Dorsal raphe nucleus serotonergic neurons innervate the rostral ventrolateral medulla in rat

Stimulation of the dorsal raphe nucleus (DRN) alters arterial pressure, heart rate and cerebral blood flow, yet projections from the DRN to medullary autonomic nuclei have not been described. We examined whether serotonergic (5-HT) projections from the DRN terminate in the rostral ventrolateral medulla (RVL) and if so, whether the projection mediates cardiovascular responses to DRN stimulation. Studies were performed in adult male Sprague-Dawley rats. Horseradish peroxidase or choleratoxin B was injected unilaterally or bilaterally into the RVL. Levels of 5-HT, its precursors L-tryptophan and 5-hydroxytryptophan and the metabolite 5-hydroxyindole acetic acid were measured in the ventral medulla by HPLC three weeks following placement of electrolytic lesions in DRN. Serotonin transporter (3H-cyanoimipramine binding) was quantified by autoradiography in DRN-lesioned animals. Horseradish peroxidase or choleratoxin B injections into the medulla at the level of the RVL resulted in retrogradely labeled neurons bilaterally, with ipsilateral predominance, in the DRN. Labeled cells were preponderant in rostral ventrolateral portions of the DRN, but were also observed in the dorsal, lateral and interfascicular DRN subnuclei; fewer neurons were observed in caudal portions of the DRN. Three weeks following placement of electrolytic lesions in the DRN, the concentrations of 5-HT and 5-hydroxyindole acetic acid, but not L-tryptophan or 5-hydroxytryptophan, were reduced in the medulla by 45 and 48%, respectively, compared to sham-operated or unoperated controls. DRN lesions reduced binding to the 5-HT transporter in the RVL by approximately 30% compared to unlesioned controls. Unilateral lesions of the RVL reduced the evoked blood pressure response by 53+/-15%; bilateral RVL lesions reduced the response by 86+/-9%. The increase in cortical blood flow elicited by DRN stimulation was unchanged after unilateral or bilateral RVL lesions. These studies demonstrate that there is a descending serotonergic projection from the DRN to the RVL. This projection may mediate autonomic changes elicited by DRN stimulation.     

Vasopressor neurons in the rostral ventrolateral medulla of the rabbit

Neurons within the rostral ventrolateral medulla oblongata project directly to the intermediolateral column in the thoracolumbar spinal cord. This paper reviews evidence obtained from experiments in the rabbit regarding the anatomical connections and physiological, pharmacological and histochemical properties of these cells. The following hypotheses are discussed: an increase in the firing rate of these neurons leads to a rise in arterial pressure due to sympathetic vasoconstriction, but does not affect respiratory or other somatomotor activity; the bulbospinal pathway originating from these neurons is an essential component of the central pathways mediating baroreceptor and other cardiovascular reflexes; these neurons receive tonic GABAergic inhibitory inputs, which are not all of baroreceptor origin; many of these bulbospinal neurons synthesize adrenalize. The possible role of adrenaline in the function of these neurons is considered.     

8-OH-DPAT-induced hypotensive action and sympathoexcitatory neurons in the rostral ventrolateral medulla of the rat

We examined whether the selective 5-hydroxytryptamine 1A (5-HT_1A) receptor agonist 8-hydroxy-2-(di-n-propylamino)-tetralin (8-OH-DPAT) injected systemically can act directly on sympathoexcitatory neurons located in the rostral ventrolateral medulla (RVLM) to cause the hypotensive effect of this agent in rats. Microinjections of 8-OH-DPAT and buspirone into the RVLM produced a dose-dependent decrease in blood pressure. Microinjections of spiperone and pindolol, 5-HT_1A antagonists, into the RVLM inhibited the depressor response to 8-OH-DPAT intravenously injected or injected into the RVLM. Microiontophoretic application of 8-OH-DPAT onto RVLM sympathoexcitatory neurons inhibited the firing of RVLM sympathoexcitatory neurons and the inhibition of unit activity by 8-OH-DPAT was blocked by rrmicroiontophoretic spiperone. Intravenous administration of 8-OH-DPAT also inhibited the firing of these neurons. Microiontophoretic application of spiperone onto the RVLM sympathoexcitatory neurons reversed the inhibitory response to intravenous 8-OH-DPAT. These results are consistent with the hypothesis that 8-OH-DPAT may exert a portion of its hypotensive effect through a direct inhibition of RVLM sympathoexcitatory neurons in rats. The receptor involved is probably the 5-HT_1A type.     

