Biomedical subjects

R M McAllen

Publications and source records attributed to R M McAllen.

At least 19 recordsLinked to original sources

PubMed2005

Interactive drives from two brain stem premotor nuclei are essential to support rat tail sympathetic activity.

Anatomical studies indicate that sympathetic preganglionic neurons receive inputs from several brain stem cell groups, but the functional significance of this organization for vasomotor control is not known. We studied the roles of two brain stem premotor cell groups, the medullary raphé and the rostral ventrolateral medulla (RVLM), in determining the activity of sympathetic vasomotor supply to the tail of urethane-anesthetized, artificially ventilated rats. Chemical inactivation of either RVLM (bilaterally) or raphé cells by microinjecting glycine (120-200 nl, 0.5 M) or muscimol (40-160 nl, 2.1-8 mM) was sufficient to inhibit ongoing tail sympathetic fiber activity and to block its normally strong response to mild cooling via the trunk skin (reducing rectal temperature from 38.5 to 37 degrees C). After bilateral RVLM inactivation, tail sympathetic fibers could still be excited by chemical stimulation of raphé neurons (l-glutamate, 120 nl, 50 mM), and strong cooling (rectal temperature approximately 33 degrees C) caused a low level of ongoing activity. After chemical inhibition of raphé neurons, however, neither strong cooling nor chemical stimulation of RVLM neurons activated tail sympathetic fibers. Electrical stimulation of the RVLM elicited tail sympathetic fiber volleys before and after local anesthesia of the raphé (150-500 nl of 5% tetracaine), demonstrating the existence of an independent descending excitatory pathway from the RVLM. The data show that neurons in both the medullary raphé and the RVLM, acting together, provide the essential drive to support vasomotor tone to the tail. Inputs from these two premotor nuclei interact in a mutually facilitatory manner to determine tonic, and cold-induced, tail sympathetic activity.

Action Potentials↗

PubMed2004

Descending vasomotor pathways from the dorsomedial hypothalamic nucleus: role of medullary raphe and RVLM.

The dorsomedial hypothalamic nucleus (DMH) is believed to play a key role in mediating vasomotor and cardiac responses evoked by an acute stress. Inhibition of neurons in the rostral ventrolateral medulla (RVLM) greatly reduces the increase in renal sympathetic nerve activity (RSNA) evoked by activation of the DMH, indicating that RVLM neurons mediate, at least in part, the vasomotor component of the DMH-evoked response. In this study, the first aim was to determine whether neurons in the medullary raphe pallidus (RP) region also contribute to the DMH-evoked vasomotor response, because it has been shown that the DMH-evoked tachycardia is mediated by the RP region. The second aim was to directly assess the effect of DMH activation on the firing rate of RVLM sympathetic premotor neurons. In urethane-anesthetized rats, injection of the GABA(A) receptor agonist muscimol (but not vehicle solution) in the RP region caused a modest ( approximately 25%) but significant reduction in the increase in RSNA evoked by DMH disinhibition (by microinjection of bicuculline). In other experiments, disinhibition of the DMH resulted in a powerful excitation (increase in firing rate of approximately 400%) of 5 out of 6 spinally projecting barosensitive neurons in the RVLM. The results indicate that neurons in the RP region make a modest contribution to the renal sympathoexcitatory response evoked from the DMH and also that sympathetic premotor neurons in the RVLM receive strong excitatory inputs from DMH neurons, consistent with the view that the RVLM plays a key role in mediating sympathetic vasomotor responses arising from the DMH.

Animals↗

PubMed2004

Vasopressin secretion: osmotic and hormonal regulation by the lamina terminalis.

