Previous findings show that rats with
electrolytic or excitotoxic lesions in the dorsomedial hypothalamic
nucleus (DMN) are hypophagic and hypodipsic and have reduced ponderal
and linear growth but normal body composition. DMN-lesioned (DMNL) rats
also show altered ingestive responses to naloxone. The present study investigated the intrahypothalamic nerve pathways involved in these
DMNL effects and the response of the pathways to deprivation challenges
by placing knife cuts posterior (Post), lateral (Lat), ventral
(Vent), dorsal, or anterior to the DMN or by administering sham operations. One major finding was that rats with Post
or Vent were hypophagic (P < 0.05)
and had reduced body weight but responded normally to deprivation
challenges. Post and Lat groups were hypodipsic
(P < 0.05), but plasma
Na+,
K+, and osmolality and 24-h
post-water-deprivation drinking responses were similar in all groups.
Naloxone did not suppress the intake of Post rats. It appears that the
hypophagia and the reduced body weight after DMNL involve fibers
entering or leaving the DMN from ventral and posterior directions, and
they may be part of an opioid feeding system.
 |
INTRODUCTION |
SMALL ELECTROLYTIC LESIONS of the dorsomedial
hypothalamic nucleus (DMN) of rats produce animals that are hypophagic
and hypodipsic and show reduced body weight and linear growth but have
normal body composition when compared with sham-operated (Sham) rats (10-12, 16). Although the DMN-lesioned (DMNL) rats are hypodipsic, they regulate water consumption just as well as Sham rats
(2). Similar effects have been noted after kainic acid (9)
and ibotenic acid (1) excitotoxin destruction of neuronal cell bodies,
but not of fibers of passage, in the DMN. Notably, the secretion of anabolic hormones and intermediary metabolism is normal in DMNL rats
(11). The above changes have been termed the DMNL syndrome (11).
Although DMNL rats are hypophagic, they consume adequate calories for
their body size, show normal efficiency of food utilization (11), and
actively defend their lower body weights (5, 11). These findings
indicate that DMNL rats adequately regulate long-term energy intake and
body weight. Nevertheless, after food deprivation, excitotoxin-lesioned, but not electrolytic-lesioned, DMNL rats initially consume more food relative to body size than do Sham rats (1,
9, 11). This suggests that DMNL rats have deficits in mechanisms that
regulate short-term food intake (1, 11). This was supported by the
finding that the DMN contains glucosensitive and glucose-responsive
neurons (see Ref. 11) and that DMNL rats have deficiencies (4, 11) in
their ability to respond to short-term changes in glucose utilization
caused by infusions of insulin, glucose, or
2-deoxy-D-glucose (2-DG).
Additionally, the short-term food intake suppressor (14, 23) CCK does
not affect the intake of DMNL rats (3, 6), and DMNL rats initially overconsume an imbalanced amino acid diet (8). Therefore, the initial
overconsumption of food after food deprivation may be caused by a loss
of one or more of these short-term regulatory mechanisms. As noted
above, despite these short-term deficits in food intake regulation
after food deprivation, DMNL rats competently regulate their intake
over longer periods, i.e., days. This indicates that DMNL rats have
other intact regulatory mechanisms that adequately control long-term
caloric intake (7, 11).
The DMN contains a variety of neurotransmitters and receptors (11, 12),
including norepinephrine, neuropeptide Y (NPY), CCK, opioids, and, as
discovered most recently, leptin receptors (17). All of
these are known to affect feeding behavior and may work, at least in
part, through the DMN (11, 12, 24). With regard to opioids, naloxone
(NOX) does not suppress the food intake of DMNL rats (6), and it was
suggested that the DMN contains an opioid system, which in turn
inhibits a satiety system. In support of this was the later finding
(24) that activation of µ- and 
-receptors in the DMN increases the
animal's food intake. Still later, it was suggested that DMN opioids
play a role in eating after food deprivation (13).
