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College of Dentistry, Ohio State University, Columbus, Ohio 43218
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ABSTRACT |
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 TOP
 ABSTRACT
 INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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Previous studies have localized a central pattern generator for mastication to the midline pontomedullary reticular formation (RF) based on cortically induced ororhythmic movements. The present study determined whether this same substrate mediated licking responses evoked by more natural stimuli. Licking in the awake rat was initiated either through an appetitive response to sucrose presented in a bottle or by intraoral (IO) infusions. Oral rejection responses also were obtained by IO infusions of quinine hydrochloride. Small volumes of the GABAA agonist muscimol bilaterally infused into the lateral medullary RF significantly reduced licking and oral rejection responses measured electromyographically from the anterior digastric and geniohyoid muscles. Other than the decrement or absence of ororhythmic activity, rats appeared normal and actively approached and probed the water bottle. The suppression was reversible and returned to baseline within 3 h. In contrast, midline infusions of muscimol did not affect licking or rejection responses. We postulate that the lateral medullary RF is an essential final common path for ingestive consummatory responses.
central pattern generator; licking; mastication; feeding
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INTRODUCTION |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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EXPERIMENTS WITH DECEREBRATE preparations conclusively demonstrate that the caudal brain stem contains a substrate sufficient to produce the consummatory responses of ingestion (licking and mastication), as well as the oral component of the rejection response elicited by unpalatable substances (13, 31). The location of this substrate is generally thought to include the brain stem reticular formation (RF); however, the precise site remains somewhat unclear.
Studies employing electrical stimulation of the orbital (masticatory) cortex combined with knife cuts in the lower brain stem suggest an essential role for nucleus gigantocellularis and paragigantocellularis (6, 34), reviewed by Nakamura and Katakura (33) and Travers et al. (44). Neurons that are premotor to the oromotor nuclei, however, are concentrated more laterally in the intermediate and to a lesser extent the parvocellular RF, suggesting the necessity of more lateral regions of the RF for the production of coordinated oromotor behavior (6, 18, 47). In addition, these lateral regions are the recipients of efferent projections from brain stem sensory nuclei and thus appear to be part of the circuitry through which gustatory and orotactile inputs pass to influence oromotor responses (2, 16, 22). The lateral RF is also the target of descending input from forebrain structures related to feeding (26, 32, 37, 49, 51). In addition to anatomic studies, chronic unit recording confirms the presence of orosensory and ororhythmic responsive neurons in the lateral and intermediate subdivisions of the RF (17, 41, 45).
Despite the wealth of anatomic, physiological, and lesion data, direct evidence for the necessity of any particular RF structure in producing oromotor behavior in awake preparations is lacking. Moreover, most lesion studies, aimed at identifying critical substrates underlying ororhythmic function, have not only used anesthetized preparations but have focused on mastication, with relatively little attention directed to lingual movement. Consummatory responses usually require the coordinated movement of both tongue and jaws, as well as facial musculature (43). It seems likely, although as yet unproven, that coordination of this diversely innervated oral musculature employs a common brain stem substrate (21).
In a previous study, we demonstrated that microinfusions of lidocaine
into the RF reversibly suppressed licking and gaping (rejection) in the
awake, freely moving rat (8). Because lidocaine blocks
conductance of both cell soma and axons, this suppression could not
unambiguously be attributed to loss of cell function at the site of
infusion (25). Thus the present study used microinfusions of the 
-aminobutyric acidA (GABAA) agonist
muscimol. GABAA receptors are located on or near cell
bodies, and the effect of muscimol is thus not likely to be
attributable to fibers of passage. GABAA receptors are
nearly ubiquitous throughout the brain, and muscimol has been used
extensively in chronic preparations to produce temporary reversible
lesions (25, 30). In the present study,
ingestion and rejection behavior was quantified from electromyographic
activity from subsets of tongue and jaw muscles in awake, freely moving rats in response to the intraoral (IO) infusion of taste stimulants. Consummatory responses following more natural, appetitive behavior were
also recorded during licking from a bottle.
