Lateral Tegmental Field Neurons Research Articles

Responses of Neurons in the Medullary Lateral Tegmental Field and Nucleus Tractus Solitarius to Vestibular Stimuli in Conscious Felines.

Considerable evidence shows that the vestibular system contributes to adjusting sympathetic nervous system activity to maintain adequate blood pressure during movement and changes in posture. However, only a few prior experiments entailed recordings in conscious animals from brainstem neurons presumed to convey baroreceptor and vestibular inputs to neurons in the rostral ventrolateral medulla (RVLM) that provide inputs to sympathetic preganglionic neurons in the spinal cord. In this study, recordings were made in conscious felines from neurons in the medullary lateral tegmental field (LTF) and nucleus tractus solitarius (NTS) identified as regulating sympathetic nervous system activity by exhibiting changes in firing rate related to the cardiac cycle, or cardiac-related activity (CRA). Approximately 38% of LTF and NTS neurons responded to static 40° head up tilts with a change in firing rate (increase for 60% of the neurons, decrease for 40%) of ~50%. However, few of these neurons responded to 10° sinusoidal rotations in the pitch plane, in contrast to prior findings in decerebrate animals that the firing rates of both NTS and LTF neurons are modulated by small-amplitude body rotations. Thus, as previously demonstrated for RVLM neurons, in conscious animals NTS and LTF neurons only respond to large rotations that lead to changes in sympathetic nervous system activity. The similar responses to head-up rotations of LTF and NTS neurons with those documented for RVLM neurons suggest that LTF and NTS neurons are components of the vestibulo-sympathetic reflex pathway. However, a difference between NTS/LTF and RVLM neurons was variability in CRA over time. This variability was significantly greater for RVLM neurons, raising the hypothesis that the responsiveness of these neurons to baroreceptor input is adjusted based on the animal's vigilance and alertness.

Carotid chemoreceptors tune breathing via multipath routing: reticular chain and loop operations supported by parallel spike train correlations.

We tested the hypothesis that carotid chemoreceptors tune breathing through parallel circuit paths that target distinct elements of an inspiratory neuron chain in the ventral respiratory column (VRC). Microelectrode arrays were used to monitor neuronal spike trains simultaneously in the VRC, peri-nucleus tractus solitarius (p-NTS)-medial medulla, the dorsal parafacial region of the lateral tegmental field (FTL-pF), and medullary raphe nuclei together with phrenic nerve activity during selective stimulation of carotid chemoreceptors or transient hypoxia in 19 decerebrate, neuromuscularly blocked, and artificially ventilated cats. Of 994 neurons tested, 56% had a significant change in firing rate. A total of 33,422 cell pairs were evaluated for signs of functional interaction; 63% of chemoresponsive neurons were elements of at least one pair with correlational signatures indicative of paucisynaptic relationships. We detected evidence for postinspiratory neuron inhibition of rostral VRC I-Driver (pre-Bötzinger) neurons, an interaction predicted to modulate breathing frequency, and for reciprocal excitation between chemoresponsive p-NTS neurons and more downstream VRC inspiratory neurons for control of breathing depth. Chemoresponsive pericolumnar tonic expiratory neurons, proposed to amplify inspiratory drive by disinhibition, were correlationally linked to afferent and efferent "chains" of chemoresponsive neurons extending to all monitored regions. The chains included coordinated clusters of chemoresponsive FTL-pF neurons with functional links to widespread medullary sites involved in the control of breathing. The results support long-standing concepts on brain stem network architecture and a circuit model for peripheral chemoreceptor modulation of breathing with multiple circuit loops and chains tuned by tegmental field neurons with quasi-periodic discharge patterns. NEW & NOTEWORTHY We tested the long-standing hypothesis that carotid chemoreceptors tune the frequency and depth of breathing through parallel circuit operations targeting the ventral respiratory column. Responses to stimulation of the chemoreceptors and identified functional connectivity support differential tuning of inspiratory neuron burst duration and firing rate and a model of brain stem network architecture incorporating tonic expiratory "hub" neurons regulated by convergent neuronal chains and loops through rostral lateral tegmental field neurons with quasi-periodic discharge patterns.

