Midcollicular Level Research Articles

Pivotal role of the ventral tegmental area in spontaneous motor activity and concomitant cardiovascular responses in decerebrate rats

Central command, a feedforward signal from higher brain centers, regulates the cardiovascular system in association with exercise. Previous evidence suggests that nucleus (or nuclei) around the midbrain may contribute to generating spontaneous motor activity and concomitant cardiovascular responses. To examine which area within the midbrain is important for the spontaneous and synchronized responses, 18 rats were decerebrated at three levels (pre-midbrain, rostroventral midbrain, and caudal midbrain levels) and paralyzed with a neuromuscular blocker. Individual brain sections showed decerebration rostral to the pre-collicular level in the pre-midbrain preparation and, additionally, removal of the periaqueductal gray in the rostroventral midbrain preparation, and decerebration around the midcollicular level in the caudal midbrain preparation. Spontaneous motor activity occurred at frequency of 69 ± 27 times/h and accompanied increases in heart rate (by 15 ± 4 beats/min) and mean arterial blood pressure (by 54 ± 4 mmHg) in the pre-midbrain preparation. Similar motor and cardiovascular responses took place in the rostroventral midbrain preparation, while such responses hardly occurred in the caudal midbrain preparation. We next examined whether injection of a GABAergic receptor agonist (muscimol) in the ventral tegmental area (VTA) inhibits the spontaneous motor and cardiovascular responses in 6 pre-midbrain preparations. The occurrence of spontaneous motor activity and concomitant cardiovascular responses was inhibited clearly (P < 0.05) by injection of muscimol, but not saline. It is concluded that the VTA plays a pivotal role in the spontaneous and synchronized activation of the motor and cardiovascular systems in decerebrate rats.

Central command: control of cardiac sympathetic and vagal efferent nerve activity and the arterial baroreflex during spontaneous motor behaviour in animals

Feedforward control by higher brain centres (termed central command) plays a role in the autonomic regulation of the cardiovascular system during exercise. Over the past 20 years, workers in our laboratory have used the precollicular-premammillary decerebrate animal model to identify the neural circuitry involved in the CNS control of cardiac autonomic outflow and arterial baroreflex function. Contrary to the traditional idea that vagal withdrawal at the onset of exercise causes the increase in heart rate, central command did not decrease cardiac vagal efferent nerve activity but did allow cardiac sympathetic efferent nerve activity to produce cardiac acceleration. In addition, central command-evoked inhibition of the aortic baroreceptor-heart rate reflex blunted the baroreflex-mediated bradycardia elicited by aortic nerve stimulation, further increasing the heart rate at the onset of exercise. Spontaneous motor activity and associated cardiovascular responses disappeared in animals decerebrated at the midcollicular level. These findings indicate that the brain region including the caudal diencephalon and extending to the rostral mesencephalon may play a role in generating central command. Bicuculline microinjected into the midbrain ventral tegmental area of decerebrate rats produced a long-lasting repetitive activation of renal sympathetic nerve activity that was synchronized with the motor nerve discharge. When lidocaine was microinjected into the ventral tegmental area, the spontaneous motor activity and associated cardiovascular responses ceased. From these findings, we conclude that cerebral cortical outputs trigger activation of neural circuits within the caudal brain, including the ventral tegmental area, which causes central command to augment cardiac sympathetic outflow at the onset of exercise in decerebrate animal models.

Chronic femoral artery occlusion augments exercise pressor reflex in decerebrated rats

Although the exercise pressor reflex evoked by static muscle contraction has been reported to be potentiated by acute ischemia of skeletal muscles, the effect of chronic muscle ischemia on the exercise pressor reflex remains unclear. We, therefore, determined if ligation of the femoral artery 72 hours prior to static contraction augmented the exercise pressor reflex in male rats. 72 hours after ligation of one femoral artery, rats were decerebrated at midcollicular level. The pressor responses to static muscle contraction were compared between the side ligated previously for 72 hours and the contralateral side. The pressor response to contraction of the side whose femoral artery was ligated 72 hours previously averaged 28 ± 8 mmHg whereas the pressor response to contraction of the contralateral freely perfused side averaged 10 ± 8 mmHg (n=4, P&lt;0.05). Likewise the pressor response to contraction on the side whose femoral artery was ligated for 72 hours previously averaged 28 ± 8 mmHg, whereas the pressor response to contraction on the contralateral side whose femoral artery was ligated for only 3 minutes averaged 8 ± 3 mmHg (n=4, P&lt;0.05). We conclude that chronic femoral arterial occlusion augments exercise pressor reflex. Supported by NIH grant HL30710.