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METHODS |
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ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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Surgical preparation. Adult male Sprague-Dawley rats (270-450 g) were maintained on a normal 12:12-h light-dark cycle and trained to lick from a bottle containing 0.3 M sucrose for 3-4 days. After training, rats were anesthetized with pentobarbital sodium (Nembutal, 50 mg/kg ip). Supplemental doses of Nembutal (5 mg) were given to maintain a surgical level of anesthesia characterized by hindlimb areflexia. Body temperature was maintained throughout the surgery at 37°C with a body warmer. Animals were fitted with two IO cannulas to allow delivery of taste solutions into the oral cavity (12). The cannulas were inserted into oral mucosa and exited through an incision on the skull. Bipolar electromyogram (EMG) electrodes, consisting of a pair of twisted fine wires (67 µm NiCr) insulated except for 0.5 mm at the tip, were implanted via a 26-gauge needle into anterior digastric (AD) and geniohyoid (Gen) muscles (48). Leads from the EMG electrodes were guided subcutaneously to the top of the head and attached into an Amphenol connector (46).
After the IO cannulas and EMG electrodes were implanted, the head of the rat was fixed in a conventional stereotaxic instrument equipped with blunt ear bars, and the skull was made horizontal with respect to bregma and lambda. After removal of a small portion of bone 4 mm posterior to lambda, the dura was cut and removed. A 26-gauge stainless steel guide cannula (24 mm) was positioned after the anterior pole of the nucleus of the solitary tract (NST) was located and identified on the basis of recording electrophysiological responses to gustatory stimulation of the anterior tongue using a tungsten electrode (15). After this landmark was located, the guide cannula was positioned over sites including the midline (n = 7) and the lateral RF (n = 23) at various locations along the rostrocaudal extent of the medulla. An additional set of targets included the NST (n = 4). In many instances, recording from a fine-wire extending through the guide cannulas (subsequently removed) ensured accurate placement because various landmarks could be discerned, e.g., fourth ventricle, brain stem surface, NST, etc. We found that the added effort of electrophysiological guidance usually led to more accurate placement than relying on stereotaxic coordinates alone; however, all locations were subsequently verified histologically. In three instances, the guide cannulas were implanted into the RF at an angle (either across the midline or posteriorly directed) to avoid the overlying NST. The guide cannulas, as well as the IO cannulas and Amphenol strip connector, were secured to the skull with dental acrylic. A 33-gauge stainless steel tube was used as a stylet (obturator). The incision was closed with suture, and rats were given penicillin-G procaine (30,000 U im daily) for 3-4 days postoperatively. During the recovery period rats were fed a mixture of powdered rat chow and Crisco to enhance weight gain. All procedures were approved by the Institutional Animal Care and Use Committee.Adaptation and stimulation. After 2 days of recovery, rats were adapted to the testing chamber and to IO stimulation with distilled water. On the last day of adaptation and on subsequent test days, rats received three to six blocks of IO taste stimuli. Each block consisted of a 50-µl IO infusion of 0.1 M sucrose, 0.003 M quinine monohydrochloride (QHCl), and 0.1 M NaCl. Each taste stimulus was followed by three (or 6 following QHCl) infusions of water. After the water rinses to NaCl, the rat was given access to a bottle containing 0.3 M sucrose for 10 s. Each block lasted ~15 min, and consecutive blocks were separated by 30 min.
Recording and drug infusion.
There were four main groups of rats. One group with bilateral guide
cannulas in the lateral RF (n = 15) received the
"standard" dose of muscimol (0.06 nmol in 100 nl volume or 0.06 nmol/100 nl). A second group with bilateral cannulas
(n = 7), received a "low" dose of muscimol (0.03 nmol/50 nl). Two rats in the low-dose group also received bilateral
infusions of muscimol intermediate to the low and high dose (0.045 nmol/75 nl) and two rats in the bilateral standard dose group also
received a "very high" dose (
Data analysis. Rectified and integrated EMG activity (Payntor filter, 0.02-s time constant, Bak Electronics) was analyzed off-line with Modular Instruments XYZ Spreadsheet software. For each stimulus trial, the mean amplitude and rate of EMG activity were determined. To compare across animals, EMG amplitudes and rates were normalized to their respective responses obtained from the first stimulus block. These normalized responses were used in ANOVAs to test for block, stimulus, and location effects across animals. Oral rejection responses to QHCl (gapes) were identifiable in the EMG records and treated separately from licks. Gapes were characterized by larger amplitude contractions compared with licks and occurred at a slower rate (12, 48). Although data were collected for IO stimulation following both 0.1 M sucrose and 0.1 M NaCl, preliminary analyses revealed virtually identical effects and so only the 0.1 M sucrose response data are presented.