Ultrastructure of the rostral ventral respiratory group neurons in the ventrolateral medulla of the rat

The neurons in the ventrolateral medulla that project to the spinal cord are called the rostral ventral respiratory group (rVRG) because they activate spinal respiratory motor neurons. We retrogradely labeled rVRG neurons with Fluoro-Gold (FG) injections into the fourth cervical spinal cord segment to determine their distribution. The rostral half of the rVRG was located in the area ventral to the semicompact formation of the nucleus ambiguus (AmS). A cluster of the neurons moved dorsally and intermingled with the palatopharyngeal motor neurons at the caudal end of the AmS. The caudal half of the rVRG was located in the area including the loose formation of the nucleus ambiguus caudal to the AmS. We also labeled the rVRG neurons retrogradely with wheat germ agglutinin-horseradish peroxidase (WGA-HRP) to determine their ultrastructural characteristics. The neurons of the rVRG were medium to large (38.1 x 22.1 microm), oval or ellipsoid in shape, and had a dark cytoplasm containing numerous free ribosomes, rough endoplasmic reticulum (rER), mitochondria, Golgi apparatuses, lipofuscin granules and a round nucleus with an invaginated nuclear membrane. The average number of axosomatic terminals in a profile was 33.2. The number of axosomatic terminals containing round vesicles and making asymmetric synaptic contacts (Gray's type I) was almost equal to those containing pleomorphic vesicles and making symmetric synaptic contacts (Gray's type II). The axodendritic terminals were large (1.55 microm), and about 60% of them were Gray's type I. The rVRG neurons have ultrastructural characteristics, which are different from the palatopharyngeal motor neurons or the prorpiobulbar neurons.     

Different types of barosensory synaptic inputs to rostral ventrolateral medulla neurons of the rat

Neurons situated in the rostral ventrolateral medulla (RVLM) with descending axons to the spinal cord and that are modulated by different baroreceptor inputs are considered the main central generators of vasomotor activity. In the urethane-anesthetized, curarized rat, we recorded intracellular potentials from 14 neurons located in the RVLM and investigated their barosensory properties by analysis of the relation between neuronal membrane potential (MP), including spike potentials, and high-pressure barosensory activity, which was indicated by arterial blood pressure (BLPR). Time-domain (cross-correlations or triggered averaging) and frequency-domain (autospectra and coherences) analysis showed that 7 of 14 neurons had cardiac-cycle-correlated rhythms. EXCITATORY CARDIAC-CYCLE-RELATED MODULATION: One type of barosensitive neuron, with strong cardiac-related activity, was antidromically activated from the spinal cord and received inhibitory inputs from aortic nerve stimulation. These neurons had strong pulse-modulated activity consisting of EPSPs and spike potentials locked to the cardiac cycle and occurring at the end of diastole. INHIBITORY CARDIAC-CYCLE-RELATED MODULATION: Another type of barosensitive neuron showed hyperpolarizations locked to the cardiac cycle that started during late diastole and ended during the systolic period, but which had little relation to spike firing. The hyperpolarizations might be due to either IPSPs or disfacilitation. RESPIRATORY AND CARDIAC MODULATION: Some neurons also showed modulation of synaptic potentials and/or spike firing locked to the oscillation produced by ventilator pressure. It is suggested that the different types of cardiac- and respiratory-related rhythm reflect different functional roles of neurons in baroreceptor regulation of vasomotor activity.     

Glutamate in spinally projecting neurons of the rostral ventral medulla

Phosphate activated glutaminase (PAG), an enzyme of glutamate synthesis, was localized by immunohistochemistry in all PNMT-immunoreactive and all serotonin-immunoreactive neurons in the rostral ventral medulla of the rat. Between 71 and 83% of bulbospinal neurons localised in the rostral ventral medulla projecting to the intermediolateral cell column in the upper thoracic spinal cord contained PAG immunoreactivity. Of these bulbospinal PAG-immunoreactive neurons 17-27% contained PNMT immunoreactivity and 9-16% contained serotonin immunoreactivity. Other bulbospinal PAG-immunoreactive neurons (60-70%) contained neither PNMT- nor serotonin immunoreactivity. The results provide anatomical evidence suggestive of a glutamatergic input to the sympathetic preganglionic neurons of the spinal cord arising from different populations of neurons located in the rostral ventral medulla.     