The DMN is thought to contain one or more systems controlling ingestive
behavior. However, the functional brain connections of the DMN that
produce the DMNL syndrome are unknown. The present study investigated
the effects of knife cuts of fiber tracts entering or leaving the DMN
on production of the DMN syndrome.
| |
MATERIALS AND METHODS |
In trial
1, 134 male Sprague-Dawley rats
(Harlan Industries, Houston, TX) were caged individually in a
light-controlled (12:12-h light-dark cycle, lights off at 1545) and
temperature-controlled (23°C) room. The rats were given laboratory
chow (Purina) and tap water (in Wahmann calibrated bottles) ad libitum
unless otherwise specified. Food intake, corrected for spillage, and
water intake were measured daily, and body weight was recorded as noted
in Fig. 4. At the time of surgery, the rats were anesthetized with pentobarbital sodium (4.2 mg/100 g body wt). Body weight and nasoanal length were recorded (Table
1) for indirect computation
of body composition via the Lee obesity index method (see Ref. 4). The
rats were divided into six groups and given either bilateral knife cuts
or sham operations with a Scouten knife (David Kopf Instruments,
Tujunga, CA). In group
1, cuts were made (19) just posterior
(Post) to the DMN [anterior-posterior 3.8 mm, lateral to midline
0.8 mm, depth 2.5 mm (above ear bar zero)]. The knife was
extended 1.0 mm medially and then lowered 1.3 mm and retracted. In
group
2, cuts were made lateral (Lat) to the
DMN (anterior-posterior 3.8 mm, lateral to midline 0.7 mm, depth 2.5 mm). The knife was extended anteriorly 1.3 mm at an 11.5° angle
lateral to the sagittal plane, lowered 1.2 mm, and retracted. In
group
3, cuts were made ventral (Vent) to
the DMN (anterior-posterior 3.8 mm, lateral to midline 0.7 mm, depth
1.4 mm). The knife was extended 1.4 mm at an 11.5° angle lateral to
the sagittal plane. The knife was moved medially 45° so that the
knife contacted the third ventricle. Next the knife was retracted 0.1 mm and a medial 8° cut made; this was repeated until a total
101.5° (11.5° + 90°) cut was made. In
group
4, cuts were made dorsal (Dor) to the
DMN. The anterior-posterior positioning of the knife shaft on the
rat's right side was 4.9 mm, 0.8 mm lateral to the midline, and 2.6 mm
deep. The knife was extended 1.4 mm in the direction of the midline,
rotated posteriorly 78.5°, and then retracted and brought back to
the original starting position. The knife was then extended in the
direction of the midline 1.9 mm and rotated 13° posteriorly. Next
the knife shaft was inserted on the rats' left side
(anterior-posterior 3.8 mm, lateral to midline 0.7 mm, depth 2.6 mm),
and the knife was extended to the midline. The cuts were made as noted
above, but the knife was rotated in the anterior direction. In
group
5, cuts were made just anterior (Ant)
to the DMN (anterior-posterior 4.9 mm, lateral to midline 0.9 mm, depth
2.9 mm), and the knife was extended 1.1 mm medially and then lowered
1.6 mm and retracted. In group
6, sham operations were made with the
various AP positions of groups 1-5. The knife shaft was lowered
to a depth of 1 mm higher than was used in
groups
1-5. The incisions were closed
with stainless steel wound clips, and the rats were returned to their
cages.
Nineteen days after surgery, the rats were deprived of food, but not
water, for 24 h to ascertain whether the knife-cut rats would drink in
the absence of food. Food was returned, and 1- and 24-h consumptions
were recorded to determine the rats' feeding response after a period
of food deprivation (1, 9). Twenty-three days after surgery, 1.0 ml of
blood was removed from the rats by heart puncture under light ether
anesthesia. The heparinized blood was chilled, and plasma was separated
by centrifugation. Sodium and potassium concentrations of the plasma
were determined using a flame photometer, model 51 (Perkins Elmer,
Norwalk, CT). Plasma osmolality was determined with an Osmomat 300 (UIC, Joliet, IL). Next, a test for glucoprivic feeding was conducted.
Rats were given intraperitoneal injections of saline (~1.8 ml) at
1000 for several days. Food intake, corrected for spillage, was
recorded for 1-, 2-, and 3-h cumulative totals. The rats were then
injected with 2-DG (ICN Pharmaceuticals, Cleveland, OH) at a dose of
300 mg/kg body wt that was in a concentration of 5% wt/vol (4). Food
intake was recorded as described above. Five days later the rats were
tested to observe whether they would eat in the absence of water, and,
on return of water, their drinking response to the water deprivation,
i.e., combination of intracellular and extracellular dehydration, was
determined (1, 2, 9). Therefore, the rats were deprived of water for 24 h, and at the end of this period their food cups were removed, water
was returned, and water consumption was recorded for a 1-h duration.
