consistent with the existence of direct and indirect projections between the cuneiform nucleus and the aforementioned activated areas, the functions of which may include the control of reproduction and metabolism, as well as cardiovascular regulation. The ipsilateral nature of responses in certain brain areas may be explained by the absence of decussating pathways and/or the presence of multisynaptic connections which attenuate bilateral signal transmission. The existence of structures that are known to receive afferent projections from the cuneiform nucleus, but that were not activated, may be explained by synaptic depolarization not reaching the threshold for immediate early gene expression or by a net inhibitory effect on innervated neurons. Characterization of these activated forebrain regions using other compatible labelling techniques should further elucidate the mechanisms by which these central nervous system structures are integrated in the response to stimulation of the cuneiform nucleus.

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PubMed1996

An electrophysiological study of the medial prefrontal cortical projection to the nucleus of the solitary tract in rat.

The medial prefrontal cortex (MPFC) has been described as a "visceromotor" cortical area, since autonomic effects such as depressor responses may be elicited from this area. The central circuitry which mediates these depressor responses may include a projection from the MPFC to the nucleus of the solitary tract (NTS). Neurones were recorded extracellularly in the MPFC and were tested for antidromic (AD) activation from the NTS. These were all tested for (1) constant spike latency, (2) ability to follow high-frequency stimulation to more than 200 Hz, and (3) where possible, collision of stimulation-evoked spike with spontaneous spike or spikes evoked by iontophoretic application of glutamate. Of the 34 cells studied, all had constant AD latency (30 +/- 1 ms, range 16-46 ms); they followed high-frequency stimulation up to 354 +/- 19 Hz, and only seven cells were spontaneously active (range 1-19 spikes/s). The threshold stimulation intensity for AD activation was 102 +/- 9 microA (n = 34, range 8-200 microA). Depth-threshold curves (n = 7) showed minimum-threshold AD activation currents that corresponded to the dorsal and ventral subdivisions of the NTS. Small shifts in AD latency were found in the depth-threshold curves, suggesting axonal branching. Analysis of recording sites showed that NTS-projecting MPFC neurones were predominantly found in the infralimbic and ventral prelimbic regions of the MPFC. These findings indicate that there is a population of neurones in the MPFC that projects to, and probably terminates within, the NTS. It is possible that this projection may, in part, mediate the cardiovascular response to MPFC stimulation.

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PubMed1996

Increased nerve growth factor inducible-A gene and c-fos messenger RNA levels in the rat midbrain and hindbrain associated with the cardiovascular response to electrical stimulation of the mesencephalic cuneiform nucleus.

Functional neuronal connections associated with the cardiovascular response to unilateral low-intensity electrical stimulation of the mesencephalic cuneiform nucleus were examined in the halothane-anaesthetized and paralysed rat by in situ hybridization histochemistry using specific 35S-labelled oligonucleotides for detection of nerve growth factor inducible-A gene (NGFI-A) and c-fos messenger RNAs. Stimulation of the cuneiform nucleus increased mean arterial pressure and heart rate by 20 +/- 0.5 mmHg and 35 +/- 3 b.p.m., respectively, while no significant cardiovascular response was observed in animals stimulated in the inferior colliculus or in sham-operated animals. Cuneiform nucleus stimulation produced increased NGFI-A and c-fos messenger RNA levels in the Kölliker-Fuse and parabrachial nuclei ipsilaterally, and the cuneiform nucleus, dorsal periaqueductal gray and caudal ventrolateral medulla bilaterally at levels significantly greater than those in inferior colliculus-stimulated, sham-operated and naive, unoperated animals. NGFI-A, but not c-fos, messenger RNA expression was increased bilaterally in the caudal portion of the nucleus of the solitary tract and inferior olive. These results are consistent with previous neuroanatomical tract-tracing studies of afferent and efferent pathways from the cuneiform nucleus and indicate that these midbrain and hindbrain structures may be involved in the pressor and tachycardic responses associated with stimulation of the cuneiform nucleus. The ipsilateral nature of responses in certain brain areas may be explained by the absence of decussating pathways and/or the presence of multisynaptic connections which attenuate bilateral signal transmission. Characterization of these activated neuronal structures using other compatible labelling techniques should further elucidate the mechanisms by which these central nervous system structures are integrated in the cardiovascular responses to stimulation of the cuneiform nucleus.

Animals↗

PubMed1996

Medullary sympathoexcitatory neurons are inhibited by activation of the medial prefrontal cortex in the rat.

