Serotonergic Mechanisms of The Lateral Parabrachial PDF

Serotonergic mechanisms of the lateral parabrachial
nucleus and cholinergic-induced sodium appetite

Jos Vanderlei Menani, Silas Pereira Barbosa, Laurival Antonio De Luca, Jr.,
Juliana Irani Fratucci De Gobbi and Alan Kim Johnson
Am J Physiol Regul Integr Comp Physiol 282:R837-R841, 2002. doi:10.1152/ajpregu.00311.2001
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Sertraline, a selective serotonin reuptake inhibitor, affects thirst, salt appetite and plasma
levels of oxytocin and vasopressin in rats
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Guedes, Jr, Jacqueline Pereira Arajo, Priscila Camargo Granadeiro, Hevellyn Katarine
Milanez-Barbosa, Ricardo Henrique da Costa-e-Sousa, Magda Alves de Medeiros, Jos
Antunes-Rodrigues and Lus Carlos Reis
Exp Physiol, September 1, 2007; 92 (5): 913-922.
Am J Physiol Regulatory Integrative Comp Physiol 282: R837R841, 2002;

10.1152/ajpregu.00311.2001.
Serotonergic mechanisms of the lateral parabrachial

nucleus and cholinergic-induced sodium appetite
VANDERLEI MENANI, SILAS PEREIRA BARBOSA,
JOSE
LAURIVAL ANTONIO DE LUCA, JR., JULIANA IRANI FRATUCCI DE GOBBI,
AND ALAN KIM JOHNSON
Departments of Psychology, Pharmacology, and Exercise Science and the Cardiovascular Center,
University of Iowa, Iowa City, Iowa 52242-1407; and Department of Physiology and Pathology,
School of Dentistry, Paulista State University, Araraquara, Sao Paulo 14801-903, Brazil
Received 1 June 2001; accepted in final form 14 November 2001
carbachol; water intake; thirst; salt intake; salt appetite;

5-hydroxytryptamine
(LPBN) is a hindbrain structure that has been implicated in body fluid

regulation (3, 4, 6, 1724). The LPBN receives afferent
projections from the area postrema (AP) and adjacent
portions of the medial nucleus of the solitary tract
(mNTS) and sends efferent projections to forebrain
THE LATERAL PARABRACHIAL NUCLEUS
Address for reprint requests and other correspondence: A. K.

Johnson, Dept. of Psychology, Univ. of Iowa, 11 Seashore Hall E.,
Iowa City, IA 52242-1407 (E-mail: alan-johnson@uiowa.edu).
http://www.ajpregu.org
areas involved in fluid and electrolyte balance such as