Disuse atrophy increases the muscle mechanoreflex in rats

We investigated the effect of disuse atrophy on the magnitude of the muscle mechanoreflex. The left leg of eight rats (6-7 wk, male) was put in a plaster cast for 1 wk. The rats were decerebrated at the midcollicular level. We recorded the pressor and cardioaccelerator responses to 30-s stretch of the calcaneal tendon, which selectively stimulated the muscle mechanosensitive receptors in the left atrophied and right control triceps surae muscles. Atrophied muscles showed significantly lower mass control muscles (1.0 +/- 0.1 vs. 1.4 +/- 0.1 g; P < 0.05). At the same stretch tension (229 +/- 20 g), the pressor response to stretch was significantly greater in the atrophied muscles than in the control muscles (13 +/- 3 vs. 4 +/- 2 mmHg, P < 0.05). The cardioaccelerator response was not significantly different (8 +/- 4 vs. 4 +/- 2 beats/min). Comparing responses at the same relative tension (57 +/- 6 vs. 51 +/- 8% of maximal tension), the pressor response was still significantly greater in the atrophied triceps surae than in the control (14 +/- 4 vs. 4 +/- 2 mmHg; P < 0.05). These results suggest that disuse atrophy increases the magnitude of muscle mechanoreflex.

Effect of enflurane on the baroreflex control of heart rate in decerebrate rats.

Volatile anesthetics alter the arterial baroreflex (BRX) but its mechanisms are poorly understood. This study was designed to determine the effect of 1 and 2 minimal alveolar concentrations (MAC) of enflurane on the BRX parameters in unanesthetized brain stem-intact and decerebrate rats. Under enflurane anesthesia, the femoral artery and both femoral vein were catheterized for pressor (phenylephrine) and depressor (nitroprusside) drug delivery and continuous blood pressure measurements. Decerebration was performed at midcollicular level. BRX tests were performed in 3 time periods; before enflurane (conscious brain-intact), during 1 or 2 MAC enflurane exposure 1 hour after a sham operation or a decerebration operation, and 2 hours after the termination of enflurane (zero enflurane). Mean arterial pressure (MAP) and heart rate (HR) were fitted to a sigmoid logistic equation, the Boltzman equation. The curve of best fit was obtained with a computer program. 1 MAC and 2 MAC of enflurane shifted MAP-HR baroreflex curves to the left in the all groups and significantly attenuated the baroreflex range. The slope of conscious intact period and zero enflurane period of each group did not change significantly, but during the enflurane period the slope was significantly lowered. Enflurane depressed the baroreflex sensitivity (slope) and the HR range in a similar dose-dependent manner in both brain stem-intact and decerebrate rats. Such results draw into question whether the suprapontine sites contribute to enflurane's actions on cardiovascular autonomic regulation.

HISTORICAL NOTE: Frédéric Bremer 1892–1982: a pioneer in sleep research

Frédéric Bremer was one of the pioneer neurophysiologists who dedicated their career to understanding the neural mechanisms involved in the control of sleep-wake regulation. This paper follows his career and his major achievements. We found that Bremer's interest in sleep resulted from his unexpected observations after transecting the brain at the midcollicular level in the "encéphale isolé" preparation. The sleep-like behaviour of the animal, accompanied by slow waves in the cortex, convinced him that sleep resulted from cortical deafferentation. He was further convinced that deafferentation was the cause of sleep when he found that transecting the brain at the medullary level did not much affect the sleep-wake cycle. As we show, Bremer's views that sleep is a passive phenomenon imposed on the brain because of deafferentation was shared by most of his contemporaries. Years later Bremer admitted that he interpreted his experimental findings wrongly. He continued to investigate sleep using his preparations and made important contributions to understanding the relationships between the brainstem reticular formation and the basal forebrain hypnogenic centres, as well as the importance of light on these relationships.

The neural mechanism of rectal motility response induced by the epicardial application of lactic acid.