The lamina terminalis, located in the anterior wall of the third ventricle, is comprised of the subfornical organ, median preoptic nucleus (MnPO) and organum vasculosum of the lamina terminalis (OVLT). The subfornical organ and OVLT are two of the brain's circumventricular organs that lack the blood-brain barrier, and are therefore exposed to the ionic and hormonal environment of the systemic circulation. Previous investigations in sheep and rats show that this region of the brain has a crucial role in osmoregulatory vasopressin secretion and thirst. The effects of lesions of the lamina terminalis, studies of immediate-early gene expression and electrophysiological data show that all three regions of the lamina terminalis are involved in osmoregulation. There is considerable evidence that physiological osmoreceptors subserving vasopressin release are located in the dorsal cap region of the OVLT and possibly also around the periphery of the subfornical organ and in the MnPO. The circulating peptide hormones angiotensin II and relaxin also have access to peptide specific receptors (AT(1) and LGR7 receptors, respectively) in the subfornical organ and OVLT, and both angiotensin II and relaxin act on the subfornical organ to stimulate water drinking in the rat. Studies that combined neuroanatomical tracing and detection of c-fos expression in response to angiotensin II or relaxin suggest that both of these circulating peptides act on neurones within the dorsal cap of the OVLT and the periphery of the subfornical organ to stimulate vasopressin release.

Animals↗

PubMed2003

The sensory circumventricular organs of the mammalian brain.

The brain's three sensory circumventricular organs, the subfornical organ, organum vasculosum of the lamina terminalis and the area postrema lack a blood brain barrier and are the only regions in the brain in which neurons are exposed to the chemical environment of the systemic circulation. Therefore they are ideally placed to monitor the changes in osmotic, ionic and hormonal composition of the blood. This book describes their. General structure and relationship to the cerebral ventricles Regional subdivisions Vasculature and barrier properties Neurons, glia and ependymal cells Receptors, neurotransmitters, neuropeptides and enzymes Neuroanatomical connections Functions.

Animals↗

PubMed2003

The brain renin-angiotensin system: location and physiological roles.

Angiotensinogen, the precursor molecule for angiotensins I, II and III, and the enzymes renin, angiotensin-converting enzyme (ACE), and aminopeptidases A and N may all be synthesised within the brain. Angiotensin (Ang) AT(1), AT(2) and AT(4) receptors are also plentiful in the brain. AT(1) receptors are found in several brain regions, such as the hypothalamic paraventricular and supraoptic nuclei, the lamina terminalis, lateral parabrachial nucleus, ventrolateral medulla and nucleus of the solitary tract (NTS), which are known to have roles in the regulation of the cardiovascular system and/or body fluid and electrolyte balance. Immunohistochemical and neuropharmacological studies suggest that angiotensinergic neural pathways utilise Ang II and/or Ang III as a neurotransmitter or neuromodulator in the aforementioned brain regions. Angiotensinogen is synthesised predominantly in astrocytes, but the processes by which Ang II is generated or incorporated in neurons for utilisation as a neurotransmitter is unknown. Centrally administered AT(1) receptor antagonists or angiotensinogen antisense oligonucleotides inhibit sympathetic activity and reduce arterial blood pressure in certain physiological or pathophysiological conditions, as well as disrupting water drinking and sodium appetite, vasopressin secretion, sodium excretion, renin release and thermoregulation. The AT(4) receptor is identical to insulin-regulated aminopeptidase (IRAP) and plays a role in memory mechanisms. In conclusion, angiotensinergic neural pathways and angiotensin peptides are important in neural function and may have important homeostatic roles, particularly related to cardiovascular function, osmoregulation and thermoregulation.

Animals↗

PubMed2003

Are pre-ganglionic neurones recruited in a set order?