the subfornical organ, median preoptic nucleus, paraventricular hypothalamic nucleus, and the amygdala
(e.g., central nucleus) (2, 9, 10, 13, 15, 25). Functional
studies have implicated the LPBN and its afferent
connections in the neural control of body fluid and
cardiovascular homeostasis (14).
A prominent serotonergic pathway from the AP/
mNTS to the parabrachial nucleus has been described
(16). Previous experimental results have led to the
hypothesis that information arising from this pathway
acts to inhibit thirst- and sodium appetite-related behaviors. Bilateral injections of the nonselective 5-hydroxytryptamine (5-HT)1/2 receptor antagonist methysergide into the LPBN significantly increases salt
intake in a number of forms of experimentally induced
sodium appetite. These include intracerebroventricular angiotensin (22), systemic administration of a diuretic (furosemide; Furo) plus angiotensin-converting
enzyme inhibitor (22), chronic sodium depletion [24 h
(18)], water deprivation (18), and chronic treatment
with DOCA (4). Conversely, the administration of the
5-HT receptor agonist 2,5-dimethoxy-4-iodoamphetamine into the LPBN substantially reduces salt intake
produced by dipsogenic/natriorexigenic treatments.
In addition to the increase of an already existing
sodium intake, injection of methysergide into the
LPBN also results in marked sodium intake by conditions where this behavior is usually not activated.
Specifically, subcutaneous treatment with the -adrenergic agonist isoproterenol or acute (12 h after) subcutaneous Furo (19) induces significant intakes of salt
solution when methysergide is administered into the
LPBN.
Central cholinergic activation, particularly with carbachol, is another special situation that stimulates
water consumption but not hypertonic saline intake.
Some studies have even suggested that central injections of carbachol might actually inhibit sodium intake
in rats (7, 8). Considering the results from previous
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0363-6119/02 $5.00 Copyright 2002 the American Physiological Society
R837
Menani, Jose Vanderlei, Silas Pereira Barbosa, Laurival Antonio De Luca, Jr., Juliana Irani Fratucci
De Gobbi, and Alan Kim Johnson. Serotonergic mechanisms of the lateral parabrachial nucleus and cholinergicinduced sodium appetite. Am J Physiol Regulatory Integrative Comp Physiol 282: R837R841, 2002; 10.1152/ajpregu.
00311.2001.Central cholinergic mechanisms are suggested to participate in osmoreceptor-induced water intake. Therefore, central injections of the cholinergic agonist carbachol usually produce water intake (i.e., thirst)
and are ineffective in inducing the intake of hypertonic
saline solutions (i.e., the operational definition of sodium
appetite). Recent studies have indicated that bilateral
injections of the serotonin receptor antagonist methysergide into the lateral parabrachial nucleus (LPBN) markedly increases salt intake in models involving the activation of the renin-angiotensin system or mineralocorticoid
hormones. The present studies investigated whether sodium appetite could be induced by central cholinergic
activation with carbachol (an experimental condition where
only water is typically ingested) after the blockade of LPBN
serotonergic mechanisms with methysergide treatment in
rats. When administered intracerebroventricularly in combination with injections of vehicle into both LPBN, carbachol (4
nmol) caused water drinking but insignificant intake of hypertonic saline. In contrast, after bilateral LPBN injections of
methysergide (4 g), intracerebroventricular carbachol induced the intake of 0.3 M NaCl. Water intake stimulated by
intracerebroventricular carbachol was not changed by LPBN
methysergide injections. The results indicate that central
cholinergic activation can induce marked intake of hypertonic NaCl if the inhibitory serotonergic mechanisms of the
LPBN are attenuated.
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LPBN 5-HT AND SALT APPETITE
studies that have shown increases of an already existing sodium intake (3, 4, 17, 18, 22) or induction of a de
novo sodium appetite (19) after the blockade of the
LPBN inhibitory serotonergic mechanism, the present
experiments investigated whether treatment of the
LPBN with methysergide in conjunction with central
(intracerebroventricular) injections of carbachol may
induce hypertonic NaCl intake in addition to water,
which is typically the only fluid consumed.
MATERIALS AND METHODS
RESULTS
Histological analysis. As seen in studies conducted

previously (3, 4, 20, 22), LPBN injection sites were
centered in the central lateral and dorsal lateral portions of the LPBN [see Fulwiler and Saper (9) for
definitions of LPBN subnuclei]. Injections reaching the
ventral lateral and external lateral portions, as well as
the Ko lliker-Fuse nucleus, were observed in some rats,
and the results from these rats were included in the
analysis. As estimated from the injection of Evans blue
dye, the spread of the injection was almost completely
confined above the brachium. In some rats there was a
small, limited spread of the injection into the brachium.
Effects of LPBN methysergide injection on the intake
of water and 0.3 M NaCl induced by intracerebroventricular injection of carbachol. After the injection of
vehicle into the LPBN, carbachol (4 nmol) injected
intracerebroventricularly induced significant water intake and only a small amount of 0.3 M saline over the
90-min period after the injection (Fig. 1). Bilateral
injections of methysergide (4 g/200 nl each site) into
the LPBN combined with intracerebroventricular carbachol significantly increased the intake of 0.3 M NaCl
[F(1,22) 7.24; P 0.05] (Fig. 1). Water intake induced by intracerebroventricular carbachol was not
significantly increased by LPBN methysergide treatment [F(1,22) 0.15; P 0.05] (Fig. 1).
When water was the only fluid available for drinking, bilateral LPBN injections of methysergide also
produced no change in carbachol-induced water intake
[F(1,18) 0,083; P 0.05] (Fig. 2).
Bilateral LPBN injections of methysergide, in the
absence of any other treatment, produced no effect on
AJP-Regulatory Integrative Comp Physiol VOL
282 MARCH 2002
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Animals. Male Holtzman rats weighing 280320 g were