Effects of visceral inputs on the processing of labyrinthine signals by the inferior and caudal medial vestibular nuclei: ramifications for the production of motion sickness

Neurons located in the caudal aspect of the vestibular nucleus complex have been shown to receive visceral inputs and project to brainstem regions that participate in generating emesis, such as nucleus tractus solitarius and the "vomiting region" in the lateral tegmental field (LTF). Consequently, it has been hypothesized that neurons in the caudal vestibular nuclei participate in triggering motion sickness and that visceral inputs to the vestibular nucleus complex can affect motion sickness susceptibility. To obtain supporting evidence for this hypothesis, we determined the effects of intragastric infusion of copper sulfate (CuSO4) on responses of neurons in the inferior and caudal medial vestibular nuclei to rotations in vertical planes. CuSO4 readily elicits nausea and emesis by activating gastrointestinal (GI) afferents. Infusion of CuSO4 produced a >30% change in spontaneous firing rate of approximately one-third of neurons in the caudal aspect of the vestibular nucleus complex. These changes in firing rate developed over several minutes, presumably in tandem with the emetic response. The gains of responses to vertical vestibular stimulation of a larger fraction (approximately two-thirds) of caudal vestibular nucleus neurons were altered over 30% by administration of CuSO4. The response gains of some units went up, and others went down, and there was no significant relationship with concurrent spontaneous firing rate change. These findings support the notion that the effects of visceral inputs on motion sickness susceptibility are mediated in part through the caudal vestibular nuclei. However, our previous studies showed that infusion of CuSO4 produced larger changes in response to vestibular stimulation of LTF neurons, as well as parabrachial nucleus neurons that are believed to participate in generating nausea. Thus, integrative effects of GI inputs on the processing of labyrinthine inputs must occur at brain sites that participate in eliciting motion sickness in addition to the caudal vestibular nuclei. It seems likely that the occurrence of motion sickness requires converging inputs to brain areas that generate nausea and vomiting from a variety of regions that process vestibular signals.

Processing of vestibular inputs by the medullary lateral tegmental field of conscious cats: implications for generation of motion sickness

The dorsolateral reticular formation of the caudal medulla, the lateral tegmental field (LTF), participates in generating vomiting. LTF neurons exhibited complex responses to vestibular stimulation in decerebrate cats appropriate for a brain region that generates motion sickness. Since responses of brainstem neurons to vestibular stimulation can differ between decerebrate and conscious animals, the current study examined the effects of vestibular stimulation on the activity of LTF neurons in conscious felines. We examined whether LTF neurons had spatial‐temporal convergence (STC) behavior, which is due to the convergence of vestibular inputs with different spatial and temporal properties. The proportion of LTF neurons with STC behavior in conscious animals (25%) was similar to that in decerebrate cats. Far fewer neurons in other regions of the feline brainstem had STC behavior. However, responses to vertical plane vestibular stimulation were considerably different in decerebrate and conscious felines for LTF neurons lacking STC behavior. In decerebrate cats, most LTF neurons had responses similar to those of otolith organ afferents; in conscious animals, the response properties were similar to those of semicircular canal afferents. These differences show that higher centers of the brain regulate the labyrinthine inputs relayed to the LTF.

Responses of neurons in the caudal medullary lateral tegmental field to visceral inputs and vestibular stimulation in vertical planes

The dorsolateral reticular formation of the caudal medulla, or lateral tegmental field (LTF), has been classified as the brain's “vomiting center” as well as an important region in regulating blood pressure. We examined in cats the responses of LTF neurons to rotations of the body that activate vertical semicircular canals and otolith organs, as well as to stimulation of baroreceptors and gastrointestinal receptors (through the intragastric administration of the emetic compound copper sulfate). Half of the LTF neurons exhibited graviceptive responses to vestibular stimulation, similar to primary afferents innervating otolith organs. The other half of the neurons had complex responses, suggesting that they received convergent inputs from a variety of vestibular receptors, as expected for neurons that contribute to the generation of motion sickness. The administration of copper sulfate often modulated the gain of responses of LTF neurons to vestibular stimulation, particularly for units whose spontaneous firing rate was altered by infusion of drug (median of 459%). The present results thus raise the prospect that emetic signals from the gastrointestinal tract modify the processing of vestibular inputs by LTF neurons, thereby affecting the probability that vomiting will occur as a consequence of motion sickness.