The epicardial application of lactic acid induced a biphasic rectal motility response in lightly anaesthetised, open-chested and artificially ventilated cats. This rectal biphasic response is reflexogenic in nature as epicardial lignocaine abolished such response. This rectal biphasic response is abolished by cardiac sympathectomy and reprecipitated by left inferior cardiac afferent nerve stimulation. Such response is also abolished by sacral ventral rhizotomy and reproduced by stimulation of the peripheral cut end of split sacral ventral roots. This indicates that the afferent and efferent pathways for such reflex are lying in the cardiac sympathetic and sacral pelvic nerves, respectively. The higher centers involved for such reflex are lying above the mid-collicular level of the brain as decerebration at the mid-collicular level completely abolished such type of rectal response. Furthermore, the relaxation phase and contraction phase of such rectal response are mediated through nitric oxide release and cholinergic neurones, respectively, as NG-nitro-L-arginine and atropine abolished relaxation and contraction phase of the rectal response, respectively.

GABA receptor-mediated inhibition of reflex deglutition in the cat.

In anesthetized cats, swallowing elicited by electrical stimulation of the superior laryngeal nerves (SLNs) was inhibited by the GABA-mimetic muscimol and by diazepam, an action that was reversed by picrotoxin and bicuculline. This inhibition supports the involvement of GABA receptors, specifically those of the GABAA subtype which both antagonists have been shown to block in various areas of the central nervous system. The inhibition of reflex swallowing and its reversal were unaltered by a transection of the brainstem at a midcollicular level. Stimulation of the SLNs also caused a bradycardia that was inhibited by both muscimol and diazepam and was restored by both GABA antagonists. Data from these experiments provide suggestive evidence for a role of GABA-ergic transmission in the central control of the deglutitory reflex.

Dorsal column stimulation induces release of serotonin and substance P in the cat dorsal horn.

The neurohumoral mechanisms behind the pain-suppressing effect of dorsal column stimulation (DCS) still remain obscure. Experimental observations have indicated an inhibitory role for serotonin and, under certain conditions, also for substance P (SP), on nociceptive transmission in the spinal cord. Furthermore, some observations suggest that these substances might be involved in the effect of DCS. The present series of experiments was undertaken to investigate whether serotonin and SP are released in the dorsal horn by DCS. Twenty-one adult cats, in some experiments anesthetized, in others decerebrated at the midcollicular level, were used. Microdialysis probes were implanted bilaterally in lumbar dorsal horns (L5-L7) and perfused with Krebs' solution. Dialysates were analyzed for serotonin by high-performance liquid chromatography or for SP by radioimmunoassay. DCS was applied at the thoracolumbar junction with current parameters similar to those used clinically in humans. DCS induced a significant release of serotonin in the dorsal horn of decerebrated animals (173 +/- 83% increase; mean +/- standard error; n = 4; P less than 0.01), whereas the levels of the metabolite 5-hydroxyindoleacetic acid were not significantly influenced. In contrast, no release of SP could be recorded in response to DCS in the decerebrated preparation, although peripheral nociceptive stimulation (pinch) and noxious electric dorsal root stimulation induced an elevation of the SP levels. However, in intact animals DCS provoked a marked SP release in the dorsal horn (190 +/- 92% increase; n = 7; P less than 0.01). The release of serotonin and SP after DCS may indicate that these substances participate in the mediation of the pain alleviating effect of DCS.(ABSTRACT TRUNCATED AT 250 WORDS)

Hypoxia-mediated in vivo release of dopamine in nucleus tractus solitarii of rabbits

A wide variety of neuroactive substances have been suggested to be involved in the respiratory depression observed in response to severe hypoxia. By use of the technique of microdialysis, the release of dopamine (DA) was measured in the nucleus tractus solitarii during severe hypoxic provocations (6% O2 in N2) in the adult pentobarbital-anesthetized rabbit. DA release was analyzed by high-performance liquid chromatography with electrochemical detection. Such hypoxic provocations caused pronounced phase of depression in the phrenic nerve activity and enhanced release of DA. After bilateral carotid sinus nerve denervation, acute severe hypoxia did not give rise to enhanced release of DA or to phrenic nerve depression. Mild hypoxic (9% or 12% O2 in N2) or hypercapnic (6% CO2) stimuli resulted in an increased phrenic nerve activity without any concomitant changes in DA release. Decerebration at the midcollicular level in rabbits prevented an enhanced release of DA in the nucleus tractus solitarii during severe hypoxia. The results suggest that 1) DA is involved in the central ventilatory response to severe hypoxia, 2) not only the initial excitatory but also the second depressive phase in response to severe hypoxia is mediated partially by the peripheral chemoreceptors, and 3) the depressive phase is dependent on intact connections from suprapontine structures.

