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Institut National de la Santé et de la Recherche Médicale U.378, Université Victor Segalen, Institut François Magendie, 33077 Bordeaux, France
Submitted 10 March 2003; accepted in final form 18 April 2003
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ABSTRACT |
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 TOP ABSTRACT INTRODUCTIONMETHODSRESULTSDISCUSSIONDISCLOSURESACKNOWLEDGMENTSREFERENCES |
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INTRODUCTION |
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TOPABSTRACTINTRODUCTIONMETHODSRESULTSDISCUSSIONDISCLOSURESACKNOWLEDGMENTSREFERENCES |
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) that itself is dependent on afferent excitatory
and inhibitory synaptic inputs originating from many brain areas
(Anderson et al. 1990).
-amino butyric acid (GABA) and glutamate are the main inhibitory and
excitatory transmitters in the hypothalamus respectively
(Decavel and Van den Pol 1990;
Van den Pol et al. 1990).
Electrophysiological recordings have indicated the presence of functional
GABA-A receptors on SON neurons responsible for fast inhibitory potentials
(Randle et al. 1986). GABA-B
receptors have also been reported in the SON on both glutamatergic and
GABAergic terminals (Kombian et al.
1996; Mouginot et al.
1998) and on magnocellular neurons
(Harayama et al. 1998;
Stern et al. 2002). Studies
performed at the ultrastructural level have revealed that >40% of all
synapses on magnocellular neurons were GABAergic
(Gies and Theodosis 1994).
Accordingly, GABA has been reported to play an important role in the
regulation of firing activity both in OT and VP SON neurons (reviewed in
Renaud and Bourque 1991).
In addition to the transmitters GABA and glutamate, several other
substances have been described as neuromodulators in the SON
(Renaud and Bourque 1991). One
of them is dopamine (DA), which acts on a variety of G-protein-coupled
receptor subtypes classified in two families. The D1 family includes D1 and D5
receptors, whereas the D2 family consists of D2–D4 receptors. The D1 and
D2 families have been reported to be positively and negatively coupled to
adenylyl cyclase respectively (Missale et
al. 1998). The supraoptic nucleus receives a diffuse dopaminergic
innervation from cells located in the A14 and A15 regions
(Jourdain et al. 1999;
Van Vulpen et al. 1999).
Moreover, dopaminergic synapses have been documented on dendrites and soma of
SON neurons (Buijs et al. 1984;
Decavel et al. 1987). In vivo
experiments have shown that intracerebroventricular
(Bridges et al. 1976;
Moos and Richard 1982) or
direct injection of DA into the SON (Urano
and Kobayashi 1978) could induce or facilitate the release of
neurohypophysial hormones. In lactating rats, OT release is facilitated or
inhibited through the activation of D1 or D2 receptors, respectively
(Crowley et al. 1987;
Parker and Crowley 1992). In
vitro, dopamine has been reported to depolarize SON neurons directly through
the activation of D2-like receptors (Yang
et al. 1991), whereas activation of presynaptic D4 receptors has
been found recently to inhibit glutamatergic transmission
(Price and Pittman 2001).
Because most of the studies performed in vivo points to a general
excitatory action of DA on the hypothalamo-neurohypophysial system, we tested
the hypothesis that DA could modulate inhibitory GABAergic inputs in the SON
as is the case in other brain regions (Gonzales-Islas and Hablitz 2001;
Miyazaki and Lacey 1998;
Seamans et al. 2001). Whole
cell patch-clamp recordings performed in acute hypothalamic slices indicated
that application of DA resulted in a consistent and reversible reduction of
GABAergic synaptic activity. This inhibitory action appeared to be mediated,
at least in part, by the activation of presynaptic D4 receptors in agreement
with the presence of these receptors in the SON
(Defagot et al. 1997).