Food was then returned, and water intake was recorded for a 23-h total. Several days later a trial was started to test the rats' feeding response to CCK. Food cups were removed at 0830, and the rats were
injected with saline (0.5 ml ip) at 1600. The rats' food was returned,
and their intake, corrected for spillage, was recorded at 30 min. After
this familiarization period, one half of each group was injected
intraperitoneally with saline, whereas the other half received CCK
octapeptide (Bachem, Torrance, CA) at a dose of 3.0 µg/kg body wt (3,
6). Two days later the trial was repeated in a counterbalanced design.
Several days later the food cups were removed at 1300. The rats were
injected with saline (0.3 ml) at 1515, and food cups were returned at
1545. Food intake, corrected for spillage, was recorded for 1-, 2-, and
3-h cumulative totals. This was repeated the following day, whereas on
the third day the rats were injected with NOX dissolved in saline at a
dose of 1 mg/kg body wt (6). Food intake was recorded as described above. Forty-nine days after surgery, the rats were anesthetized to
determine body weight and nasoanal length and then killed by decapitation. The rats' brains were saved for histological evaluation with Luxol fast blue and cresyl echt violet stain as previously described (1). Serial 8-µm sections were cut, and every sixth section
was stained. If more sections were needed, they were obtained from the
unstained saved sections and stained. Only those animals with correctly
placed transections were used for statistical analysis. At this point
it was determined that there were not enough rats with Ant cuts to
perform statistical analyses. Therefore, the above experiment was
repeated (trial
2) with 26 Ant and Sham rats. Data
from the Vent, Post, Dor, Lat, and Sham groups of
trial
1 were analyzed together, as were the
Ant and Sham groups of trial 2. Data were compared by means of one-
and two-way ANOVA with and without repeated measurements, Duncan's
multiple range test, and Student's
t-test.
| |
RESULTS |
A few animals died during or became ill shortly after surgery and were
eliminated from the study. Two individuals separately determined the
location and extent of the knife cuts. Composite drawings were then
made and any disagreements resolved. A very conservative approach was
used in accepting correct knife cut placement; thus only 58 of the 134 animals used met the criteria. Histology (Fig.
1) revealed that in
trial
1 correct knife cuts were placed in 7 Post, 8 Lat, 7 Vent, and 7 Dor rats, and there were 13 Sham rats. In
trial
1, correct knife cuts were placed in
too few Ant rats to make any analysis possible (see
MATERIALS AND METHODS). When the
experiment was repeated in trial
2, correct knife cuts were placed in
seven Ant rats, and there were nine Sham rats.
View larger version (25K):
[in this window]
[in a new window]
|
Fig. 1.
Line drawing of composite knife cuts
(arrows). Cuts were made dorsal
(A; Dors), ventral
(B; Vent), anterior
(C; Ant), posterior
(D; Post), and lateral
(E; Lat) to dorsomedial hypothalamic
nucleus (DMH). Location of drawing is denoted in µm anterior (A) to
ear bar zero or lateral (L) from midline (21). MTT, mammillo-thalamic
tracts; VMH, ventromedial hypothalamic nucleus; FX, fornix; CA,
anterior commissure; CO, optic chiasm; PVN, paraventricular nucleus;
PH, posterior hypothalamic area.
|
|
At the time of surgery (Table 1), body weight and body composition, as
determined by the Lee index, were similar in the five groups of
trial
1 and the two groups of
trial
2.
In trial
1 there was a significant
(P < 0.001) group effect on food
consumption after the surgery. Further analysis revealed that the Post
(Fig.
2A) and
Vent (Fig. 2B) groups consumed
significantly (P < 0.05-0.01)
less food than did the Sham group throughout the experiment [mean
daily food intake during experiment: Sham 22.0 ± 0.6 vs. Post 19.0 ± 0.6 g (P < 0.01) and vs. Vent
19.6 ± 0.5 g (P < 0.01)].
The food intake of the Ant group of
trial
2 did not differ significantly
[F(1,14) = 0.74; NS] from
its Sham group over the course of the study.
View larger version (17K):
[in this window]
[in a new window]
|
Fig. 2.
Food intake of sham-operated (Sham) rats and Post
(A) and Vent
(B) knife-cut rats. Post and Vent
groups were significantly (P < 0.05-0.01) hypophagic compared with Sham group over period of
measurement. On day
19 rats were food deprived for 24 h.
SE range, 0.24-2.23.
|
|
In trial
1 there was also a significant
(P < 0.001) group effect on water
intake subsequent to the operations. Additional analysis showed that
the Post (Fig.