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RESULTS |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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Suppression of oromotor EMG.
In 7 of 23 cases, infusing muscimol into the lateral medullary RF
completely eliminated ingestion and rejection responses (Fig.
1). In other cases, EMG responses were
attenuated but not eliminated (Fig. 2).
These effects were both dose and location dependent.
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; ANOVA, block P = 0.926; stimulus
P = 0.486; stimulus × block interaction
P = 0.125).
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Location of effective sites.
The effect of infusion location on suppressing oromotor responses is
summarized on a horizontal schematic of the brain stem in Fig.
5 and again on coronal sections in Fig.
6. Cases were divided into three groups
based on their rostrocaudal location. Level I was anterior
to the rostral pole of the NST (rNST), level II was between
the rNST and the junction of the NST with the fourth ventricle, and
level III was caudal to the junction. Summarized for each
level are the mean percent reductions of the amplitude collapsed over
the three stimulus conditions (IO licking, bottle licking, and QHCl
stimulation) as a function of stimulus block. Two ANOVAs were
performed. The first ANOVA compared the lateral cases in level
II with midline cases (predominantly also in level II)
as a function of stimulus and block. Mediolateral location was highly
significant (P < 0.001) as was trial block
(P < 0.001), but there was no effect of stimulus
condition (P = 0.596). The interaction between block
and location was also significant (P < 0.001), but
there was no stimulus × block interaction (P = 0.724). The lack of a stimulus effect in the ANOVA justified the use of plotting the mean of the three stimulus conditions in Figs. 5 and 6.
The second ANOVA compared the eight lateral cases in level II with the five cases in level I. As with the previous
ANOVA there was a location (P < 0.001), block
(P < 0.001), and location × block (P < 0.001) effect, but no stimulus (P = 0.927) or
stimulus × block interaction (P = 0.787). A modest
mean reduction in blocks 3 and 4 was noted for the two cases in
level III at the standard dose but the small "n"
precluded any statistical treatment. Two cases using the low dose at
level III (not shown) had no effect.
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) were
intermediate to the standard and low dose.
Five cases with infusions centered rostral to rNST (level I)
were ineffective in suppressing oromotor responses at the standard dose. However, in two of these cases (and one additional case at this
level), high doses of muscimol (0.22 nmol/150 nl) greatly attenuated
oromotor responses. These three cases were made at an angle either
across the midline or from the anterior direction. Control infusions of
muscimol into the overlying the NST (n = 4, 0.06 nmol/50 nl) did not significantly alter either the AD EMG amplitude or
the lick/gape rate.
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DISCUSSION |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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The present study confirms the results of a previous study making reversible lesions in the medullary RF with 2% lidocaine (8). The use of muscimol, however, obviates the role of fibers of passage in mediating the diminution of oromotor responses. In addition, smaller volumes of muscimol (50-100 nl) were equally effective as larger volumes of lidocaine (200-400 nl), thus allowing better spatial resolution of effective sites. As others have reported, muscimol blocks last longer than lidocaine, permitting a more complete battery of tests to be performed (30).
Specificity of location. Bilateral infusions of muscimol into the lateral medullary RF profoundly reduced both licking and gaping. Similar-sized infusions centered along the midline, just 1.5 mm medial, were completely ineffective. The conclusion that the muscimol effects were restricted to a relatively small area at this dose and volume is supported by results using similar doses of muscimol in the hypothalamus (40). In that study, bilateral infusions of muscimol into the dorsomedial subnucleus were quite effective in attenuating cardiovascular responses to stress, but infusions 1 mm away in the paraventricular nucleus were ineffective.