Relative effects of different spinal autonomic nuclei on cardiac sympathoexcitatory function

Mean arterial pressure and heart rate were monitored in immobilized and artificially ventilated male Wistar rats either anesthetized with pentobarbital or decerebrated at midcollicular level. The rate of increase in the left ventricular pressure was also monitored in order to compute contractility index. L-glutamate (1.77 nmole) was microinjected (10 nl) into the following autonomic nuclei of the spinal cord at C 8 to T 4 levels: 1) intermediolateral column (IML), 2) n. intercalates spinalis (IC) and 3) n. intercalates pars paraependymalis (ICpe); this region is commonly known as the central autonomic area (CA). The site of microinjection was marked by injection of a dye; these studies suggested that microinjections of glutamate into the IML are likely to encompass the neurons in the nucleus (n.) intermediolateralis thoracolumbalis pars principalis (ILp) and n. intermediolateralis thoracolumbalis pars funicularis (ILf). Sympathoexcitatory cardiac responses to glutamate microinjections were elicited from T 1 to T 3 levels; these responses could not be evoked at C 8 and T 4 levels. In each of these segments, maximum responses were obtained from the IML while the responses evoked from the IC and the CA were minimal. These results suggest that at T 1 to T 3 levels of the spinal cord, IML is the main cell group regulating sympathetic cardiac function; CA and IC may play a relatively minor role in this function.

Microinjections of cholinergic agonists into the intermediolateral cell column of the spinal cord at T 1-T 3 increase heart rate and contractility

Cardiovascular responses to the microinjections of cholinergic agonists into the intermediolateral cell column (IML) of the spinal cord at T 1-T 3 level were studied. Mean arterial pressure (MAP), heart rate (HR), the rate of increase in the left ventricular pressure (d p/d t) and contractility index (CI) were monitored in immobilized and artificially ventilated male Wistar rats either anesthetized with pentobarbital or decerebrated at mid-collicular level. Microinjections (20 nl) of carbachol (110–660 pmol) into the right IML elicited a marked increase in HR and a small increase in CI. A marked increase in the CI with relatively little effect on the HR was observed when carbachol was injected into the left IML. The cardioacceleratory effects of carbachol, but not those of l-glutamate, were blocked by prior microinjections of scopolamine (18 nmol) into the IML. Intravenous injections of chlorisondamine (a ganglion blocker) also blocked these effects of carbachol. Spinal transections at C 4 or T 6 level did not alter these responses. Microinjections of acetylcholine (0.01–1 nmol) into the right IML also produced tachycardic effects. The responses to acetylcholine were blocked by prior injections of a muscarinic receptor blocker (atropine hemisulfate, 0.2 nmol). Microinjections of a selective M 2 muscarinic receptor agonist, cis-methyldioxolane (CD; 0.2–0.8 nmol), but not those of a relatively selective M 1 receptor agonist (McN-A343; 2–3 nmol), into the right IML elicited an increase in HR. Previous microinjections of a selective competitive M 2 receptor antagonist (AFDX-116; 0.8 nmol), but not those of a potent selective M 1 receptor antagonist (pirenzepine; 2 nmol), into the IML blocked the effects of CD. Nicotine (0.25–1 nmol)_when injected into the right INL also produced positive chronotropic effects. These responses were blocked by prior microinjections of hexamethonium (5 nmol). The above-mentioned results suggest that cholinoceptive neurons, interneurons or terminals are located in the areas of IML which control cardiac functions. Muscarinic as well as nicotinic receptors are present in this area. Muscarinic receptors are predominantly of the M 2 type. The physiological significance of the presence of cholinergic receptors in this area in controlling cardiac functions remains to be established.