Processing of vestibular inputs by the medullary lateral tegmental field of conscious cats: implications for generation of motion sickness

The dorsolateral reticular formation of the caudal medulla, the lateral tegmental field (LTF), participates in generating vomiting. LTF neurons exhibited complex responses to vestibular stimulation in decerebrate cats, indicating that they received converging inputs from a variety of labyrinthine receptors. Such a convergence pattern of vestibular inputs is appropriate for a brain region that participates in generating motion sickness. Since responses of brainstem neurons to vestibular stimulation can differ between decerebrate and conscious animals, the current study examined the effects of whole-body rotations in vertical planes on the activity of LTF neurons in conscious felines. Wobble stimuli, fixed-amplitude tilts, the direction of which moves around the animal at a constant speed, were used to determine the response vector orientation, and also to ascertain whether neurons had spatial-temporal convergence (STC) behavior (which is due to the convergence of vestibular inputs with different spatial and temporal properties). The proportion of LTF neurons with STC behavior in conscious animals (25%) was similar to that in decerebrate cats. Far fewer neurons in other regions of the feline brainstem had STC behavior, confirming findings that many LTF neurons receive converging inputs from a variety of labyrinthine receptors. However, responses to vertical plane vestibular stimulation were considerably different in decerebrate and conscious felines for LTF neurons lacking STC behavior. In decerebrate cats, most LTF neurons had graviceptive responses to rotations, similar to those of otolith organ afferents. However, in conscious animals, the response properties were similar to those of semicircular canal afferents. These differences show that higher centers of the brain that are removed during decerebration regulate the labyrinthine inputs relayed to the LTF, either by gating connections in the brainstem or by conveying vestibular inputs directly to the region.

Responses of neurons in the caudal medullary lateral tegmental field to visceral inputs and vestibular stimulation in vertical planes.

The dorsolateral reticular formation of the caudal medulla, or the lateral tegmental field (LTF), has been classified as the brain's "vomiting center", as well as an important region in regulating sympathetic outflow. We examined the responses of LTF neurons in cats to rotations of the body that activate vestibular receptors, as well as to stimulation of baroreceptors (through mechanical stretch of the carotid sinus) and gastrointestinal receptors (through the intragastric administration of the emetic compound copper sulfate). Approximately half of the LTF neurons exhibited graviceptive responses to vestibular stimulation, similar to primary afferents innervating otolith organs. The other half of the neurons had complex responses, including spatiotemporal convergence behavior, suggesting that they received convergent inputs from a variety of vestibular receptors. Neurons that received gastrointestinal and baroreceptor inputs had similar complex responses to vestibular stimulation; such responses are expected for neurons that contribute to the generation of motion sickness. LTF units with convergent baroreceptor and vestibular inputs may participate in producing the cardiovascular system components of motion sickness, such as the changes in skin blood flow that result in pallor. The administration of copper sulfate often modulated the gain of responses of LTF neurons to vestibular stimulation, particularly for units whose spontaneous firing rate was altered by infusion of drug (median of 459%). The present results raise the prospect that emetic signals from the gastrointestinal tract modify the processing of vestibular inputs by LTF neurons, thereby affecting the probability that vomiting will occur as a consequence of motion sickness.

Medullary lateral tegmental field neurons influence the timing and pattern of phrenic nerve activity in cats

In an effort to characterize the role of the medullary lateral tegmental field (LTF) in regulating respiration, we tested the effects of selective blockade of excitatory (EAA) and inhibitory amino acid (IAA) receptors in this region on phrenic nerve activity (PNA) of vagus-intact and vagotomized cats anesthetized with dial-urethane. We found distinct patterns of changes in central respiratory rate, duration of inspiratory and expiratory phases of PNA (Ti and Te, respectively), and I-burst amplitude after selective blockade of EAA and IAA receptors in the LTF. First, blockade of N-methyl-D-aspartate (NMDA) receptors significantly (P < 0.05) decreased central respiratory rate primarily by increasing Ti but did not alter I-burst amplitude. Second, blockade of non-NMDA receptors significantly reduced I-burst amplitude without affecting central respiratory rate. Third, blockade of GABAA receptors significantly decreased central respiratory rate by increasing Te and significantly reduced I-burst amplitude. Fourth, blockade of glycine receptors significantly decreased central respiratory rate by causing proportional increases in Ti and Te and significantly reduced I-burst amplitude. These changes in PNA were markedly different from those produced by blockade of EAA or IAA receptors in the pre-Bötzinger complex. We propose that a proper balance of excitatory and inhibitory inputs to several functionally distinct pools of LTF neurons is essential for maintaining the normal pattern of PNA in anesthetized cats.