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METHODS |
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TOPABSTRACTINTRODUCTIONMETHODSRESULTSDISCUSSIONDISCLOSURESACKNOWLEDGMENTSREFERENCES |
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Acute hypothalamic slices were obtained using procedures similar to those
described previously (Oliet and Poulain
1999). Briefly, female Wistar rats (1–2 mo old) were
anesthetized and decapitated. The brain was quickly removed and placed in
ice-cold artificial cerebro-spinal fluid (ACSF) saturated with 95%
O2-5% CO2. Thin coronal slices (300 µm) were cut with
a vibratome (Leica) from a block of tissue containing the hypothalamus. Slices
including the SON were hemisected along the midline and allowed to recover for
1 h before recording. A slice was then transferred into a recording
chamber where it was submerged and continuously perfused (1–2 ml/min)
with ACSF at room temperature. The composition of the ACSF was (in mM) 123
NaCl, 2.5 KCl, 1 Na2HPO4, 26.2 NaHCO3, 1.3
MgCl2, 2.5 CaCl2, and 10 glucose (pH 7.4; 295–300
mosmol/kg). In experiments in which L745,870 was bath-applied, a different
ACSF was made to facilitate solubility of the drug. The composition of this
solution was (in mM) 150 NaCl, 2.5 KCl, 1.2 KH2PO4, 10
HEPES, 1.3 MgSO4, 2.5 CaCl2, and 10 glucose (pH 7.4;
295–300 mosmol/kg).
Patch-clamp recording
Magnocellular neurons were visually identified using infrared differential
interference contrast microscopy (Olympus). Patch-clamp recording pipettes
(3–5 M
) were filled with a solution containing (in mM) 141 CsCl,
10 HEPES, 5 QX-314, and 2 Mg-ATP (adjusted to pH 7.1 with CsOH). Membrane
currents were recorded using an Axopatch-1D amplifier (Axon Instruments).
Signals were filtered at 2 kHz and digitized at 5 kHz via a DigiData 1200
interface (Axon Instruments). Series resistance (6–20 M) was
monitored on-line and cells were excluded from data analysis if more than a
15% change occurred during the course of the experiment. All cells were held
at –60 mV in voltage-clamp mode. Spontaneous unitary synaptic currents
(miniatures) obtained in the presence of tetrodotoxin (TTX) were stored on
videotape via a pulse-code modulator (Neurodata), detected, and analyzed
off-line using Axograph (Axon Instruments). To evoke synaptic responses, a
glass stimulating electrode filled with ACSF and connected to an isolated
stimulator (Digitimer) was placed in the hypothalamic region dorsomedial to
the SON, as described previously (Kombian
et al. 1996). Synaptic responses were evoked at 0.05 Hz, using
square pulses of 0.1-ms duration, and analyzed on-line using pClamp (Axon
Instruments). To study the paired-pulse facilitation ratio (PPF ratio), two
synaptic responses (S1 and S2) were evoked by a couple of stimuli given at
60-ms intervals. PPF ratio was expressed as the ratio of the amplitude of the
second synaptic response over the first synaptic response (S2/S1).
Data were compared statistically with either the paired or the unpaired Student's t-test accordingly. Miniature amplitude and frequency distributions were compared using the nonparametric Kolmogorov-Smirnov test. Significance was assessed at P < 0.05. All data are reported as means ± SE.
Drugs
All drugs were bath-applied. Appropriate stock solutions were made and diluted with ACSF just before application. QX-314 chloride (Alomone labs) was diluted directly in the patch-solution. Drugs used were 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX, RBI), bicuculline methobromide, bromocriptine (Tocris), clozapine, dopamine, L750,667, L745,870 (Sigma), PD168077, SCH 23390, SKF 38393 (Tocris), sulpiride, and TTX (Sigma).
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RESULTS |
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TOPABSTRACTINTRODUCTIONMETHODSRESULTSDISCUSSIONDISCLOSURESACKNOWLEDGMENTSREFERENCES |
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). The mean frequency of mIPSCs varied greatly between
neurons from 0.5 to 7.7 Hz, whereas the mean amplitude ranged from –66.0
to –348.6 pA.
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Dopamine inhibits mIPSCs
Bath application of dopamine (DA; 300 µM) caused an important and
reversible reduction of mIPSC activity
(Fig. 1B). This effect
was associated with a rightward shift of the event interval distribution
(Fig. 1D; P
< 0.05), reflecting a decrease in mIPSC frequency. Conversely, DA neither
affected the amplitude distribution (P > 0.05) nor the kinetics of
the mIPSCs, as illustrated in Fig.
1C. On average, DA significantly inhibited the frequency
of mIPSCs by 60.8 ± 5.8% (n = 9; P < 0.05;
Fig. 1E), whereas the
mean amplitude of these unitary events was not significantly affected
(–7.2 ± 4.0%; P > 0.05). This specific modulation of
mIPSC frequency is usually considered to reflect a presynaptic modulation of
transmission (Redman 1990).