3A) and
the Lat (Fig. 3B) groups, but not
the Vent group, were hypodipsic (P < 0.05-0.01) compared with the Sham group throughout the experiment
[mean daily water intake during the experiment: Sham 34.9 ± 1.0 vs. Post 29.6 ± 0.9 ml (P < 0.01), vs. Lat 29.4 ± 1.0 ml (P < 0.01), and vs. Vent 33.6 ± 0.8 ml (NS)]. The water intake
of the Ant group of trial
2 did not differ significantly
[F(1,14) = 0.26; NS] from its Sham group throughout the study.
View larger version (18K):
[in this window]
[in a new window]
|
Fig. 3.
Water intake of Sham and Post (A)
and Lat (B) knife-cut rats. Post and
Vent groups were significantly (P < 0.05-0.01) hypodipsic compared with Sham group over period of
measurement. On day
35 rats were water deprived for 24 h.
SE range, 0.24-5.93.
|
|
In trial
1 the lower food intake of the Post
and Vent groups manifested itself in a reduced growth rate (Fig.
4) in these two groups compared with the
Sham group (group effect, P < 0.001). Further analysis revealed that the body weight of the two
groups differed (P < 0.05-0.01)
from the controls by day
18 and thereafter. The Post and Vent
groups remained at ~88-90% of the weight of the controls
throughout the study. By the end of the study the Vent group was
significantly shorter than the controls (Table 1). The Post group also
had reduced body length, but significance was not reached. The body
weight of the Ant group did not differ significantly
[F(1,14) = 1.00; NS] from
the Sham group over the course of the study. The body composition, as
determined by the Lee index, of the groups of
trials
1 and
2 was normal (Table 1).
View larger version (18K):
[in this window]
[in a new window]
|
Fig. 4.
Body weight of Sham DMN knife-cut groups. Post and Vent groups were
significantly (P < 0.05-0.01)
different from Sham group from days
18-49. SE range, 1.6-7.0.
|
|
The reduced body weight of the Post and Vent groups was apparently not
a result of dehydration, inasmuch as plasma analyses of
Na+,
K+, and osmolality revealed normal
values in all groups (Table 2).
During food deprivation in trial
1, water consumption was reduced
suggestively in the Sham, Lat, and Dor groups (Table
3), whereas it was reduced significantly,
but not eliminated, in the Post group and elevated slightly in the Vent
group. In trial
2 water consumption was significantly
reduced in the Sham and Ant groups and for unexplained reasons was
greater than that observed in the Sham group of
trial
1. However, when water intake during food deprivation was expressed as a percentage of baseline intake, the
five groups of trial
1 did not differ significantly
[F(4,37) = 1.68;
NS], but the variation was large. The Ant group of
trial 2 also showed a percentage intake
similar to that of its Sham group (Table 3). On refeeding, all groups
significantly increased their 24-h food intake
[F(1,74) = 110.90;
P < 0.001]. Although the Post
and Vent groups remained hypophagic compared with the Sham group
[F(4,74) = 3.71;
P < 0.01], all groups of
trial
1 showed similar percent increases
(compared with their baseline intakes) at 1 h and 24 h postfeeding. The
Ant group of trial
2 consumed slightly more than did its
Sham group at 1 h but not at 24 h, and both showed an increase intake
during the 24 h postdeprivation.
After 24 h of water deprivation (Table 4),
during the initial hour of access to water all groups consumed a
similar amount of water. Thus the hypodipsic Post rats, on a percentage
of baseline intake, actually consumed more
(P < 0.05) water than the control animals. A similar increase was seen in the Lat group, but significance was not reached. Subsequent 24-h water intakes exceeded
[F(1,73) = 54.40;
P < 0.001] 24-h consumption
before deprivation in all groups, with the Post group, but not the Lat
group, remaining hypodipsic compared with the Sham rats [group
effect, F(4,73) = 5.45;
P < 0.001]. Notably, the Vent
group also consumed significantly less water than the Sham group. When
the 24-h water intake postdeprivation was calculated as a percentage of
baselines, all groups showed similar increases. During the 24 h of
water deprivation, the groups consumed between 70 and 76% of their
mean daily food intake before deprivation. Thus all groups in
trial
1 continued to eat in the absence of
water and to a similar degree. The Ant and Sham groups displayed the
exact same pattern of response as did the Sham group of
trial
1; however, for unexplained reasons,
during the first hour postdeprivation both groups consumed more water
than did the Sham rats of trial
1.