used. The animals were housed in individual stainless steel
cages with free access to standard sodium diet (Purina Rat
chow, sodium content 0.5%), water, and 0.3 M NaCl solution.
Temperature was maintained at 23 1C, with a 12:12-h
light-dark cycle with light onset at 7:00 AM. All experiments
were performed between 9:00 AM and 1:00 PM.
Cerebral cannulas. Rats were anesthetized with ketamine
(10 mg/100 g body wt) and placed in a Kopf stereotaxic
instrument. The skull was leveled between bregma and
lambda. Stainless steel 23-gauge cannulas were implanted
bilaterally into the LPBN by using the following coordinates:
9.4 mm caudal to bregma, 2.2 mm lateral to the midline, and
4.1 mm below the dura mater. The tips of the cannulas were
positioned to terminate 2 mm above each LPBN. A third
23-gauge stainless steel cannula was implanted into the
lateral ventricle (LV) according to the following coordinates:
0.5 caudal to bregma, 1.5 mm lateral to the midline, and 3.5
mm below the dura mater. Cannulas were fixed to the skull
with the use of dental acrylic resin and jewelers screws. A
30-gauge metal obturator filled the cannulas between tests.
After surgery, the rats were allowed to recover for 6 days
before testing.
Drugs. Carbachol hydrochloride (4 nmol/1 l) from Sigma
Chemicals (St. Louis, MO) was dissolved in isotonic saline.
Methysergide maleate (Sandoz Pharmaceutical, E. Hanover,
NJ) was dissolved in propylene glycol-water (2:1). The dose of
methysergide (4 g/200 nl) used in the present study was
based on previous studies (3, 4, 1720).
Water and 0.3 M NaCl ingestion tests. Rats were tested in
their home cages. Water and 0.3 M NaCl were provided from
burettes with 0.1-ml divisions that were fitted with metal
drinking spouts. In each experimental session, one-half of the
rats received bilateral LPBN injections of vehicle (i.e., 2:1
propylene glycol-water), and the remaining animals received
methysergide injections into the same nuclei. Fifteen minutes later, carbachol was injected into the LV. The volumes of
water and 0.3 M NaCl ingested were recorded each 30 min
during the 90 min immediately after the injection of carbachol. Each group of rats received two tests with a recovery
period of at least 3 days between tests. One group of 26 rats
had water and 0.3 M NaCl available during the test, and one
group of 18 rats had only water available during the test.
Injections were made by using 30-gauge injection cannulas
connected by polyethylene tubing (PE-10) to 10-l Hamilton
syringes. At the time of testing, the animals were taken from
their home cages, the obturators were removed, and injection
cannulas were introduced into the implanted guide cannulas.
The injection cannulas were 2 mm longer than the guide
cannulas. Injection volumes of 200 nl were delivered to each
LPBN and 1 l into the LV. After injection, the obturators
were replaced, and the rats were returned to their cages.
To control for the effects of LPBN methysergide injections
in the absence of any other treatment, one group of 22 rats
received bilateral LPBN injections of vehicle (200 nl/site) or

methysergide (4 g/200 nl/site; order randomized), and the
volumes of water and 0.3 M NaCl ingested were recorded
for 1 h.
Food intake. To assess the specificity of LPBN serotonergic
mechanisms to control sodium intake in one group of 12 rats,
the effect of LPBN injections of methysergide on food intake
was tested.
Rats were deprived of food but not water overnight (14 h).
The next day, a preweighed amount of food (pellet Purina
chow) was returned to the rats 15 min after methysergide (4
g/200 nl) or vehicle was injected bilaterally into the LPBN.
Food intake was recorded each 30 min for 90 min.
Histology. At the end of the experiments, the animals
received bilateral LPBN injections of Evans blue dye (200
nl/site). They were then deeply anesthetized with tribromoethanol (200 mg/kg body wt) and perfused transcardially
with saline followed by 10% formalin. The brains were removed, fixed in 10% formalin, frozen, cut in 50-m sections,
stained by Giemsa, and analyzed by light microscopy in
single-blind fashion to confirm the injection sites in the
LPBN. Only data from rats with confirmed injections into the
LV and bilateral placements of cannulas in the LPBN were
analyzed.
Statistical analysis. The results are reported as means
SE. Repeated-measures ANOVA and Newman-Keuls tests
were used for comparisons. Differences were considered significant at P 0.05.
R839
Fig. 1. Cumulative 1.8% NaCl intake (A) and cumulative water

intake (B) induced by intracerebroventricular (icv) injection of carbachol (4 nmol/1 l) after injection of vehicle or methysergide (4
g/200 nl each site) bilaterally into the lateral parabrachial nucleus
(LPBN). * Significantly different from carbachol vehicle tested by
Newman-Keuls test (P 0.05).
the ingestion of either water (1.0 0.6 ml in 1 h) or 0.3