Fractal noises and motions in time series of presympathetic and sympathetic neural activities

We used Allan factor analysis to classify time series of the discharges of single presympathetic neurons in the cat medullary lateral tegmental field (LTF) and rostral ventrolateral medulla (RVLM) and of the postganglionic vertebral sympathetic nerve. These time series fell into two classes of fractal signals characterized by statistically self-similar behavior reflecting long-range correlations among data points. Classification of a time series as either fractional Gaussian noise (fGn) or fractional Brownian motion (fBm) was based on the scaling exponent, alpha, of the power law in the Allan factor curve. fGn is defined as 0 < alpha < 1 and fBm as 1 < alpha < 3. All but one of the spike trains of 12 classifiable LTF neurons with sympathetic nerve-related activity were fGn. In contrast, the spike trains of 8 of 9 RVLM presympathetic neurons that could be classified were fBm. The time series of simultaneously recorded vertebral sympathetic nerve discharge and heart period fell into the fBm class. Because a fBm signal is the cumulative sum of the elements comprising the corresponding fGn signal, these results demonstrate smoothing of fractal time series in a feedforward direction from medullary presympathetic neurons to postganglionic sympathetic neurons. Whether this involves integration by RVLM neurons of their LTF inputs or independent fractal processes acting at different levels of the network controlling sympathetic nerve discharge remains to be determined. (Supported by NIH HL-33266.)

Fractal Noises and Motions in Time Series of Presympathetic and Sympathetic Neural Activities

We used Allan factor analysis to classify time series of the discharges of single presympathetic neurons in the cat medullary lateral tegmental field (LTF) and rostral ventrolateral medulla (RVLM) and of the postganglionic vertebral sympathetic nerve. These time series fell into two classes of fractal-based point processes characterized by statistically self-similar behavior reflecting long-range correlations among data points. Classification of a time series as either a fractional Gaussian noise (fGn)-or fractional Brownian motion (fBm)-based point process depended on the scaling exponent, alpha, of the power law in the Allan factor curve. fGn is defined as 0 < alpha < 1 and fBm as 1 < alpha < 3. The process responsible for the fractal spike trains of 11 of 12 classifiable LTF neurons with sympathetic nerve-related activity was fGn. In contrast, the process responsible for the fractal spike trains of eight of nine classifiable RVLM presympathetic neurons was fBm. The time series of simultaneously recorded vertebral sympathetic nerve discharge and the arterial pulse also were fBm-based signals. Because a fBm signal is the cumulative sum of the elements comprising the corresponding fGn signal, these results show smoothing of fractal time series in a feedforward direction from medullary presympathetic neurons to postganglionic sympathetic neurons. This may involve integration by RVLM neurons of their LTF inputs or independent fractal processes acting at different levels of the network controlling sympathetic nerve discharge. Whether feedforward smoothing of fractal signals is a feature in other neural systems is open to investigation.

Role of the medullary lateral tegmental field in reflex-mediated sympathoexcitation in cats.

We tested the hypothesis that blockade of N-methyl-D-aspartate (NMDA) and non-NMDA receptors on medullary lateral tegmental field (LTF) neurons would reduce the sympathoexcitatory responses elicited by electrical stimulation of vagal, trigeminal, and sciatic afferents, posterior hypothalamus, and midbrain periaqueductal gray as well as by activation of arterial chemoreceptors with intravenous NaCN. Bilateral microinjection of a non-NMDA receptor antagonist into LTF of urethane-anesthetized cats significantly decreased vagal afferent-evoked excitatory responses in inferior cardiac and vertebral nerves to 29 +/- 8 and 24 +/- 6% of control (n = 7), respectively. Likewise, blockade of non-NMDA receptors significantly reduced chemoreceptor reflex-induced increases in inferior cardiac (from 210 +/- 22 to 129 +/- 13% of control; n = 4) and vertebral nerves (from 253 +/- 41 to 154 +/- 20% of control; n = 7) and mean arterial pressure (from 39 +/- 7 to 21 +/- 5 mmHg; n = 8). Microinjection of muscimol, but not an NMDA receptor antagonist, caused similar attenuation of these excitatory responses. Sympathoexcitatory responses to the other stimuli were not attenuated by microinjection of a non-NMDA receptor antagonist or muscimol into LTF. In fact, excitatory responses elicited by stimulation of trigeminal, and in some cases sciatic, afferents were enhanced. These data reveal two new roles for the LTF in control of sympathetic nerve activity in cats. One, LTF neurons are involved in mediating sympathoexcitation elicited by activation of vagal afferents and arterial chemoreceptors, primarily via activation of non-NMDA receptors. Two, non-NMDA receptor-mediated activation of other LTF neurons tonically suppresses transmission in trigeminal-sympathetic and sciatic-sympathetic reflex pathways.