The data from the 2-DG and CCK trials are not shown because the
findings were equivocal. In the case of the 2-DG trial, the baseline
data showed differences among the groups, and in the CCK trial the Sham
group of trial
1 did not respond to CCK.
In the NOX experiment, all groups in
trial
1 showed similar intakes over the 3-h
measurement period after saline injection. Injection of NOX (Table
5) significantly [drug effect,
F(1,222) = 54.49;
P < 0.001] reduced the food
intake of the Sham group during all 3 h of measurement. NOX did not
cause a significant suppression of the Post group's food intake
[group effect, F(4,222) = 5.49;
P < 0.001]. The Lat and Dor
groups had attenuated food intakes during the first hour and a
significant depression of food consumption during the second hour. The
Ant group of trial 2 did not show a significant
attenuation in food intake after treatment with NOX, whereas the Sham
group's intake was significantly decreased at the 2- and 3-h
measurement points.
View this table:
[in this window]
[in a new window]
|
Table 5.
Effect of intraperitoneal injections of naloxone (1 mg/kg) or saline on
cummulative food intake in DMNL or Sham rats
|
|
| |
DISCUSSION |
Rats with electrolytic or excitotoxic lesions of the DMN are hypophagic
and have reduced body weights but normal body compositions (7, 11). The
present study demonstrates that transection of fiber tracts that enter
or leave the DMN from the posterior and ventral directions also
produces a reduction in food consumption, a decrease in body weight,
and a reduction in linear growth. The magnitude of the food intake
reductions after these individual cuts was about half that observed
after electrolytic or excitoxic destruction of the DMN (1, 9, 11). Thus
if the observed food intake reductions after Post and Vent cuts are
cumulated, they approach levels observed after destruction of the DMN.
Despite the reduced body weight of the Post and Vent groups, all groups in trials
1 and
2 had normal body compositions as
measured by the Lee obesity index.
The afferent and efferent neural connections of the DMN have been
extensively investigated (21, 22, 25-28). Posterior DMN cuts would
disrupt fibers originating in the premammillary, tuberomammillary, supramammillary, and posterior hypothalamic nuclei and the
periaqueductal gray area. Ventral DMN cuts would remove input fibers
from the ventral subiculum and lateral septal, suprachiasmatic,
subparaventricular, arcuate, and ventromedial hypothalamic nuclei and
amygdala. Ventral cuts would also remove fibers entering the DMN from
the lateral hypothalamic area that course under the fornix. It is also
possible that some fibers arising from the ventral medulla (A1/C1),
nucleus of the solitary tract, parabrachial nucleus, mesencephalic
reticular nucleus, and superior central nucleus would be interrupted
after ventral cuts.
The knife cuts posterior to the DMN would disrupt efferent fibers from
the DMN to the posterior hypothalamic nucleus, superior colliculus,
mesencephalic reticular nucleus, retroruberal area, dorsal nucleus of
the raphe, periaqueductal gray, cuneiform nucleus, Barrington's
nucleus, and parabrachial nucleus. The cuts ventral to the DMN would
apparently disrupt some descending efferent fibers from the DMN to the
ventral and dorsal premammillary nuclei, dorsal and ventral
tuberomammillary nucleus, posterior periventricular nucleus, nucleus of
the solitary tract, area postrema, nucleus raphe globus pallidus, and
medullary reticular nucleus. Lateral ascending connections from the DMN
exit both ventral and dorsal to the fornix and at this time cannot be
distinguished from one another. The Vent cuts would transect only those
lateral fibers leaving the DMN ventral to the fornix. With this in
mind, some laterally directed fibers innervate the perifornical region.
Other fibers enter the medial forebrain bundle to innervate the
parvocellular region of the paraventricular nucleus, anterior
hypothalamic area, preoptic area, bed nucleus of the stria terminalis,
lateral septal nucleus, nucleus accumbens, amygdala, layer 1 of the
entorhinal area, the ventral subiculum, and areas CA1 and CA3 of the
hippocampus. Another efferent DMN pathway is directed ventrally in the
periventricular region and would be disrupted by the ventral cuts. This
pathway innervates the ventromedial nucleus, arcuate nucleus, anterior hypothalamic nucleus, preoptic region, retrochiasmatic area, supraoptic nucleus, and plexus around the suprachiasmatic nucleus.
Many of these brain areas that are connected to the DMN have been shown
to be involved in the control of feeding behavior and body weight (11,
12, 21, 22, 26-28). It should be remembered that most of the DMNL
syndrome is reproduced by loss of cell bodies in the DMN (1, 9).