M 2 muscarinic receptors mediate pressor responses to cholinergic agonists in the ventrolateral medullary pressor area

Microinjections of cholinergic agonists into the ventrolateral medullary pressor area (VLPA) evoke increase in blood pressure (BP) and heart rate (HR). Recently two major subtypes of muscarinic receptors (M 1 and M 2) have been identified. This investigation was designed to study the role of these muscarinic receptor subtypes in pressor responses of cholinergic agonists in the VLPA. Male Wistar rats were anesthetized with pentobarbital or decerebrated at mid-collicular level. The rats were artificially ventilated and BP and HR were recorded. Ventral medulla was exposed and the VLPA identified bilaterally by microinjections of l-glutamate. Microinjections of cis-methyldioxolane (CD, a specific agonist of M 2 receptors) in the doses of 0.004–4 nanomol (nmol)/site into the VLPA evoked an increase in BP (13–56 mm Hg) and HR (7–24 bpm) which lasted for 10–50 min. Intravenous injections of the same doses of this agent failed to evoke a response. AFDX-116 (a specific M 2 muscarinic receptor antagonist) microinjected into the VLPA (0.2–1.6 nmol/site) evoked depressor responses (6–20 mm Hg). Microinjections of this agent into the VLPA prevented the pressor responses to subsequent microinjections of CD at the same sites, indicating that AFDX-116 blocked M 2 receptors. AFDX-116 rendered neurons in the VLPA unresponsive to l-glutamate but this effect lasted for 30–40 min while the hypotensive and M 2 receptor blocking effect lasted for 60–150 min. McN-A343 (a specific agonist for M 1 receptors) or pirenzepine (PZ, a specific antagonist of M 1 receptors) injected into the VLPA (0.4–4 nmol/site) failed to evoke any response. Microinjections of the M 2 receptor antagonist (AFDX-116), but not the M 1 receptor antagonist (PZ), into the VLPA blocked the pressor responses to physostigmine which was injected intravenously 60 min after the microinjection of AFDX. At this time interval, the neurons in the VLPA were responsive to l-glutamate microinjections. These results indicate that the pressor and tachycardic responses evoked by cholinergic agonists in the VLPA are mediated via the M 2 receptors. Since microinjections of atropine, scopolamine and AFDX-116 into the VLPA cause a fall in BP, it is tentatively hypothesized that the M 2 receptors in the VLPA may be under tonic excitatory cholinergic control.

Responses of solitary tract nucleus neurons to taste and mechanical stimulations of the oral cavity in decerebrate rats.

Physiological characteristics of 45 taste and 15 mechanoreceptive units were examined in the solitary tract nucleus (NTS) of rats decerebrated at the pre- or midcollicular level, and compared with previous findings in the intact rat. The rostro-caudal extent of the area, where taste and mechanoreceptive neurons were recorded, was almost the same in the decerebrate rat as that in intact rat. The spontaneous discharge rate was significantly lower in the decerebrate rat than in the intact rat. The taste profile of the NTS units in decerebrate rats was quite different from that in intact rats; significant decreases in correlation coefficients were found between certain pairs of taste stimuli and spontaneous discharge rate, e.g. NaCl-quinine, sucrose-quinine. A large number of taste (18 of 31) and mechanoreceptive (12 of 15) units examined had receptive fields (RFs) on the palate, and four taste and two mechanoreceptive units on the circumvallate area. This contrasts with the findings in the intact rat. Some taste (n = 1) and mechanoreceptive units (n = 2) had large RFs. Taste units with different RF locations showed different taste profiles. Acute i.v. injection of amobarbital sodium affected only the response magnitude of taste units, suggesting that most of the differences between intact and decerebrate rats might be caused by decerebration. The present findings indicate that neural structures above the pre- or midcollicular level have tonic inhibitory or facilitatory effects on the response properties of NTS taste units.

Pressor reflex evoked by muscular contraction: contributions by neuraxis levels.

The pressor reflex evoked by muscular contraction (exercise pressor reflex) is one important model of cardiovascular adjustments during static exercise. The central nervous system (CNS) structures mediating this reflex have remained largely obscure. Therefore, we examined the contribution of selected levels of the neuraxis in mediating the pressor reflex evoked by muscular contraction from stimulation of ventral roots. Decerebrate cats exhibited larger pressor reflexes than those found in intact alpha-chloralose-anesthetized cats, a difference more apparent at low (5 Hz or repeated twitch) rather than at high (50 Hz or tetanic) stimulus frequencies. Although a depressor response to 5-Hz stimulation was observed in the intact anesthetized cats, it appeared to be primarily due to anesthetic level, since a depressor response was not observed in decerebrate animals (nonanesthetized). Cerebellectomy produced no changes in the reflexes of the decerebrate animal. Further transection of the neuraxis (caudal to the midcollicular level) attenuated the exercise pressor reflex. The spinal cat demonstrated slight evidence of exercise pressor reflex activity. These results provide clarification as to representation of this pressor reflex within the CNS and establish the reflex's characteristics at several levels of neuraxis integration.