M NaCl (0.03 0.03 ml/1 h; n 10 rats).
Effects of LPBN injections of methysergide on food
intake. Bilateral LPBN injections of methysergide produced no significant change in food intake after 14 h of
food deprivation [F(1,12) 0.14; P 0.05] (Fig. 3).
dium appetite is already being expressed. That is,

sodium appetite induced by several systemic treatments [Furo captopril (22), subcutaneous Furo
24 h of sodium-deficient diet (18), 24 h of water deprivation (18), or subcutaneous DOCA (4)] are significantly increased by bilateral LPBN methysergide
treatment. In comparison to the previous studies, the
present results demonstrate that it is possible not only
to enhance an existing salt intake but also to induce
sodium appetite by LPBN 5-HT receptor antagonist
injections in combination with intracerebroventricular
carbachol, a treatment that typically produces only
water drinking (i.e., thirst).
Evidence available at the present time indicates that
there is a reasonable degree of specificity for the enhancement of NaCl solution intake by bilateral LPBN
DISCUSSION
The results of these experiments are consistent with

others (7, 8) indicating that intracerebroventricular
injection of carbachol immediately induces water intake but little hypertonic NaCl intake. However, the
present results demonstrate that when the nonselective 5-HT receptor antagonist methysergide is administered into the LPBN in conjunction with intracerebroventricular carbachol, there is substantial 0.3 M
NaCl intake. Unlike the intake of hypertonic saline,
water intake in rats treated with central carbachol or
food intake was not modified by LPBN injections of
methysergide.
Previous studies (3, 4, 18, 22) have demonstrated
that injections of methysergide into the LPBN enhance
hypertonic saline intake under conditions where a so-
Fig. 3. Cumulative food intake induced by 14 h of food deprivation

after injection of vehicle or methysergide (4 g/200 nl each site)
bilaterally into the LPBN.
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Fig. 2. Cumulative water intake induced by icv injections of carbachol (4 nmol/1 l) after injections of vehicle or methysergide (4
g/200 nl each site) bilaterally into the LPBN when only water was
available for the rats.
R840
be discounted. This anatomic organization suggests