Therefore, cell bodies in the DMN are actively participating in the
regulation of feeding behavior and body weight through their efferent
connections with other brain areas. The DMN may also have a role in
integrating afferent signals from other brain areas controlling
ingestion and body weight (11, 12). It is noteworthy that Ant and Dor
cuts would have disrupted most connections between the DMN and the
paraventricular nucleus. The paraventricular nucleus is thought to have
a major role in the control of feeding behavior (15, 18, 24, 29), and yet disconnecting the DMN and paraventricular nucleus did not affect
food or water intake or body weight.
The DMN of rats contains both opioid fiber tracts and cell bodies (see
Refs. 6, 11), and infusion of µ- and -receptor agonists into the
DMN increases food intake of rats (24). In the present study, rats with
Post cuts, and to a lesser degree rats with Ant cuts, did not show food
intake suppression after NOX. On the other hand, rats with Vent cuts
overresponded to the food intake-suppressive effects of NOX. In a
previous study (6) rats with electrolytic DMN lesions showed no food
intake suppression when given 1.0 mg/kg of NOX. It was proposed that an
opioid system in the DMN increases feeding by inhibiting a satiety
system (6). Destruction of the DMN would leave the satiety system
uninhibited and thus would produce hypophagia. Hypophagia is a
characteristic of the DMNL syndrome. It was further (6) suggested that
lesions of the DMN do not destroy a feeding system. This was supported by the observation that DMNL rats enhance their food intake after food
deprivation (1, 9, 11). Additional evidence (5) comes from the finding
that if the body weight of the rat before DMNL is reduced below the
lesion-induced lowered body weight "set point," the DMNL rat
actually becomes hyperphagic. The rats' intake remains elevated until
they reach the DMNL-induced body weight "set point." Finally,
DMNL rats are not aphagic, and thus feeding system(s) remain
operational (6) but are unable to maintain food intake at control
levels. Lambert et al. (20) reported that giving NOX to
intact rats caused them to decrease their food intake while at the same
time increasing NPY concentrations in the DMN. Recently, Carr et al.
(13) suggested a role for DMN opioids and NPY in the control of feeding
behavior. They noted that NPY from the arcuate nucleus may modulate
DMN-induced feeding and that a feedback loop from the DMN to the
arcuate nucleus may exist. Whether the enhanced NOX response in the
Vent group is caused by a loss of efferent or afferent connections
between the arcuate nucleus and DMN awaits further investigation.
Finally, Carr et al. (13) proposed that the DMN may be one of multiple brain sites involved in NPY and opioid orexigenic activity.
Like electrolytic- or excitotoxic-lesioned DMN rats, the knife-cut
groups elevated their intake after food deprivation. This demonstrates
that although DMNL, Post, and Vent rats are hypophagic, they retain the
ability to respond to caloric deficits and regulate their body weight,
albeit at a lower "set point."
Rats with Post and Lat cuts were hypodipsic, but the magnitude of the
decrease in water consumption was less than that observed after
electrolytic or excitotoxic DMNL (1, 2, 9). However, the additive
decreases observed after these two types of cuts approximated that
measured after DMNL. Earlier, it was demonstrated (2) that the drinking
responses of DMNL rats to a variety of extra- and intracellular
dehydration challenges were normal. Like DMNL rats, the knife-cut
groups ate in the absence of water, drank in the absence of food, and
responded normally to water deprivation.
The DMN knife-cut data indicate that the same neural pathways appear to
be involved in the attenuation of both feeding and body weight. The
hypodipsia observed after DMNL involve some neural pathways separate
from feeding systems. The data also suggest that the loss of DMN opioid
pathways that enter or leave the DMN from the posterior direction are
involved in the attenuation of feeding after DMNL. The data indicate
that the DMN influences ingestive behavior through complex neural connections.
We are grateful to Dr. L. Fliedner (Endocrine Laboratories, Garden
City, NY) for the generous supply of the naloxone. We also thank Connie
Tillberg for technical assistance.
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. §1734 solely to indicate this fact.
Address for reprint requests and other correspondence: L. L. Bellinger,
Dept. of Biomedical Sciences, Texas A & M Univ. System Health Science
Center, Baylor College of Dentistry, 3302 Gaston Ave., Dallas, TX 75246 (E-mail: lbellinger{at}tambcd.edu).
TOP
ABSTRACT
INTRODUCTION