Our results, therefore indicate that dopamine acts presynaptically to inhibit
GABA release in the SON. Because DA did not change the amplitude distribution
or the kinetics of the unitary synaptic GABAergic currents, we have focused
the rest of our study on mIPSC frequency except when otherwise stated.
We next investigated the dose-dependent profile of this inhibition by using
varying concentrations of DA (Fig.
2A). The frequency of mIPSCs was reduced, on average, by
4.1 ± 4.8% (n = 5 cells), 2.9 ± 4.3% (n = 5),
53.0 ± 7.0% (n = 5), 69.0 ± 8.2% (n = 3) and
60.8 ± 5.8% (n = 9) for 0.3, 3, 30, 100, and 300 µM
dopamine, respectively. As illustrated in
Fig. 2B, fitting these
data with a Boltzmann function revealed values for half-maximal inhibition
(IC50) of 20.8 ± 2.2 µM and a threshold of 3 µM.
Maximal inhibitory responses were obtained for concentrations of 100
µM.
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Dopamine-mediated inhibition of mIPSCs is affected by D4 receptor antagonist
To identify the subtype of receptor involved in the modulation of
inhibitory GABAergic transmission by DA, we used several dopaminergic
antagonists. In this set of experiments, the antagonist was first added to the
bathing solution and DA (300 µM) was subsequently applied
(Fig. 3, A and
B). In the presence of the D2/D3 receptor antagonist
sulpiride (10 µM), dopamine retained its full ability to inhibit mIPSC
frequency (–57.6 ± 0.7%; n = 4; P > 0.05).
Similarly, blockade of D1/D5 receptors with SCH 23390 (100 µM) failed to
prevent the dopamine-dependent inhibition (–62.0 ± 0.7%;
n = 4; P > 0.05). These findings suggested that D1, D2,
D3, and D5 receptors are not implicated in the inhibitory response induced by
DA. We next investigated whether D4 dopamine receptors could be involved in
the inhibition of GABA release because it has been recently reported that
activation of these receptors inhibited glutamate release in the SON
(Price and Pittman 2001).
Interestingly, in the presence of the atypical antipsychotic drug clozapine
(50 µM), an antagonist of dopamine receptors that has a higher affinity
than for D4 over D2/D3 receptors (Seeman
and Van Tol 1994), dopamine-induced inhibition of mIPSC frequency
was partially prevented (–39.9 ± 4.3%; n = 6; P
< 0.05). The involvement of D4 receptors was confirmed by the use of
L750,667 and L745,870, two highly specific antagonists of these receptors
(Kulagowski et al. 1996;
Patel et al. 1996). In the
presence of L750,667 (50 µM) and L745,870 (50 µM), dopamine reduced
mIPSC frequency by 27.7 ± 6.4% (n = 6) and 19.8 ± 5.6%
(n = 5) respectively (Fig. 3,
A and B). These values were significantly
different from those obtained by DA alone in the absence of these antagonists
(P < 0.05), indicating that D4 receptors mediate part of, if not
all, the action of dopamine on mIPSCs in the SON. Clozapine, L750,667, nor
L745,870 affected mIPSC frequency by themselves, suggesting that D4 receptors
were not activated tonically by endogenous dopamine.
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Dopamine-mediated inhibition of mIPSCs is mimicked by a D4 receptor agonist
If D4 receptors mediate the inhibition of GABAergic transmission, a
specific agonist of this receptor subtype should mimic this action. On the
other hand, agonists of D1, D2, D3, and D5 receptors should be without effect
on GABAergic synaptic currents. We first examined the action of PD168077, a
potent and selective D4 receptor agonist
(Glase et al. 1997). Bath
application of PD168077 (30 µM; n = 8) reduced the frequency
(–51.6 ± 4.2%; P < 0.05) but not the amplitude
(–3.6 ± 1.8%; P > 0.05) of mIPSCs
(Fig. 4). This finding confirms
the existence of presynaptic D4 receptors on GABAergic terminals in the SON
whose activation leads to an inhibition of transmitter release. Conversely,
exposure of SON neurons to SKF 38393 (30 µM; n = 4), a specific
D1/D5 receptor agonist, and bromocriptine (50 µM; n = 4), a
specific D2/D3 receptor agonist, was without effect on mIPSC frequency
(–5.2 ± 6.7 and –2.1 ± 4.4%, respectively;
P > 0.05; Fig.