The role of the medullary lateral tegmental field in the generation and baroreceptor reflex control of sympathetic nerve discharge in the cat.

Data from experiments with single neuron recordings as well as central microinjections of N-methyl-D-aspartate (NMDA) and non-NMDA excitatory amino receptor antagonists that have led to a model of central sympathetic pathways that includes synaptic relays in the medullary lateral tegmental field (LTF) of the cat are summarized. Evidence is presented that (1) the LTF contains a population of tonically active sympathoexcitatory neurons that drive rostral ventrolateral medullary neurons, (2) blockade of non-NMDA receptors in the LTF significantly reduces basal levels of sympathetic nerve discharge (SND) and mean arterial pressure in baroreceptor-denervated cats, and (3) blockade of NMDA-mediated neurotransmission in the LTF prevents baroreceptor reflex control of SND. Thus, LTF neurons play an important role in the generation and baroreceptor reflex control of SND in the cat.

Lateral tegmental field neurons with activity correlated to the 10-Hz rhythm in sympathetic nerve discharge

Neurons in the lateral tegmental field (FTL) has been previously reported to have activity only minimally correlated (<1% of neurons tested) with the 10-Hz rhythm of the slow wave of the sympathetic nerve discharge. We report here that 10% of the neurons recently tested in the FTL could be shown to correlate with the 10-Hz rhythm. The neuron-to-nerve coherence is weaker than in other medullary areas, but is nonetheless significant.

Lateral Tegmental Field Neurons Sensitive to Muscular Contraction: A Role in Pressor Reflexes?

Lateral Tegmental Field Neurons Sensitive to Muscular Contraction: A Role in Pressor Reflexes?

Lateral tegmental field neurons sensitive to muscular contraction: A role in pressor reflexes?

The medullary lateral tegmental field (LTF) has a major role in sympathetic nerve discharge (SND) rhythmicity, but its role in pressor reflexes generated by hindlimb muscular contraction (MC) is unknown. Therefore, two sets of experiments were performed in 17 chloralose-urethane anesthetized cats. First, response of single LTF neurons to MC induced by L7-S1 ventral root stimulation were examined. The majority (30 of 47) of LTF neurons increased firing during MC. Most LTF neurons had a basal discharge correlated with the 2–10 Hz rhythm of SND or the cardiac cycle and responded to increases in blood pressure. Only seven neurons were inhibited by MC, most having a respiratory rhythm. Second, pressor responses to MC and to caudal hypothalamic stimulation were examined before and after bilateral LTF microinjections of a synaptic blocker (CoCl 2) as well as with lidocaine. Microinjection of CoCl 2 or lidocaine significantly attenuating the dominant 2–10 Hz power coefficient of SND had no effect on the pressor responses to MC or caudal hypothalamic stimulation. Therefore, LTF may be important for basal rhythms in SND and may help synchronize SND during MC, but its contribution to basal rhythms is apparently not required for pressor reflexes evoked by hindlimb MC or hypothalamic stimulation.

Vestibular inputs to the lateral tegmental field of the cat: potential role in autonomic control

The lateral tegmental field (LTF), which is comprised of the lateral reticular formation near the obex, is an important integrative area involved in cardiovascular control and the production of emesis. Using neuroanatomical and electrophysiological techniques, we tested the hypothesis that LTF neurons receive vestibular inputs; the neurons studied include those projecting into the subretrofacial rostral ventrolateral medulla (sRVLM), which contains cells that make direct connections with sympathetic preganglionic neurons. Injections of the anterograde tracer PHA-L into the medial and inferior vestibular nuclei produced labeled terminals in the LTF. Electrical stimulation of the vestibular nerve affected the firing rate of LTF neurons, including approximately one-third of those antidromically activated from the sRVLM. The response latencies ranged from 1.5 to 20 ms, suggesting that the neurons received both direct and polysynaptic vestibular inputs from the vestibular nuclei. The LTF may be involved in the production of vestibulosympathetic reflexes and vestibular-elicited vomiting.