AIM: The idea that, like somatic motor neurones, sympathetic pre-ganglionic neurones are engaged to fire in a pre-determined recruitment order, was investigated in chloralose-anaesthetized cats. METHOD: Ongoing pre-ganglionic spike activity was recorded from fine filaments of otherwise intact thoracic white rami, while post-ganglionic activity was recorded from the whole inferior cardiac nerve (ICN). Spikes of individual pre-ganglionic fibres were extracted from few-fibre recordings by spike shape analysis. Presumed cardiac pre-ganglionic fibres were further selected by the spike-triggered average of ICN activity, which showed a clear peak when triggered by their spikes. RESULTS: To test whether particular pre-ganglionic neurones were recruited to fire in a set time sequence, the spontaneous spike trains of fibres in the same white ramus were compared by cross correlation. In all 24 cases the cross correlograms showed a central peak (width 163 +/- 15 ms), indicating that the two neurones tended to fire together. In 23 of the 24 cases that peak spanned the zero point on the time axis, showing that each neurone could fire either first or second. To test whether pre-ganglionic neurones were recruited in a set order with respect to burst amplitude, the firing of individual pre-ganglionic neurones was compared with the strength of the corresponding post-ganglionic burst discharge, on a heartbeat-by-heartbeat basis. Pre-ganglionic neurone firing was probabilistic: each neurone fired with only a minority of post-ganglionic bursts. Firing probability increased linearly with burst amplitude (30 of 30 cases). The slope of the relation varied between units, but its intercept was always close to the origin (zero pre-ganglionic firing probability at zero post-ganglionic burst size). CONCLUSION: The data indicate that, at least under these conditions, sympathetic pre-ganglionic neurones follow no set recruitment sequence in either their firing times or with respect to the strength of the autonomic motor output.

Action Potentials↗

PubMed2002

Thermoregulatory control of sympathetic fibres supplying the rat's tail.

We investigated the thermoregulatory responses of sympathetic fibres supplying the tail in urethane-anaesthetised rats. When skin and rectal temperatures were kept above 39 degrees C, tail sympathetic fibre activity was low or absent. When the trunk skin was cooled episodically by 2-7 degrees C by a water jacket, tail sympathetic activity increased in a graded fashion below a threshold skin temperature of 37.8 +/- 0.6 degrees C, whether or not core (rectal) temperature changed. Repeated cooling episodes lowered body core temperature by 1.3-3.1 degrees C, and this independently activated tail sympathetic fibre activity, in a graded fashion, below a threshold rectal temperature of 38.4 +/- 0.2 degrees C. Tail blood flow showed corresponding graded vasoconstrictor responses to skin and core cooling, albeit over a limited range. Tail sympathetic activity was more sensitive to core than to trunk skin cooling by a factor that varied widely (24-fold) between animals. Combined skin and core cooling gave additive or facilitatory responses near threshold but occlusive interactions with stronger stimuli. Unilateral warming of the preoptic area reversibly inhibited tail sympathetic activity. This was true for activity generated by either skin or core cooling. Single tail sympathetic units behaved homogeneously. Their sensitivity to trunk skin cooling was 0.3 +/- 0.08 spikes s(-1) degrees C(-1) and to core cooling was 2.2 +/- 0.5 spikes s(-1) degrees C(-1). Their maximum sustained firing rate in the cold was 1.82 +/- 0.35 spikes s(-1).

Adrenergic Fibers↗

PubMed2002

Activity patterns of cardiac vagal motoneurons in rat nucleus ambiguus.

Extracellular recordings were made in the right nucleus ambiguus of urethane-anesthetized rats from 33 neurons that were activated at constant latency from the craniovagal cardiac branch. Their calculated conduction velocities were in the B-fiber range (1.6-13.8 m/s, median 4.2), and most (22/33) were silent. Active units were confirmed as cardiac vagal motoneurons (CVM) by the collision test for antidromic activation and by the presence of cardiac rhythmicity in their resting discharge (9/9). Brief arterial pressure rises of 20-50 mmHg increased the activity in five of five CVM by 0.1 +/- 0.02 spikes. s(-1). mmHg(-1) from a resting 3.8 +/- 1.2 spikes/s; they also recruited activity in two of four previously silent cardiac branch-projecting neurons. CVM firing was modulated by the central respiratory cycle, showing peak activity during inspiration (8/8). Rat CVM thus show firing properties similar to those in other species, but their respiratory pattern is distinct. These findings are discussed in relation to mechanisms of respiratory sinus arrhythmia.