4D). Taken together, these data indicate that, in the
SON, indeed dopamine inhibits mIPSCs through the activation of D4
receptors.
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Dopamine-mediated inhibition of evoked IPSC amplitude
Although our data indicate that DA inhibits spontaneous GABA-A
receptor-mediated currents, it remained to be determined whether GABA release
evoked by electrical stimulation was also sensitive to dopamine. As
illustrated in Fig. 5, A and
B, bath application of DA (300 µM) was found to
reversibly reduce the amplitude of evoked IPSCs by 60.5 ± 5.4%
(n = 9). This inhibitory action of DA was accompanied by an increase
in paired-pulse facilitation ratio from 1.21 ± 0.15 to 2.22 ±
0.34 (n = 9; Fig. 5, C
and D) as expected from a presynaptic reduction of
transmitter release (Zucker and Regehr
2002). To make sure that the action of DA on evoked GABA release
was mediated through D4 receptors, we tested the effect of PD168077 (30 µM)
on evoked inhibitory postsynaptic currents (IPSCs;
Fig. 5, A and
B). In the presence of the D4 agonist, the amplitude of
the response was inhibited by 54.6 ± 8.6% (n = 5), an effect
similar to that obtained with 300 µM DA. These results are in agreement
with those obtained on mIPSCs and confirm the presence of presynaptic D4
receptors whose activation depresses the release of GABA in the SON.
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DISCUSSION |
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TOPABSTRACTINTRODUCTIONMETHODSRESULTSDISCUSSIONDISCLOSURESACKNOWLEDGMENTSREFERENCES |
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) and the substantia nigra
(Miyazaki and Lacey 1998).
This disinhibitory process represents a potent regulatory mechanism of
neuronal excitability. Our data indicate that, in the SON, it is through a
similar mechanism that dopamine could contribute to the regulation of
neurohypophysial hormone secretion (Bridges
et al. 1976; Forsling and
Williams 1984; Ivanyi et al.
1986; Moos and Richard
1982; Urano and Kobayashi
1978; Yamagushi and Hama
1989). Presynaptic inhibition of GABAergic transmission
Suprathreshold applications of dopamine inhibited GABAergic synaptic
currents in all SON neurons tested. Because we did not record from a specific
area in the SON, it is very likely that DA modulates GABAergic transmission in
both OT and VP neurons in agreement with the observation that DA modulates the
release of both neurohypophysial hormones
(Bridges et al. 1976;
Moos and Richard 1982).
The inhibitory action of DA was associated with a reduction in the
frequency, but not the amplitude, of mIPSCs and with an increased PPF of
evoked IPSCs. These findings are consistent with an inhibition of presynaptic
origin (Redman 1990;
Zucker and Regehr 2002). DA
receptors mediating this action are almost certainly located on the terminals
rather than on the cell bodies of GABAergic neurons because mIPSCs were
obtained in the absence of presynaptic action potentials due to the blockade
of voltage-gated Na+ channels by TTX. The mechanism by which
activation of presynaptic DA receptors elicits an inhibition of GABA release
remains to be determined. One possible explanation could be an inhibition of
the voltage-gated Ca2+ channels involved in transmitter
release (Mei et al. 1995). The
reduction of Ca2+ entry in the terminals would alter the
coupling between action potential and exocytosis of vesicles
(Augustine et al. 1987).
However, this mechanism cannot account for the reduction of mIPSC activity in
the present study because these unitary events are known to be independent of
Ca2+ entry (Brussaard
et al. 1996; Oliet and Poulain
1999).
Alternatively, the activation of presynaptic DA receptors could affect the
proteins involved in the intracellular signaling cascade leading to
exocytosis. Because most of the effects of dopamine are associated with the
modulation of a cAMP-dependent protein kinase (PKA)
(Missale et al. 1998) and
because transmitter release has been shown to be sensitive to PKA (Kondo et
al. 1997; Trudeau et al.
1996), the action of DA observed in our experiments could reflect
a change in cAMP level in the terminals. Interestingly, presynaptic inhibition
of GABAergic release in the SON appears to be inhibited through the activation
of several presynaptic receptors coupled to adenylyl cyclase activity. This
includes group III mGluRs (Piet et al.
2003; Schrader and Tasker
1997), GABA-B (Mouginot et al.