Lateralisation of projections from the rostral ventrolateral medulla to sympathetic preganglionic neurons in the rat

Spinally projecting sympathoexcitatory neurons in the rostral ventrolateral medulla (RVLM), synapse with sympathetic preganglionic neurons (SPN) and regulate the activity of sympathetic nerves that control the heart, blood pressure and the adrenal medulla (AM). However, the degree of lateralization of the bulbospinal projections to SPN innervating specific targets is poorly understood. Three approaches were used in this study. Anterograde tracer was iontophoresed into a pressor site in the RVLM (left or right) and retrograde tracer injected into the superior cervical ganglion (SCG, right) and the AM (left). Close appositions between anterogradely labelled axons and retrogradely labelled SCG- or AM-SPN were counted. Projections to the SCG were bilateral. Projections to the AM were markedly ipsilateral. In the second part, retrograde tracers were injected unilaterally into the region of the intermediolateral cell column at spinal segment T2 or T8 on one side and the number of labelled neurons in the RVLM counted. The results from each level of injection were similar showing that 63–64% of the neurons were ipsilateral. Responses to glutamate microinjection into the RVLM on adrenal nerve (left) and superior cervical nerve (left) activity were measured. The ratio of the nerve responses was the same even when different sides of the RVLM were injected. The anterograde data strongly suggest that the RVLM projections to AM-SPN are predominantly ipsilateral. Although other experimental approaches also attempted to investigate lateralization, the retrograde data target different and functionally heterogeneous pools of SPN that may mask the ipsilateral projection to the AM. Similarly, chemical stimulation of the RVLM will excite not only monosynaptic projections but also polysynaptic projections that may also mask the predominant ipsilateral monosynaptic projection to AM.     

Effects of clonidine on sympathoexcitatory neurons in the rostral ventrolateral medulla

The effects of intravenous and iontophoretic clonidine were determined on the firing rates of sympathoexcitatory neurons in the rostral ventrolateral medulla of the cat. As previously reported in the rat, we found that sympathoexcitatory neurons could be differentiated based on their sensitivity in clonidine. Approximately 50% of the neurons were inhibited by clonidine. There was only a weak correlation between the inhibition of unit activity and whole sympathetic nerve activity. The discharge rates of the remaining neurons were either not altered or were increased by clonidine. Unlike the rat, these two groups of neurons could not be further differentiated on the basis of axonal conduction velocity or discharge frequency. These data are discussed and the effects of clonidine and 8-hydroxy-2-(di-n-propylamino)tetralin (8-OH-DPAT) on sympathoexcitatory neurons are compared.     

Mu-opioid receptors are present in functionally identified sympathoexcitatory neurons in the rat rostral ventrolateral medulla

Agonists of the mu-opioid receptor (MOR) produce profound hypotension and sympathoinhibition when microinjected into the rostral ventrolateral medulla (RVL). These effects are likely to be mediated by the inhibition of adrenergic and other presympathetic vasomotor neurons located in the RVL. The present ultrastructural studies were designed to determine whether these vasomotor neurons, or their afferents, contain MORs. RVL bulbospinal barosensitive neurons were recorded in anesthetized rats and filled individually with biotinamide by using a juxtacellular labeling method. Biotinamide was visualized by using a peroxidase method and MOR was identified by using immunogold localization of an antipeptide antibody that recognizes the cloned MOR, MOR1. The subcellular relationship of MOR1 to RVL neurons with fast- or slow-conducting spinal axons was examined by electron microscopy. Fast- and slow-conducting cells were not morphologically distinguishable. Immunogold-labeling for MOR1 was found in all RVL bulbospinal barosensitive neurons examined (9 of 9). MOR1 was present in 52% of the dendrites from both types of cells and in approximately half of these dendrites the MOR1 was at nonsynaptic plasmalemmal sites. A smaller portion of biotinamide-labeled dendrites (16%) from both types of cells were contacted by MOR1-containing axons or axon terminals. Together, these results suggest that MOR agonists can directly influence the activity of all types of RVL sympathoexcitatory neurons and that MOR agonists may also influence the activity of afferent inputs to these cells. The heterogenous distribution of MORs within individual RVL neurons indicates that the receptor is selectively targeted to specific pre- and postsynaptic sites.     