Electrical stimulation of the medial prefrontal cortex (MPFC) reduces arterial blood pressure. To investigate the mechanism of this response, the effects of electrical and chemical stimulation of the MPFC on splanchnic and lumbar sympathetic nerve discharge and on the discharges of barosensitive neurons of the rostral ventrolateral medulla (RVLM) were studied in halothane-anesthetized rats. Electrical stimulation (20 Hz, 1 ms, 100 and sympathoinhibitory responses (reduced discharge of the splanchnic sympathetic nerve). Microinjection of glutamate (10 nmol/100 nl) into the MPFC also reduced arterial blood pressure and sympathetic discharge. Electrical stimulation (0.5 Hz, 1-ms pulse pairs, 3-ms interval, 150-300 microA) produced distinct patterns of splanchnic and lumbar sympathetic nerve discharge. A clear sympathoinhibitory phase with an onset latency of 146 +/- 14 ms was observed only in the case of the splanchnic sympathetic nerve activity. Electrical stimulation at depressor sites within the MPFC also inhibited the discharge of 10 of 21 RVLM barosensitive neurons tested. RVLM neurons were never excited by MPFC stimulation. These results indicate that the MPFC contains neurons that form part of a central sympathoinhibitory pathway.

Animals↗

PubMed1995

Effect of dorsal periaqueductal grey lesion on baroreflex and cardiovascular response to air-jet stress.

Certain areas within the periaqueductal grey (PAG) have been implicated in cardiovascular regulation. The influence of excitotoxic lesions of the caudal dorsal periaqueductal grey on the baroreceptor-heart rate reflex and the cardiovascular response to air-jet stress was examined in awake Wistar-Kyoto rats. Pressor (11 +/- 2 mmHg) and tachycardic (25 +/- 4 beats/min) responses to air-jet were not influenced by the lesion. Similarly, the resting MAP and HR were unchanged. However, the gain of the baroreflex was reduced from -3.9 +/- 0.1 to -2.8 +/- 0.3 beats/min per mmHg and the upper threshold was increased from 120 +/- 5 to 135 +/- 7 mmHg in the lesioned group. These observations suggest that although the caudal dorsal PAG does not appear to exert a tonic influence on vasomotor tone or mediate the air-jet response, it may provide a facilitatory input to the baroreceptor-heart rate reflex.

Animals↗

PubMed1995

A simple and reliable method for construction of parallel multibarrel microelectrodes.

A modification to the method of construction of parallel or "piggy-back" electrodes for extracellular single-unit recording combined with iontophoresis is described that facilitates the alignment of the two components of the array. The method involves the use of an orthogonal viewing device (a pair of mirrors mounted symmetrically at 45 degrees to the horizontal), which produces a pair of virtual images of the electrode components that can be viewed with a microscope. A slight displacement between the electrodes is easily detected as an uneven separation between the electrode images. The positions of the electrode components are adjusted until there is no visible separation of the electrodes or their virtual images.

Animals↗

PubMed1995

Cuneiform nucleus stimulation produces activation of medullary sympathoexcitatory neurons in rats.

Activation of the cuneiform nucleus (CNF) of the midbrain produces elevation of arterial blood pressure. This study examined the influence of the CNF on arterial blood pressure, sympathetic vasomotor outflow, and the discharges of barosensitive sympathoexcitatory neurons of the rostral ventrolateral medulla (RVLM) in halothane-anesthetized, paralyzed rats. Electrical stimulation (50 Hz, 25-75 microA, 10 s) of the CNF elicited intensity-dependent elevations in arterial blood pressure associated with excitation of the sympathetic vasomotor discharge (elevated discharge of the lumbar sympathetic nerve). Intermittent paired-pulse electrical stimulation of the CNF elicited an excitatory response in the discharge of the lumbar sympathetic outflow that consisted of an early peak (onset latency 84 +/- 4 ms) and a smaller late peak (onset latency 217 +/- 6 ms). Seventeen of 22 RVLM sympathoexcitatory neurons tested were excited by stimulation of the CNF. Twelve of 14 units tested projected to the thoracic spinal cord, and of these, 10 units were excited by CNF stimulation with an onset latency of 16 +/- 1 ms. These findings support the hypothesis that the sympathoexcitatory and pressor responses elicited by activation of the CNF are mediated by RVLM sympathoexcitatory neurons.

Animals↗

PubMed1993

Central respiratory control of A5 and A6 pontine noradrenergic neurons.

Sympathetic nerve discharge (SND), phrenic nerve discharge (PND), and unit activity of locus ceruleus (LC) and of putative A5 noradrenergic cells were recorded in vagotomized rats anesthetized with urethan. SND was activated by stimulation of carotid chemoreceptors with hypoxia (N2 inhalation, 5-15 s or 12% O2 inhalation, 2-5 min) and displayed a prominent central respiratory modulation during the hypoxic challenge (postinspiratory pattern). LC cells were also activated by peripheral chemoreceptor stimulation. The discharge of most LC units (28 of 31) exhibited central respiratory modulation. 15 LC units had a postinspiratory pattern and 11 had an inspiratory one. Putative A5 cells were also excited by hypoxia and also displayed a clear central respiratory modulation (mostly postinspiratory pattern). These experiments indicate that 1) the firing rate of most pontine noradrenergic cells is increased by peripheral chemoreceptor stimulation, and 2) pontine noradrenergic neurons receive afferent information of a respiratory nature, possibly from their ventrolateral medullary inputs.