that information derived from the peripheral visceral
afferents may alter activity in the anatomically defined
AP/mNTS-LPBN serotonergic pathway (16). Accumulating evidence indicates that the LPBN is an important component of a central neural network that is
related to control of cardiovascular and body fluid homeostasis. The LPBN projects to several forebrain areas (e.g., paraventricular nucleus of the hypothalamus,
central nucleus of the amygdala, bed nucleus of the
stria terminalis, median preoptic nucleus) that have
been implicated in the control of water and electrolyte
balance (24, 6, 9, 10, 13, 15, 17, 18, 20, 22).
Perspectives
The present study extends previous results showing
that the blockade of LPBN serotonergic mechanisms
combined with a central stimulus (cholinergic activation) that usually induces only thirst (i.e., no salt intake) can induce sodium appetite. Thus it seems the
control of water and sodium appetite may have similar
input signals that are modified by LPBN serotonergic
mechanisms to determine whether sodium intake vs.
water intake will be initiated. The presence or absence
of 5-HT activity in the LPBN seems to act as a switch
to turn off or turn on sodium appetite. Future research
will be necessary to show whether other stimuli or
experimental manipulations that usually evoke only
thirst also activate brain circuits that control sodium
appetite. This confirmation will provide new concepts
for the understanding of the control mechanisms subserving water and sodium intake.
We thank T. G. Beltz for expert technical assistance.
This research was supported by National Heart, Lung, and Blood
Institute Grants HL-14338 and HL-57472, Office of Naval Research
Grant N-00014-97-1-0145, and Brazilian public funding (Fundac a o
de Amparo a Pesquisa do Estado de Sao Paulo Proc. 93/0167-7 and
CNPq).
REFERENCES
1. Bradd J, Dubin J, Due B, Miselis RR, Montor S, Rogers
WT, Spyer KM, and Schwaber JS. Mapping of carotid sinus
inputs and vagal cardiac outputs in the rat (Abstract). Soc
Neurosci Abstr 15: 593, 1989.
2. Ciriello J, Lawrence D, and Pittman QJ. Electrophysiological identification of neurons in the parabrachial nucleus projecting directly to the hypothalamus in the rat. Brain Res 322:
388392, 1984.
3. Colombari DSA, Menani JV, and Johnson AK. Forebrain
angiotensin type 1 receptors and parabrachial serotonin in the
control of NaCl and water intake. Am J Physiol Regulatory
Integrative Comp Physiol 271: R1470R1476, 1996.
4. De Gobbi JIF, De Luca LA Jr, and Menani JV. Serotonergic
mechanisms of the lateral parabrachial nucleus on DOCA-induced sodium intake. Brain Res 880: 131138, 2000.
5. Edwards GL, Beltz TG, Power JD, and Johnson AK. Rapidonset need-free sodium appetite after lesions of the dorsomedial medulla. Am J Physiol Regulatory Integrative Comp Physiol
264: R1242R1247, 1993.
6. Edwards GL and Johnson AK. Enhanced drinking after excitotoxic lesions of the parabrachial nucleus in the rat. Am J
Physiol Regulatory Integrative Comp Physiol 261: R1039R1044,
1991.
282 MARCH 2002
www.ajpregu.org
methysergide injections given in conjunction with natriorexigenic or dipsogenic treatments. Previous research (18) has shown that sucrose solution intake
motivated only by the hedonic qualities of the fluid (i.e.,
sweet taste offered to nondeprived animals) was not
increased by bilateral LPBN methysergide treatment.
Similarly, the present study examining the effects of
LPBN methysergide injections on food intake after a
moderate period (overnight) of food deprivation showed
no evidence of facilitating eating.
Most experimental situations that induce a sodium
appetite take a long time (usually on the order of hours
to days) for enhanced salt ingestion (i.e., sodium appetite) to clearly manifest itself. This is in contrast with
the shorter latencies for the onset of drinking (26). It
has been hypothesized that the relatively long latency
required for a sodium appetite to become apparent is
due to the presence of some form(s) of tonic inhibition,
which must be reduced before hypertonic NaCl is consumed (26). Mechanisms hypothesized to be involved
in the reduction of such inhibition include 1) further
reductions in blood volume, 2) osmotic dilution of the
blood as a consequence of water intake, and 3) moderate reductions in arterial blood pressure [i.e., decreases
of 20 mmHg below normal; see Johnson and Thunhorst (14) and Stricker and Verbalis (26) for review].
Therefore, previous studies have suggested that the
5-HT action in the LPBN might be associated with one
or more of the mechanisms hypothesized to be inhibitory mechanisms. In the present study with the deactivation of LPBN serotonergic inhibitory mechanisms,
sodium appetite arose in the presence of central cholinergic activation, an experimental condition that typically produces water consumption but not sodium intake. Central carbachol induces ingestion of water
simultaneously with increases in arterial pressure and
vasopressin release, which are all responses associated
with a condition of plasma hyperosmolarity (11, 12).
Previous studies have suggested that carbachol may
actually inhibit sodium intake in rats (7, 8). The
present findings suggest that central carbachol also
activates mechanisms that drive sodium intake, but
the result of such cholinergic activation can be observed only after the blockade of LPBN serotonergic
inhibitory mechanisms. Part of the inhibitory effect of
carbachol on sodium intake in rats may be a consequence of inhibitory input due to the marked increase
in arterial pressure produced by intracerebroventricular carbachol. LPBN methysergide treatment may
block such inhibitory influences derived from systemic
arterial baroreceptor input.
Neural afferents from the viscera, including those
from arterial and cardiac baroreceptors, terminate in
the NTS and in portions of the AP (1). As noted previously, a prominent serotonergic pathway originates in
the AP and mNTS and projects to the lateral regions of
the LPBN (16). Of course, the possibility that manipulation of the LPBN 5-HT mechanisms may alter some
other type of inhibitory input (e.g., osmotic or gastric
distension) arising from other systemic receptors that
are carried in the AP/mNTS-LPBN projection cannot
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17. Menani JV, Colombari DSA, Beltz TG, Thunhorst RL, and
Johnson AK. Salt appetite: interaction of forebrain angiotensinergic and hindbrain serotonergic mechanisms. Brain Res
801: 2935, 1998.
18. Menani JV, De Luca LA Jr, and Johnson AK. Lateral parabrachial nucleus serotonergic mechanisms and salt appetite induced by sodium depletion. Am J Physiol Regulatory Integrative
Comp Physiol 274: R555R560, 1998.
19. Menani JV, De Luca LA Jr, Thunhorst RL, and Johnson
AK. Hindbrain serotonin and the rapid induction of sodium
appetite. Am J Physiol Regulatory Integrative Comp Physiol 279:
R126R131, 2000.
20. Menani JV and Johnson AK. Lateral parabrachial serotonergic mechanisms: angiotensin-induced pressor and drinking responses. Am J Physiol Regulatory Integrative Comp Physiol 269:
R1044R1049, 1995.
21. Menani JV and Johnson AK. Cholecystokinin actions in the
parabrachial nucleus: effects on thirst and salt appetite. Am J
Physiol Regulatory Integrative Comp Physiol 275: R1431R1437,
1998.
22. Menani JV, Thunhorst RL, and Johnson AK. Lateral parabrachial nucleus and serotonergic mechanisms in the control of
salt appetite in rats. Am J Physiol Regulatory Integrative Comp
Physiol 270: R162R168, 1996.
23. Ohman LE and Johnson AK. Lesions in the lateral parabrachial nucleus enhance drinking to angiotensin II and isoproterenol. Am J Physiol Regulatory Integrative Comp Physiol 251:
R504R509, 1986.
24. Ohman LE and Johnson AK. Role of the lateral parabrachial
nucleus in the inhibition of water intake produced by right atrial
stretch. Brain Res 695: 275278, 1995.
25. Saper CB and Loewy AD. Efferent connections of the parabrachial nucleus in the rat. Brain Res 197: 291317, 1980.
26. Stricker EM and Verbalis JG. Sodium appetite. In: Handbook
of Behavioral Neurobiology. Neurobiology of Food and Fluid
Intake, edited by Stricker EM. New York: Plenum, 1990, vol. 10,
p. 389393.
282 MARCH 2002
www.ajpregu.org
7. Fitts DA, Thunhorst RL, and Simpson JB. Fluid intake,