大鼠头端延髓腹外侧区前交感神经元的电生理研究

采用细胞外记录方法,研究氨基甲酸乙酯麻醉大鼠头端延髓腹外侧区前交感神经元的电生理特性。观察到１２５个ＲＶＬＭ神经元中有２４个的自发放电被电刺激主动脉神经和静脉注射苯肾上腺素后抑制,同时其放电具有心必节律,以上２４个中有１８个单位能被 脊髓侧索电刺激逆行激活。     

Phenylethanolamine N-methyltransferase-containing neurons in the rostral ventrolateral medulla of the rat. I. Normal ultrastructure

The electron microscopic localization of the adrenaline-synthesizing enzyme, phenylethanolamine N-methyltransferase (PNMT) was examined in the rostral ventrolateral medulla (RVL) of adult rats. The brains were fixed by perfusion with 3.75% acrolein and 2.0% paraformaldehyde in phosphate buffer. Coronal Vibratome sections through the RVL were immunocytochemically labeled using a rabbit polyclonal antiserum to PNMT and the peroxidase-antiperoxidase method. A semi-quantitative ultrastructure analysis revealed that the perikarya constituted 9% of the total immunoreactive profiles observed in the RVL. The labeled somata were large (18-24 microns) and were characterized by an indented nucleus and abundant cytoplasm with numerous mitochondria. An average of 136.8 +/- 11.6 mitochondria were present per 100 microns2 cytoplasm, which is 38% greater than the numbers found for PNMT-immunoreactive neurons in the nucleus of the solitary tract. Moreover, the labeled somata were often found in direct apposition to the basal lamina of small capillaries and neighboring astrocytic processes. The remaining labeled profiles were neuronal processes of which 72% were dendrites. Both the PNMT-labeled somata and dendrites received primarily symmetric contacts from unlabeled axon terminals. Only a few axons and terminals containing immunoreactivity for PNMT were observed. The axons were both unmyelinated and myelinated. The PNMT-immunoreactive terminals were characterized by a mixed population of vesicles and by the formation of synaptic junctions with both unlabeled dendrites and PNMT-labeled perikarya and dendrites. The ultrastructural morphology and proximity to blood vessels and glia suggest a high metabolic activity and possibly a chemosensory function of PNMT neurons in the RVL. The existence of myelinated and unmyelinated axons could imply that PNMT-containing neurons have different conduction velocities in efferent pathways to the spinal cord or other brain regions. Furthermore, the multiple types of synaptic interactions between labeled and unlabeled axons and dendrites support the concept that adrenergic neurons modulate and are modulated by neurons containing the same or other putative transmitters in the RVL.     

大鼠头端延髓腹外侧区前交感神经元的电生理研究

采用细胞外记录方法,研究氨基甲酸乙酯麻醉大鼠头端延髓腹外侧区(RVLM)前交感神经元的电生理特性.观察到125个RVLM神经元中有24个的自发放电被电刺激主动脉神经(ADN)和静脉注射苯肾上腺素后抑制,同时其放电具有心性节律,以上24个中有18个单位(75%)能被脊髓(T2)侧索电刺激逆行激活.提示RVLM前交感神经元具有压力敏感性和对脊髓的投射等特点,在压力感受器反射等交感心血管活动调节中具有十分重要的作用.     

Intracellular analysis in vivo of different barosensitive bulbospinal neurons in the rat rostral ventrolateral medulla.