Action Potentials↗

PubMed2002

Control of postganglionic neurone phenotype by the rat pineal gland.

As neurones develop they are faced with choices as to which genes to express, to match their final phenotype to their role in the nervous system. A number of processes can guide these decisions. Within the autonomic and sensory nervous systems, there are a handful of examples that suggest that one mechanism that may match phenotype to function is the presence of target-derived differentiation factors. We tested whether the rat pineal gland controls the expression of a neuropeptide (neuropeptide Y) and a calcium-binding protein (calbindin) in sympathetic postganglionic neurones that innervate it. We first showed that the chemical phenotype of sympathetic neurones innervating the rat pineal includes the expression of both neuropeptide Y and the calcium-binding protein, calbindin. After transplanting the pineal gland of neonatal rats into the submandibular salivary gland of neonatal hosts, it was innervated by sympathetic axons from the surrounding salivary gland tissue, which do not normally express neuropeptide Y and calbindin. The presence of the pineal gland led to the appearance of neuropeptide Y and calbindin in many of the postganglionic neurones that innervated the graft. From these findings we suggest that, like the rodent sweat gland, the pineal gland generates a signal that can direct the neurochemical phenotype of innervating sympathetic neurones.

Animals↗

PubMed2001

Cold-activated raphé-spinal neurons in rats.

1. In a search for sympathetic premotor neurons subserving thermoregulatory functions, medullary raphé-spinal neurons were studied in urethane-anaesthetized, artificially ventilated, paralysed rats. Extracellular unit recordings were made from a region previously shown to drive the sympathetic supplies to tail vessels and brown adipose tissue. Neurons that were antidromically activated by stimulation across the intermediate region of the upper lumbar cord (the origin of the tail sympathetic outflow) were selected for study. 2. Non-noxious cooling stimuli were delivered to the animal's shaved trunk by circulating cold instead of warm water through a water jacket. Cooling increased the activity of 21 out of 76 raphé-spinal neurons by 1.0 +/- 0.2 spikes x s(-1) degrees C(-1) for falls in skin temperature of 3-5 degrees C below a threshold of 35.0 +/- 0.6 degrees C. Their responses followed skin temperature in a graded manner, and did so whether or not there was any change in core (rectal) temperature. 3. Indirect observations suggested that seven of the neurons that were activated by skin cooling were also activated by falls in core temperature (by 2.1 +/- 0.7 spikes x s(-1) x degrees C(-1) below a threshold of 36.1 +/- 0.7 degrees C), while the remainder were unaffected by core cooling. 4. An additional 7/76 raphé-spinal neurons showed evidence of inhibition (activity reduced by 2.1 +/- 0.5 spikes x s(-1) x degrees C(-1)) when the trunk skin was cooled. 5. Cold-activated raphé-spinal neurons were found in the nuclei raphé magnus and pallidus, centred at the level of the caudal part of the facial nucleus. Their spinal axons conducted at velocities between 3.4 and 29 m x s(-1) (median 6.8). 6. Drug-induced rises in arterial pressure partially inhibited the discharge of 6/14 cold-activated raphé-spinal neurons. Weak-to-moderate cardiac modulation (10-70 %) was present in arterial pulse-triggered histograms of the activity of 11/21 cold-activated raphé-spinal neurons, and 6/6 showed evidence of ventilatory modulation (two strongly, four weakly) in pump-triggered histograms. 7. Raphé-spinal neurons responded to cooling in the absence of any change in the electroencephalogram pattern (6/6 neurons). 8. Most cold-activated raphé-spinal neurons responded to noxious tail pinch (13/21 inhibited, 6/21 excited), as did most thermally unresponsive raphé-spinal cells in the same region (19/41 excited, 9/41 inhibited). 9. It is suggested that these cold-activated raphé-spinal neurons may constitute a premotor pathway that drives sympathetically mediated cold defences, such as cutaneous vasoconstriction or thermogenesis. The data are consistent with the hypothesis that a brainstem reflex, with additional descending input signalling body core temperature, may mediate autonomic responses to environmental cooling.