distribution, and excretion during lateral ventricular infusions of
carbachol in rats. Brain Res 332: 237245, 1985.
8. Fitts DA, Thunhorst RL, and Simpson JB. Modulation of salt
appetite by lateral ventricular infusions of angiotensin II and
carbachol during sodium depletion. Brain Res 346: 273280,
1985.
9. Fulwiler CE and Saper CB. Subnuclear organization of the
efferent connections of the parabrachial nucleus in the rat. Brain
Res 319: 229259, 1984.
10. Herbert H, Moga MM, and Saper CB. Connections of the
parabrachial nucleus with the nucleus to the solitary tract and
the medullary reticular formation in the rat. J Comp Neurol 293:
540580, 1990.
11. Hoffman WE, Philips MI, Schmid PG, Falcon J, and Weet
JF. Antidiuretic hormone release and the pressor response to
central angiotensin II and cholinergic stimulation. Neuropharmacology 16: 463472, 1977.
12. Imai Y, Abe K, Sasaki S, Minami N, Munakata M, Yumita S,
Nobunaga T, Sekino H, and Yoshinaga K. Role of vasopressin in cardiovascular response to central cholinergic stimulation
in rats. Hypertension 13: 549557, 1989.
13. Jhamandas JH, Harris KH, Petrov T, and Krukoff TL.
Characterization of the parabrachial nucleus input to the hypothalamic paraventricular nucleus in the rat. J Neuroendocrinol
4: 461471, 1992.
14. Johnson AK and Thunhorst RL. The neuroendocrinology of
thirst and salt appetite: visceral sensory signals and mechanisms of central integration. Front Neuroendocrinol 18: 292
353, 1997.
15. Krukoff TL, Harris KH, and Jhamandas JH. Efferent projections from the parabrachial nucleus demonstrated with the
anterograde tracer Phaseolus vulgaris leucoagglutinin. Brain
Res Bull 30: 163172, 1993.
16. Lanc a AJ and van der Kooy D. A serotonin-containing pathway from the area postrema to the parabrachial nucleus in the
rat. Neuroscience 14: 11171126, 1985.

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