Neurons located in the rostral ventrolateral medulla (RVLM) with projections to the intermediolateral column (IML) in the spinal cord were electrophysiologically characterized and anatomically identified using an intracellular recording technique in vivo. A group of spontaneously active neurons was antidromically activated by electrical stimulation of the IML in the thoracic spinal cord (T2-T3 level). The axonal conduction velocities ranged from 1.5 m/sec to 11.0 m/sec; mean value, 5.5 +/- 2.6 m/sec (+/- SD). The firing pattern and changes in membrane potential in relation to the cardiac cycle were investigated in these bulbospinal neurons. A first group discharged action potentials with higher frequency at the end of the diastolic/beginning of the systolic period. The average of the neuronal membrane potentials demonstrated depolarizing potentials at the end of the diastolic/beginning of the systolic period. These depolarizing potentials increased in magnitude when the neurons were hyperpolarized. Therefore, they were characterized as EPSPs. The baroreceptor reflex activation produced by the increase in systemic arterial pressure following intravenous injection of phenylephrine elicited hyperpolarization, a decrease in the rate of discharge, and an increase in the membrane input resistance, suggesting that a disfacilitatory effect was produced by the activation of baroreceptor inputs on these bulbospinal neurons. Conversely, the inactivation of the baroreceptor reflex by intravenous injection of sodium nitroprusside produced depolarization and an increase in the firing rate. These neurons were characterized as baroreceptor-sensitive type I neurons. A second group of bulbospinal neuron in the RVLM was differentiated from the first group because it demonstrated a decrease in the frequency of discharge at the end of the diastolic/beginning of the systolic period. The average of the membrane potentials showed hyperpolarizing potentials that decreased in magnitude when the neuron was hyperpolarized. These hyperpolarizing potentials occurred at the end of the diastolic/beginning of the systolic period and were reversed in polarity after intracellular injections of chloride ions for several minutes. Therefore, these potentials were characterized as chloride-dependent IPSPs locked to the cardiac cycle. In some of these neurons, the electrical stimulation of the IML produced, in addition to the antidromic action potential, a monosynaptic EPSP with a shorter latency. Based on these unique characteristics, these neurons were defined as barosensitive type II neurons. During constant baroreceptor inactivation achieved by the hypotension produced by intravenous infusions of sodium nitroprusside, the pattern of discharge of barosensitive type II neurons became very regular, and the IPSPs locked to the cardiac cycle were absent.(ABSTRACT TRUNCATED AT 400 WORDS)     

Cholinergic inputs to rostral ventrolateral medulla pressor neurons from hypothalamus

The rostral ventrolateral medulla (RVLM) has cholinergic mechanisms responsible for pressor responses. Stimulation of the hypothalamic paraventricular nucleus (PVN) causes an increase of arterial pressure via activation of neurons in the RVLM. In this study, we examined whether PVN stimulation causes a pressor response via activation of cholinergic mechanisms in the RVLM. Male Wistar rats were used and they were anesthetized, paralyzed and artificially ventilated. Electrical stimulation of the PVN produced a pressor response. Microinjection of the muscarinic receptor antagonist scopolamine and the cholinesterase inhibitor physostigmine into the RVLM inhibited and potentiated, respectively, the pressor response induced by PVN stimulation. PVN stimulation also increased the firing rate of RVLM barosensitive neurons and the increase in the firing rate was inhibited and potentiated by scopolamine and physostigmine, respectively, iontophoretically applied on neurons. Microinjection of L-glutamate into the PVN produced a release of ACh in the RVLM. The inhibitory amino acid gamma-aminobutyric acid injected into the lateral parabrachial nucleus (LPBN) inhibited the pressor response induced by PVN stimulation. These results suggest that PVN stimulation causes an increase in arterial pressure via activation of cholinergic inputs in the RVLM. It appears that the pressor response is mediated, at least in part, via cholinergic inputs from the LPBN.     

Effects of morphine and morphine withdrawal on adrenergic neurons of the rat rostral ventrolateral medulla