Some effects of substance P on central respiratory control in rabbit pups

Respiratory effects of substance P (SP) have been studied in rabbit pups (I-30 days). Rabbits were either anaesthetized with urethane or decerebrated at mid-collicular level. Respiratory activity was measured with a pneumotachograph or in some cases as efferent phrenic nerve activity. SP applied to the exposed medulla oblongata from the dorsal side caused an increase of both tidal volume and respiratory frequency. The respiratory stimulation was more pronounced in decerebrate animals than in anesthetized ones. Moreover, this effect was most prominent in the youngest animals. A SP analogue (D-Arg1-D-Pro2, D-Trp7,9, Leu11)-SP was found to block the ventilatory effects of SP and to decrease the hypoxic response, while the hypercapnic response was preserved. The results suggest that SP is involved in the control of respiration, possibly mediating the hypoxic response, and that this role is more important in the neonatal period.

Naloxone-reversible respiratory inhibition induced by muscular thin-fiber afferents in decerebrated cats

Stimulation of muscular thin-fiber afferents of cats causes two types of respiratory suppression: one is stimulus-locked suppression which is not affected by naloxone, and the other is naloxone-reversible respiratory suppression after cessation of the stimulation. Both types of respiratory suppression could still be evoked after decerebration of cats at the midcollicular level. The present experiment revealed that muscular thin-fiber afferents, presumably polymodal receptor afferents, caused respiratory inhibition mediated through an opiate system in the brain structure below the caudal part of the brain stem

Properties of ventromedial hypothalamic neurons with axons to midbrain central gray.

In female rats anesthetized with urethane, 151 neurons in and around the ventromedial nucleus of the hypothalamus were identified by antidromic activation as having axonal projection to the mesencephalic central gray at the midcollicular level. Identified neurons were most numerous in the rostral part and at the borders of the nucleus.

Procedure for the decerebration of the rat

SAPRU, H. N. AND A. J. KRIEGER. Procedure for the decerebration of the rat. BRAIN. RES. BULL. 3(6) 675–679, 1978.—A procedure for the decerebration of the rat was devised. The internal and external carotid arteries were ligated under halothane anesthesia. A transection was made at the mid-collicular level of the brain and the transected forebrain was removed. The posterior communicating arteries were occluded by suction and oxidized cellulose was packed around these vessels. The cut surface of the brain was covered with oxidized cellulose and the cranial cavity was filled with cotton balls. Head-up tilt, carotid occlusion and sodium cyanide responses indicated that the orthostatic, baro-, and chemo- reflexes were intact in these preparations. The stability of the preparation (for at least 8–10 hr) and the integrity of these reflexes indicate that the decerebrate rat may be a suitable alternative for studies involving brain stem regulatory mechanisms in this species when it is desirable to avoid general anesthetics.

Ventilatory effects accompanying spontaneous movement in the suckling opossum

To determine whether spontaneous movement was associated with an organized respiratory response during early stages of mammalian development, we studied immature suckling opossums ( Didelphis virginiana) between 30 and 60 days of age. Rate and depth of breathing were measured using pressure plethysmography and movement was assessed using electromyography of neck muscles. During airbreathing as well as during ventilatory chemostimulation with hypoxic, hypercapnic, and asphyxiant test gases, the onset of spontaneous movement was often marked by an increase in minute-ventilation, dominated by an increase in breathing frequency. In the absence of respiratory irregularities, ventilation and breathing frequency remained elevated throughout an episode of movement. After decerebration at the midcollicular level, the onset of spontaneous movement was accompanied by respiratory effects similar to those found in the intact preparation. The ventilation response with spontaneous movement contrasted to results during ventilatory chemostimulation at rest, where increases in breathing resulted primarily from increases in tidal volume. It is concluded that a hyperpnea with spontaneous movement is present in the suckling opossum, and that the effect is primarily organized in the lower brainstem.