1998), and adenosine A1 (Oliet
and Poulain 1999) receptors. It is also possible that other
intracellular signaling mediators, like protein kinase C, are involved in this
process.
Receptor identification
To identify the dopamine receptors involved in the inhibition of GABA
release, we used various antagonists and agonists exhibiting different
selectivity for DA receptor subtypes. In all likelihood, the receptor
responsible for inhibition of mIPSC activity is the D4 receptor. This is based
on the sensitivity of DA-induced response to L750,667 and L745,870, which are
specific D4 antagonists, and on the observation that the specific D4 agonist
PD168077 mimicked DA inhibitory action on both miniatures and evoked IPSCs.
This finding was strengthened by the lack of effect of sulpiride and SCH
23390, D2/D3 and D1/D5 antagonists respectively, on DA-mediated inhibition of
GABAergic transmission. Furthermore, SKF 81297 and bromocriptine, D1/D5 and
D2/D3 specific agonists, respectively, did not affect mIPSC activity. Finally,
clozapine, an antagonist that has a 10-fold greater affinity for D4 than D2
and D3 receptors (Seeman and Van Tol
1994), was able to partially prevent the inhibitory action of DA.
Taken together, these results demonstrate that DA-induced inhibition of GABA
release in the SON is mediated by the activation of dopamine D4 receptors.
Dopamine D4 receptor activation has also been reported to inhibit GABAergic
transmission in the prefrontal cortex through a PKA-dependent mechanism
(Wang et al. 2002), but in
this structure, D4 receptor appears to have an action on postsynaptic GABA-A
receptors rather than on transmitter release.
Functional implications
The inhibitory action of DA on GABAergic transmission in the SON neurons
should lead to a disinhibition of magnocellular neurons and, as a consequence,
to an augmented excitability of the hypothalamo-neurohypophysial system. This
is in agreement with the excitatory effects observed in vivo in response to
injections of DA in the SON or intracerebroventricularly
(Bridges et al. 1976;
Moos and Richard 1982;
Urano and Kobayashi 1978).
However, to understand better the action of DA in the SON, it is important to
take into consideration the various actions of DA that have been reported in
previous in vitro studies. In particular, it has been shown that DA, at
concentrations similar to those used in the present study, inhibits glutamate
release via the activation of presynaptic D4 receptors
(Price and Pittman 2001), an
effect that should reduce cell excitability and hormone secretion. Conversely,
DA within the same range of concentrations acts on postsynaptic D2 receptors
causing a membrane depolarization due to the activation of a cationic
conductance (Yang et al.
1991). In view of these different effects, the overall action of
DA on SON neurons and its consequence on hypothalamo-neurohypophysial hormones
secretion remains speculative. In particular, whether one of these dopamine
responses is predominant in situ has to be determined. Inhibiting
glutamatergic and GABAergic synaptic activity, and therefore reducing
background synaptic noise, could have several consequences on the postsynaptic
cell. It could make the neuron more electrically compact by increasing input
resistance (Paré et al.
1997), reduce shunting inhibition and increase the gain of the
input-output neuronal response (Chance et
al. 2002; Prescott and De
Koninck 2003) as well as render the cell less sensitive to weak
signals (Wiesenfeld and Moss 1995). One attractive hypothesis could be that
DA-mediated inhibition of both GABA and glutamate synaptic activities in the
SON isolates, to some extent, the neurons from excitatory and inhibitory
drives mediated through these inputs. This will make SON neurons more
responsive to the activation of D2 postsynaptic receptors, for instance. In
other words, this process could serve to significantly enhance the
signal-to-noise ratio for the information originating from dopaminergic
inputs.
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DISCLOSURES |
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TOPABSTRACTINTRODUCTIONMETHODSRESULTSDISCUSSIONDISCLOSURESACKNOWLEDGMENTSREFERENCES |
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ACKNOWLEDGMENTS |
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TOPABSTRACTINTRODUCTIONMETHODSRESULTSDISCUSSIONDISCLOSURESACKNOWLEDGMENTSREFERENCES |
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FOOTNOTES |
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Address for reprint requests: S.H.R. Oliet, INSERM U378 - Institut François Magendie, 1, rue Camille St-Saëns, 33077 Bordeaux Cedex, France (E-mail: stephane.oliet{at}bordeaux.inserm.fr).
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