Central control of breathing in mammals: neuronal circuitry, membrane properties, and neurotransmitters

Central control of breathing in mammals: neuronal circuitry, membrane properties, and neurotransmitters

Sensory innervation of the viscera: peripheral basis of visceral pain.

Sensory innervation of the viscera: peripheral basis of visceral pain.

Lateral tegmental field neurons play a permissive role in governing the 10-Hz rhythm in sympathetic nerve discharge.

Recordings from sympathetic nerves in decerebrate cats show a variable mixture of 10-Hz and 2- to 6-Hz discharges. Although medullary lateral tegmental field (LTF) neurons are considered to be a source of the 2- to 6-Hz oscillation in sympathetic nerve discharge (SND), their role in the control of the 10-Hz rhythm has not been critically evaluated. This issue served as the focus of the current study. In the first series of experiments, spike-triggered averaging of inferior cardiac SND was used in an attempt to identify LTF neurons with activity correlated to the 10-Hz rhythm in SND. The discharges of only one of the 120 LTF neurons studied were correlated to this component of SND. In contrast, 17 of 79 neurons had activity correlated to the 2- to 6-Hz oscillation in experiments in which this component of SND was prominent. These data indicate that LTF neurons neither receive input from nor are components of the 10-Hz rhythm generator. In a second series of experiments, muscimol was microinjected into the LTF bilaterally. Chemical inactivation of the LTF either eliminated the 10-Hz rhythm or reduced the power and peak frequency in this band of SND. These data support the view that LTF neurons have a permissive role in governing the 10-Hz rhythm in SND, probably by acting on elements of the rhythm generator located elsewhere. As expected, muscimol microinjections reduced the power in the 2- to 6-Hz band in SND in some experiments.

Lateral tegmental field neurons of cat medulla: a source of basal activity of raphespinal sympathoinhibitory neurons.

1. We tested the hypothesis that sympathoinhibitory (SI) neurons in the lateral tegmental field (LTF) of the cat medulla exert their actions over a pathway that includes raphe neurons whose axons innervate the thoracic intermediolateral nucleus (IML). 2. We recorded from 32 LTF neurons with sympathetic nerve-related activity [as demonstrated with spike-triggered averaging of inferior cardiac sympathetic nerve discharge (SND)] whose firing rate increased during the inhibition of SND produced by baroreceptor reflex activation. These neurons were classified as SI in function. 3. Twenty-three of these 32 LTF-SI neurons were antidromically activated by microstimulation of the raphe nuclei, 2-4 mm rostral to the obex and 3-4.5 mm below the dorsal surface of the medulla. The threshold current for eliciting the longest-latency antidromic responses [18.9 +/- 2.4 (SE) ms] was increased when the stimulating microelectrode was moved more dorsally in the midline. With one exception, these neurons could not be antidromically activated by stimulation of sites either 1.5-2.0 mm lateral to the midline, contralateral to the site of unit recording or raphe sites caudal to the obex. Threshold stimuli applied 2-4 mm rostral to the obex and 1 mm lateral to the midline, ipsilateral to the site of unit recording, elicited antidromic responses whose onset latencies were shorter than those produced by raphe stimulation. These data support the view that the axons of LTF-SI neurons terminated in the region of the raphe that contains SI neurons whose axons innervate the IML. 4. We recorded from 32 raphe neurons with sympathetic nerve-related activity whose firing rate increased during baroreceptor reflex activation. These neurons were classified as SI in function. Twenty-five of the 32 raphe-SI neurons were antidromically activated by microstimulation of the third thoracic (T3) IML. Seven (including 5 with spinal axons) of 24 raphe-SI neurons tested were synaptically activated by microstimulation of the region of the LTF containing SI neurons. The modal onset latency of synaptic activation was 22.8 +/- 8.4 ms. This value is close to the difference in spontaneous firing times (26 ms on the average) of LTF-SI and raphe-SI neurons, relative to the peak of the cardiac-related burst of SND. 5. Taken together, these data are consistent with the hypothesis that LTF-SI neurons are a source of the background discharges of raphespinal-SI neurons. 6. Thirteen raphe-SI neurons were antidromically activated by stimulation of both the medulla and T3 IML.(ABSTRACT TRUNCATED AT 400 WORDS)