Although we did not observe other motor disturbances following muscimol infusions into the lateral RF, additional functional changes following the infusions cannot be ruled out. In particular, this region of the RF has been implicated in autonomic function (19, 20). Muscimol infusions, comparable in dose and volume to those used in the present study, produced apnea or attenuated phrenic nerve activity when infused into the pre-Botzinger complex in anesthetized rats (39). Some of the more ventral sites in the present study appear to overlap the distribution of those effective sites producing apnea (see Fig. 4 in Ref. 39). Likewise, the infusion of muscimol into midline ventral RF sites, in areas overlapping those of the present study, blocked pinna vasoconstriction in response to trigeminal stimulation (3). Control infusions of muscimol into the overlying NST had no observable effect on oromotor behavior. Volumes of 50 nl were deliberately chosen for these control infusions because it was reasoned that only a fraction of the infusion into the deeper RF sites might have traveled up the cannula track into this structure. Moreover, in two instances, 50 nl of muscimol into the lateral RF were highly effective in attenuating the amplitude of the EMG responses, thus indicating the potential efficacy of this dose. The NST as the effective site of action of muscimol following RF infusions was also ruled out based on three infusions into the RF from an angle across the midline or from a posteriorly directed guide cannula, approaches that completely avoided the overlying NST. Although other studies making nonreversible (electrolytic) lesions in the NST have demonstrated somewhat diminished licking to water in a dehydrated state, which could be interpreted as evidence of a motor dysfunction (38), in no instances was licking totally eliminated (4, 11, 38). In summary, it appears unlikely that muscimol spread into the gustatory-responsive NST could account for the lack of oromotor responses observed in the present study.Location of a central pattern generator for ororhythmic function. Earlier studies directed at determining an essential substrate for the generation of rhythmic oromotor activity used electrical stimulation of orbital (masticatory) cortex to elicit rhythmic trigeminal activity (6, 34). By combining this electrically evoked activity with brain stem transections, a minimal substrate was deduced that appeared to require the midline RF, i.e., nucleus gigantocellularis and paragigantocellularis. However, the recognition that most preoromotor neurons were more laterally located in the RF led to their inclusion in schematics of brain stem circuitry necessary to produce ororhythmic activity (6, 33, 44). The present results indicate that a critical substrate for both appetitively and intraorally induced licking includes the lateral medullary RF and that the midline RF is not likely a necessary structure for this behavior.
However, many of the sites in the current study that were effective in attenuating or eliminating oromotor activity overlapped with sites producing diminutions of cortically elicited rhythmic trigeminal activity following lidocaine infusions into the guinea pig RF (7). In contrast to the present results, the guinea pig study found effective sites rostral to, and coincident with the facial nucleus (see Fig. 3 in Ref. 7). The use of lidocaine in this study, however, prevents differentiating cell bodies from axonal projections (fibers of passage) as the critical substrate. In fact, many neurons in the lateral RF project rostrally to the motor trigeminal nucleus (7, 47), making these axons vulnerable to lidocaine infusions. More recent studies using a brain stem slice preparation in rat have also implicated the RF rostral to the facial nucleus as a minimal substrate for generating ororhythmic activity (23, 27, 42). Rhythmic activity from the exiting trigeminal nerve could be elicited in response to excitatory amino acids added to the bath solution containing the isolated brain stem. In contrast to these in vitro and electrical brain stimulation studies, our results in awake preparations responding to natural stimuli suggest that RF areas rostral to the NST and caudal to the motor trigeminal nucleus, i.e., the region coincident with the facial nucleus, may not be an essential substrate for generating licking responses. Overall, it is not easy to reconcile data on the origin of ororhythmic responses from studies in anesthetized, cortically driven preparations or rhythmic responses elicited from tissue slices with the current study in awake, freely moving animals. These data derive from different models, frequently in different species. It may well be the case that each method of producing ororhythmic activity has a minimal substrate and that these substrates do not entirely overlap. Although cortical stimulation that produces ororhythmic activity may require a midline substrate, this does not mean that the midline structures are themselves essential for generating licking and mastication. Anatomic studies provide ample evidence for descending pathways from cortical, hypothalamic, and other limbic structures to more lateral parts of the medullary RF, and these pathways may constitute the essential descending pathways for certain types of appetitively initiated consummatory activity (26, 32, 37, 44, 49, 51). Midline medullary structures or sites rostral to the rNST though not essential to licking responses potentially play important modulatory roles. Stimulating neurons in nucleus gigantocellularis and paragigantocellularis, for example, suppresses muscle tone and may play a role in the atonia that occurs during sleep cycles (14). Likewise, oral reflex function that is altered during mastication (28) may be mediated by interneurons adjacent to the motor trigeminal nucleus that respond rhythmically during cortically induced masticatory movements and receive orosensory mechanoreceptor input (reviewed in Ref. 33).Organization of oromotor control systems. Licking and gaping were concomitantly affected by the muscimol infusions. These data are consistent with recent chronic unit recording data that showed a high degree of overlap between RF cells rhythmically active during licking and gaping (45). In the present study, we further observed that the effects of muscimol on AD and Gen activity were highly correlated; a Pearson product correlation for normalized EMG activity between these muscles across stimulus blocks was 0.65 (P < 0.001). By inference, we conclude that the two opposing functions of ingestion and rejection, both of which require the coordinated activity of the tongue and jaws, share a common spatial substrate in the lower brain stem. Indeed, anatomic studies confirm the spatial overlap of interneurons projecting to multiple oromotor nuclei (18, 47), and this has been demonstrated at the single cell level (1, 24, 35).