In urethane anesthetized rats, iontophoretic application of morphine or α-methylnoradrenaline (α-MNE) inhibited (80–100%) the discharges of all putative adrenergic (C1) cells of the rostral ventrolateral medulla (RVLM). The effect of morphine was blocked selectively by naloxone while that of α-MNE was blocked selectively by theα₂-adrenergic antagonist idazoxan. Putative C1 cells were inhibited (75–100%) by low i.v. doses of clonidine (10–15 μg/kg). Most cells (7/10) were also inhibited by morphine i.v. (81% at 7 mg/kg). Two cells were slightly excited at doses below 2 mg/kg and inhibited at higher doses. Three cells were excited only. All effects of morphine i.v. were reversed by naloxone (1 mg/kg, i.v.). Intravenous administration of naloxone to morphine-dependent rats increased significantly the firing rate of all putative C1 adrenergic cells (from 5.8 ± 0.9 spikes/s to 12.3 ± 1.5 spikes/s;n = 8). During withdrawal these cells could still be inhibited (80–100%) by i.v. injection of clonidine (15 μg/kg). C-Fos expression induced by naltrexone-precipitated withdrawal was examined in the brainstem of freely moving morphine-dependent rats pretreated with clonidine or saline before injection of the opioid antagonist. The locus coeruleus (LC) of the same rats was examined for comparison. Morphine withdrawal without clonidine treatment significantly increased the number of Fos-like-immunoreactive (Fos-LIR) cells in the RVLM and LC. Clonidine pretreatment (1 mg/kg, i.p.) reduced the number of withdrawal-activated Fos-LIR cells in LC by 81%. In the RVLM this reduction averaged 37% for all cell types and 48% for C1 adrenregic cells. Further, a very large proportion of RVLM neurons that expressed c-Fos during morphine withdrawal (83%) were immunoreactive forα₂A-adrenergic receptors. This study suggests that, like noradrenergic cells of the LC, C1 adrenergic neurons of the RVLM are: (i) inhibited by both opiate andα₂-adrenergic receptor agonists; and (ii) activated during naloxone-precipitated morphine withdrawal, Since C1 cells are considered essential to sympathetic tone generation, their inhibition by morphine may contribute to the hypotensive effects of this opioid agonist in non-dependent individuals. Their excitation during opiate withdrawal may also contribute to the autonomic activation that characterizes this syndrome. Finally, inhibition of C1 cells by clonidine may contribute to the clinically recognized efficacy of this drug to attenuate autonomic signs of opiate withdrawal.     

Pancreatic vasoconstrictor responses are regulated by neurons in the rostral ventrolateral medulla

The pancreas receives sympathetic input which arises from several premotor cell groups in the CNS including the rostral ventrolateral medulla (RVLM). In this study, we examined the influence of electrical stimulation of the RVLM on pancreatic blood flow measured by laser Doppler flowmetry and gastric blood flow measured by ultrasonic Doppler flowmetry in halothane-anesthetized rats. The laser Doppler flow measurement technique was validated by demonstration that pancreatic conductance was reduced by systemic administration of the vasoconstrictor phenylephrine and increased by the vasodilator sodium nitroprusside. Sympathetic vasomotor withdrawal induced by either administration of phenylbiguanide (2 and 10 microg/kg, i.v.) or electrical stimulation of the central end of the cervical vagal trunk (5 Hz, 2 ms, 50-150 microA) produced depressor responses and increases in pancreatic and gastric vascular conductance. Electrical stimulation of the RVLM (50 Hz, 0.5 ms, 25-75 microA) produced pressor and tachycardic responses accompanied by decreases in pancreatic and gastric vascular conductance. All responses to RVLM stimulation were abolished by blockade of ganglionic neurotransmission (hexamethonium bromide, 20 mg/kg, i.v.). These data suggest that RVLM presympathetic vasomotor neurons are a primary source of tonic sympathetic vasomotor drive to the pancreatic and gastric vasculature.     

Synaptic interactions in neurones of the rat rostral ventrolateral medulla oblongata

Increasing number of studies indicate that stimulation of peripheral nerves elicits complex postsynaptic responses in neurones of the ventral medulla oblongata. The present study describes a recommended protocol for intracellular recording of complex postsynaptic events in neurones of the ventral medulla oblongata. The aim was to provide surgical and experimental details that will enable successful recording of slow synaptic responses in vivo, in addition to the recording of fast evoked responses. The existence of slow inhibitory responses to stimulation of the cervical vagus and sciatic nerves have already been demonstrated together with the existence of convergent visceral and viscero-somatic inputs to neurones here. The data collected in over 200 neurones so far indicated that neurones of the rostral ventrolateral medulla oblongata play an important and versatile role in the integration of somato-visceral sensory inputs.     

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.