Animals↗

PubMed2001

Neural pathways from the lamina terminalis influencing cardiovascular and body fluid homeostasis.

1. The lamina terminalis, a region of the brain with a high concentration of angiotensin AT1 receptors, consists of three distinct nuclei, the median preoptic nucleus, the subfornical organ and organum vasculosum of the lamina terminalis (OVLT). These latter two regions lack a blood-brain and detect changes in plasma angiotensin (Ang) II concentration and osmolality. 2. Efferent neural pathways from the lamina terminalis to the hypothalamic paraventricular and supraoptic nuclei mediate vasopressin secretion in response to plasma hypertonicity and increased circulating levels of AngII. 3. Studies using the neurotropic virus pseudorabies, which undergoes retrograde transynaptic neuronal transport following injection into peripheral sites, show that neurons in the lamina terminalis have efferent polysynaptic neural connections to the peripheral sympathetic nervous system. Some of these neurons have been shown to have polysynaptic connections to the kidney and to express AT1 receptor mRNA. We propose that circulating AngII acts at AT1 receptors in the subfornical organ and OVLT to influence the sympathetic nervous system. It is likely that the neural pathway subserving this influence involves a synapse in the hypothalamic paraventricular nucleus. 4. The lamina terminalis may exert an inhibitory osmoregulatory influence on renin secretion by the kidney. This osmoregulatory influence may be mediated by inhibition of renal sympathetic nerve activity and appears to involve a central angiotensinergic synapse. 5. The lamina terminalis exerts an osmoregulatory influence on renal sodium excretion that is independent of the renal nerves and is probably hormonally mediated.

Angiotensin II↗

PubMed2001

Analysis of firing correlations between sympathetic premotor neuron pairs in anesthetized cats.

The activity of sympathetic premotor neurons in the rostral ventrolateral medulla (subretrofacial nucleus) supports sympathetic vasomotor tone, but the factors that drive these premotor neurons' activity have not been determined. This study examines whether either direct interconnections between subretrofacial neurons or synchronizing common inputs to them are important for generating their tonic activity. Simultaneous extracellular single-unit recordings were made from 32 pairs of sympathetic premotor neurons in the subretrofacial nucleus of chloralose-anesthetized cats. Paired spike trains were either separated by spike shape from a single-electrode recording (14 pairs) or recorded from two electrodes less than 250 microm apart (18 pairs). All neurons were inhibited by carotid baroreceptor stimulation and most had a spinal axon proven by antidromic stimulation from the spinal cord. Autocorrelation, inter-spike interval, and cardiac cycle-triggered histograms were constructed from the spontaneous activity of each neuron, and cross-correlation histograms covering several time scales were generated for each neuron pair. No significant peaks or troughs were found in short-term cross-correlation histograms (2 ms bins, +/-100 ms range), providing no support for important local synaptic interactions. On an intermediate time scale (20 ms bins, +/-1 s range), cross-correlation revealed two patterns indicating shared, synchronizing inputs. Repeating peaks and troughs (19/32 pairs) were due to the two neurons' common cardiac rhythmicity, of presumed baroreceptor origin. Single, zero time-spanning peaks of 40--180 ms width were seen in 5/32 cases. Calculations based on the prevalence and strength of these synchronizing inputs indicate that most of the ensemble spike activity of the subretrofacial neuron population is derived from asynchronous sources (be they intrinsic or extrinsic). If synchronizing sources such as neuronal oscillators were responsible for more than a minor part of the drive, they would be multiple, dispersed, and weak.

Action Potentials↗

PubMed2001

Brain angiotensin and body fluid homeostasis.