Interestingly, lick (and gape) rate was less affected than was amplitude by the muscimol infusions. A similar observation of an amplitude reduction independent of frequency (rate) was made with regard to phrenic nerve discharge following muscimol infusions into the A5 region (29). This independence of amplitude and frequency suggested that respiratory rhythm is controlled by different structures (29), and a similar view has been expressed with respect to the masticatory rhythm (28). We do not think, however, that the medial core of the medullary RF is the likely source for generating the lick frequency. Although previous studies have demonstrated that microstimulation of the medial RF could influence the timing (onset) of ororhythmic activity of cortical origin (5), infusions of muscimol into the midline RF had virtually no effect on lick rate. Hence, such a pathway may contribute to the generation of licking but is not essential to it. Other brain stem structures with projections to the lateral RF could contribute to generating or modulating the lick rate. These include orosensory structures and other reticular regions (10, 37). The production of a modal (i.e., 7 Hz), but by no means inflexible lick rate (50), as well as the production of the different oromotor patterns of ingestion and rejection by a common substrate undoubtedly require neuromodulatory inputs from multiple structures. Moreover, the lateral RF is a likely target for descending pathways from hypothalamic and other forebrain structures sensitive to metabolic signals (36). Because decerebrate rats lick following IO stimulation but rely on their forebrains to make an appetitive response, we conclude that both local brain stem and forebrain descending pathways converge on a common substrate that coordinates the action of several oromotor nuclei necessary to affect the consummatory response.Perspectives
Interoceptive signals that convey energy and electrolyte status are processed in both caudal and forebrain structures, e.g., the caudal NST and hypothalamus. Ultimately, regulatory information processed in either area must engage substrates that control consummatory components of ingestion. The lateral medullary RF at the level of the rNST appears to be a critical substrate for producing oral consummatory responses initiated appetitively or by direct sensory stimulation. It appears that this region of the RF is specific to oromotor function to the extent that locomotor, postural, and respiratory function appeared essentially normal when oromotor function was absent. Because both licking and gaping (rejection) were similarly affected by reversible lesions in the same area, they appear to share a common spatial substrate. However, it is unknown how a common interneuronal substrate for oromotor function orchestrates the rate, amplitude, and phase differences of the oromotor patterns that characterize the two different behaviors of ingestion and rejection. Moreover, the interface between the RF and critical regulatory structures in both the brain stem and forebrain remains poorly understood.| |
ACKNOWLEDGEMENTS |
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We are greatly indebted to Ken Herman for excellent technical assistance.
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FOOTNOTES |
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This research was supported by National Institute on Deafness and Other Communication Disorders Grants DC-00416 and DC-00417.
Address for reprint requests and other correspondence: J. Travers, College of Dentistry, Section of Oral Biology, PO Box 182357, 305 W at 12th Ave., Columbus, OH 43218-2357 (E-mail: travers.1{at}osu.edu).
The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
Received 17 July 2000; accepted in final form 4 December 2000.
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REFERENCES |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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) differed significantly from the
5 low-dose (0.03 nmol/50 nl) cases at level II
(
) and the 5 standard-dose cases at level I
(*P < 0.001). Gi, nucleus gigantocellularis; io,
inferior olive; IRt, intermediate zone of medullary RF; mVII, facial
nucleus; mXII, hypoglossal nucleus; nst, nucleus of the solitary tract;
PCRt, parvocellular RF. Case numbers are inside of or adjacent to
symbols.