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PubMed1992

Rostral ventrolateral medullary neurons projecting to locus coeruleus have cardiorespiratory inputs.

This study was designed to characterize some of the properties of the rostral ventrolateral medullary (RVLM) cells with axonal projection to the locus coeruleus (LC) in urethane anesthetized, vagotomized, paralyzed and artificially respirated rats. The vast majority of RVLM units antidromically (AD) activated from LC (RVLM-LC units) were silent and unresponsive to peripheral chemoreceptor stimulation or nociceptive stimulation. Twenty seven spontaneously active RVLM-LC neurons, AD activated from LC with currents below 30 microA (17 +/- 2 microA) were analyzed. AD mapping (n = 18) indicated that the lowest threshold for AD activation occurred within the LC itself. Axonal branching within or close to LC was suggested by the presence of sudden jumps in AD latency. Maximal AD latencies ranged from 7 to 37 ms. Most spontaneously active RVLM-LC neurons displayed marked central respiratory modulation characterized by either a post-inspiratory or an inspiratory pattern. The majority of the tested neurons were affected (excited or inhibited) by brief peripheral chemoreceptor stimulation (N2 inhalation). Most cells were inhibited by raising arterial pressure but none exhibited any detectable pulse synchrony. Reticulospinal sympathetic premotor neurons of RVLM were not found to project to LC (sample of 9) and very few RVLM cells with on-off respiratory discharges appeared to project to LC (2 out of 110). This study suggests that much of the information conveyed by the RVLM to LC could be of a mixed cardiorespiratory nature.

Afferent Pathways↗

PubMed1992

Midbrain central gray: influence on medullary sympathoexcitatory neurons and the baroreflex in rats.

The influence of the central gray (CG) of the midbrain on the activity of 19 barosensitive sympathoexcitatory neurons of the rostral ventrolateral medulla (RVLM) and on the sympathetic vasomotor baroreflex was studied in halothane-anesthetized rats. Eighteen RVLM barosensitive units were readily activated by train stimulation of the CG, although twin-pulse stimulation was less effective (10 of 19 neurons responded). Inhibition of neurons within the RVLM by bilateral microinjection of the GABA-mimetic drug muscimol abolished the pressor responses to CG stimulation, while the accompanying lumbar nerve sympathoexcitation was converted to sympathoinhibition. In baroreceptor-denervated vagotomized animals, unilateral microinjection of muscimol into the RVLM ipsilateral or contralateral to the site of CG stimulation resulted in approximately equal attenuation of the CG sympathoexcitatory and pressor responses. In contrast, the sympathoexcitatory response to electrical stimulation of the sciatic nerve was reduced more effectively by inhibition of the RVLM contralateral to the site of stimulation. Electrical stimulation of the CG lateral and ventrolateral to the aqueduct produced sympathoexcitation [increased discharge of the greater splanchnic and lumbar sympathetic nerves (SSN and LSN)] with an increase in mean arterial blood pressure. Activation of the SSN by CG stimulation was greater than that observed for the LSN (n = 5 rats). This differential influence of the CG on the sympathetic outflow was not a result of a differential influence of the baroreflex. Electrical stimulation of the CG produced elevations of the gain and the cut-off pressure of the baroreflex for both the SSN and LSN.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1992

Medullary pathway of the Bezold-Jarisch reflex in the rat.

The central pathway mediating the Bezold-Jarisch reflex elicited by jugular vein injection of serotonin (5-HT) and phenyl biguanide (PBG) was studied in halothane-anesthetized, paralyzed rats. 5-HT and PBG produced hypotension and inhibition of lumbar sympathetic discharge often preceded by sympathoexcitation. The Bezold-Jarish reflex was blocked by bilateral kynurenic acid (KYN; glutamate antagonist, 1.25 nmol/side) microinjection into the solitary tract nucleus. Bilateral KYN injection into the caudal ventrolateral medulla (5 nmol/side) also blocked the reflex. Bilateral injection of bicuculline methiodide (BIC; 100 pmol/side) into the rostral ventrolateral medulla (RVL) reduced the depressor and sympathoinhibitory components of the reflex and enhanced an excitatory component. Blockade or attenuation of the Bezold-Jarisch reflex was always associated with a concomitant blockade or attenuation of the arterial baroreflex. RVL barosensitive neurons (n = 61) were inhibited (> 60% reduction in firing) by PBG and 5-HT. Iontophoretic application of BIC (n = 11 cells), but not strychnine (glycine antagonist), blocked inhibition of RVL neurons by 5-HT and PBG. The sympathoinhibitory component of the Bezold-Jarisch reflex may use a central pathway similar to that of the arterial baroreflex.

Animals↗