Angiotensinogen, the precursor molecule of the peptides angiotensin I, II, and III, is synthesized in the brain and the liver. Evidence is reviewed that angiotensin II, and possibly angiotensin III, that are generated within the brain act within neural circuits of the central nervous system to regulate body fluid balance. Immunohistochemical studies in the rat brain have provided evidence of angiotensin-containing neurons, especially in the hypothalamic paraventricular nucleus, subfornical organ, periventricular region, and nucleus of the solitary tract, as well as in extensive angiotensin-containing fiber pathways. Angiotensin immunoreactivity is observed by electron microscope in synaptic vesicles in several brain regions, the most prominent of these being the central nucleus of the amygdala. Neurons in many parts of the brain (lamina terminalis, paraventricular and parabrachial nuclei, ventrolateral medulla, and nucleus of the solitary tract) known to be involved in the regulation of body fluid homeostasis exhibit angiotensin receptors of the AT(1) subtype. Pharmacological studies in several species show that intracerebroventricular administration of AT(1) receptor antagonist drugs inhibit homeostatic responses to the central administration of hypertonic saline, intravenous infusion of the hormone relaxin, or thermal dehydration. Responses affected by centrally administered AT(1) antagonists are water drinking, vasopressin secretion, natriuresis, increased arterial pressure, reduced renal renin release, salt hunger, and thermoregulatory adjustments. We conclude that angiotensinergic neural pathways in the brain probably have an important homeostatic function, especially in regard to osmoregulation and thermoregulation, and the maintenance of arterial pressure.

Angiotensin II↗

PubMed2000

Patterning of sympathetic nerve activity in response to vestibular stimulation.

Growing evidence suggests a role for the vestibular system in regulation of autonomic outflow during postural adjustments. In the present paper we review evidence for the patterning of sympathetic nerve activity elicited by vestibular stimulation. In response to electrical activation of vestibular afferents, firing of sympathetic nerves located throughout the body is altered. However, activity of the renal nerve is most sensitive to vestibular inputs. In contrast, high-intensity simultaneous activation of cutaneous and muscle inputs elicits equivalent changes in firing of the renal, superior mesenteric and lumbar colonic nerves. Responses of muscle vasoconstrictor (MVC) efferents to vestibular stimulation are either inhibitory (Type I) or are comprised of a combination of excitation and inhibition (Type II). Interestingly, single MVC units located in the hindlimb exhibited predominantly Type I responses while those located in the forelimb and face exhibited Type II responses. Furthermore, brachial and femoral arterial blood flows were dissociated in response to vestibular stimulation, such that brachial vascular resistance increased while femoral resistance decreased. These studies demonstrate that vestibulosympathetic reflexes are patterned according to both the anatomical location and innervation target of a particular sympathetic nerve, and can lead to distinct changes in local blood flow.

Animals↗

PubMed2000

Anatomic patterning in the expression of vestibulosympathetic reflexes.

To investigate the possibility that expression of vestibulosympathetic reflexes (VSR) is related to a nerve's anatomic location rather than its target organ, we compared VSR recorded from the same type of postganglionic fiber [muscle vasoconstrictor (MVC)] located at three different rostrocaudal levels: hindlimb, forelimb, and face. Experiments were performed on chloralose-anesthetized cats, and vestibular afferents were stimulated electrically. Single MVC unit activity was extracted by spike shape analysis of few-fiber recordings, and unit discrimination was confirmed by autocorrelation. Poststimulus time histogram analysis revealed that about half of the neurons were initially inhibited by vestibular stimulation (type 1 response), whereas the other MVC fibers were initially strongly excited (type 2 response). MVC units with types 1 and 2 responses were present in the same nerve fascicle. Barosensitivity was equivalent in the two groups, but fibers showing type 1 responses fired significantly faster than those giving type 2 responses (0.29 +/- 0.04 vs. 0.20 +/- 0.02 Hz). Nerve fibers with type 1 responses were most common in the hindlimb (21 of 29 units) and least common in the face (2 of 11 units), the difference in relative proportion being significant (P < 0.05, chi(2) test). These results support the hypothesis that VSR are anatomically patterned.

Action Potentials↗

PubMed2000

Renal nerve inhibition by central NaCl and ANG II is abolished by lesions of the lamina terminalis.

The lamina terminalis is situated in the anterior wall of the third ventricle and plays a major role in fluid and electrolyte homeostasis and cardiovascular regulation. The present study examined whether the effects of intracerebroventricular infusion of hypertonic saline and ANG II on renal sympathetic nerve activity (RSNA) were mediated by the lamina terminalis. In control, conscious sheep (n = 5), intracerebroventricular infusions of 0.6 M NaCl (1 ml/h for 20 min) and ANG II (10 nmol/h for 30 min) increased mean arterial pressure (MAP) by 6 +/- 1 (P < 0.001) and 14 +/- 3 mmHg (P < 0.001) and inhibited RSNA by 80 +/- 6 (P < 0.001) and 89 +/- 7% (P < 0.001), respectively. Both treatments reduced plasma renin concentration (PRC). Intracerebroventricular infusion of artificial cerebrospinal fluid (1 ml/h for 30 min) had no effect. In conscious sheep with lesions of the lamina terminalis (n = 6), all of the responses to intracerebroventricular hypertonic saline and ANG II were abolished. In conclusion, the effects of intracerebroventricular hypertonic saline and ANG II on RSNA, PRC, and MAP depend on the integrity of the lamina terminalis, indicating that this site plays an essential role in coordinating the homeostatic responses to changes in brain Na(+) concentration.

Angiotensin II↗

PubMed1999

Differential control of sympathetic drive to the rat tail artery and kidney by medullary premotor cell groups.

Sympathetic activity was recorded from the renal nerve and the ventral tail artery of anesthetized rats while neurons in three sympathetic premotor groups, the rostroventrolateral medulla (RVLM), rostroventromedial medulla (RVMM) and medullary raphe, were activated by microinjections of sodium glutamate (1-15 nl, 50 mM). RVLM activation increased renal nerve activity by 27+/-3% but caused small, inconsistent effects on the tail outflow (+15+/-10%). Raphe neuron stimulation had little effect on the renal nerve (+8+/-3%), but strongly increased tail sympathetic unit activity (+125+/-28%). RVMM neurons had little effect on either outflow. These results indicate that different premotor cell groups have different sympathetic actions.

Animals↗

PubMed1999

Cardiac inotropic, chronotropic, and dromotropic actions of subretrofacial neurons of cat RVLM.

The cardiac actions of microinjecting sodium glutamate (0.5-2 nmol) among sympathetic premotor neurons of the subretrofacial nucleus in the rostral ventrolateral medulla (RVLM) were studied in chloralose-anesthetized cats after bilateral vagotomy, sinoaortic denervation, adrenalectomy, and alpha1-receptor blockade. Glutamate microinjections increased heart rate by 25.9 +/- 1.8 beats/min (17. 5%), systolic rate of rise in left ventricular pressure (LVdP/dt) by 1,443 +/- 110 mmHg/s (119%), and arterial blood pressure by 26.9 +/- 1.7 mmHg (50%), whereas they shortened the electrocardiogram P-R interval in 85 of 103 cases by 7.5 +/- 1.2 ms (11.4%), triggering junctional rhythms on five occasions. The increase in LVdP/dt usually led the rise in blood pressure, and its magnitude greatly exceeded any increase attributable to changes in heart rate, diastolic filling, or afterload. Right-sided microinjections caused significantly greater tachycardias than did left-sided microinjections, but only left-sided microinjections triggered junctional rhythms (5 of 52 vs. 0 of 51; P < 0.05), whereas microinjections on either side raised LVdP/dt equally. Subretrofacial neurons thus drive positive chronotropic, inotropic, and dromotropic actions via the cardiac sympathetic nerves, whereas subsets among them preferentially control different aspects of cardiac function.

Animals↗