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1
Department of Basic Neurosciences, Faculty of Medicine, University of Geneva, Geneva, Switzerland.
2
INSERM U1114, University of Strasbourg Institute for Advanced Study, Strasbourg, France.
3
IGF, Université de Montpellier CNRS, Inserm, Montpellier, France.
4
Department of Basic Neurosciences, Faculty of Medicine, University of Geneva, Geneva, Switzerland. [email protected].
5
Clinic of Neurology, Department of Clinical Neurosciences, Geneva University Hospital, Geneva, Switzerland. [email protected].
1
Department of Basic Neurosciences, Faculty of Medicine, University of Geneva, Geneva, Switzerland.
2
INSERM U1114, University of Strasbourg Institute for Advanced Study, Strasbourg, France.
3
IGF, Université de Montpellier CNRS, Inserm, Montpellier, France.
4
Department of Basic Neurosciences, Faculty of Medicine, University of Geneva, Geneva, Switzerland. [email protected].
5
Clinic of Neurology, Department of Clinical Neurosciences, Geneva University Hospital, Geneva, Switzerland. [email protected].
Fentanyl is a powerful painkiller that elicits euphoria and positive reinforcement
1
. Fentanyl also leads to dependence, defined by the aversive withdrawal syndrome, which fuels negative reinforcement
2,3
(that is, individuals retake the drug to avoid withdrawal). Positive and negative reinforcement maintain opioid consumption, which leads to addiction in one-fourth of users, the largest fraction for all addictive drugs
4
. Among the opioid receptors, µ-opioid receptors have a key role
5
, yet the induction loci of circuit adaptations that eventually lead to addiction remain unknown. Here we injected mice with fentanyl to acutely inhibit γ-aminobutyric acid-expressing neurons in the ventral tegmental area (VTA), causing disinhibition of dopamine neurons, which eventually increased dopamine in the nucleus accumbens. Knockdown of µ-opioid receptors in VTA abolished dopamine transients and positive reinforcement, but withdrawal remained unchanged. We identified neurons expressing µ-opioid receptors in the central amygdala (CeA) whose activity was enhanced during withdrawal. Knockdown of µ-opioid receptors in CeA eliminated aversive symptoms, suggesting that they mediate negative reinforcement. Thus, optogenetic stimulation caused place aversion, and mice readily learned to press a lever to pause optogenetic stimulation of CeA neurons that express µ-opioid receptors. Our study parses the neuronal populations that trigger positive and negative reinforcement in VTA and CeA, respectively. We lay out the circuit organization to develop interventions for reducing fentanyl addiction and facilitating rehabilitation.
a
, Experimental schedule. i.p., intraperitoneal injection.
b
, Representative example of speed dynamics following intraperitoneal injection of fentanyl and during precipitation of withdrawal by naloxone.
c
, Box plot of jumps and immobility time in dependent mice without precipitation (grey,
n
= 14), in dependent mice with precipitation (red,
n
= 13) and in non-dependent mice with naloxone injection (white,
n
= 13; jump Kruskal–Wallis test:
H
(3) = 26.79,
P
< 0.001; immobility time Kruskal–Wallis test
H
(3) = 28.94,
P
< 0.001; Dunn’s multiple comparisons test, **
P
< 0.01, ***
P
< 0.001). F, fentanyl; N, naloxone; S, saline.
d
, Representative images of cFOS staining in prefrontal cortex (PFC), NAc shell (NAcS), NAc core (NAcC), paraventricular thalamus (PVT), basolateral amygdala (BLA), CeA, ventral hippocampus (vHIP) and VTA in a non-dependent mouse after saline injection (top row), naloxone injection (second row), dependent mice without precipitated withdrawal (third row) and dependent mice with precipitated withdrawal (bottom row). Scale bar, 100 μm.
e
, Number of cFOS-positive cells in the brain areas shown in
d
(
n
= 7–9 mice per group, two-way ANOVA; PFC: fentanyl effect
F
(1,28)
= 59.68,
P
< 0.001, naloxone effect
F
(1,28)
= 0.50,
P
> 0.05, interaction
F
(1,28)
= 0.67,
P
> 0.05; NAcS: fentanyl effect
F
(1,28)
= 30.84,
P
< 0.001, naloxone effect
F
(1,28)
= 5.64,
P
< 0.05, interaction
F
(1,28)
= 0.59,
P
> 0.05; NAcC: fentanyl effect
F
(1,29)
= 55.43,
P
< 0.001, naloxone effect
F
(1,29)
= 10.34,
P
< 0.01, interaction
F
(1,29)
= 2.13,
P
> 0.05; PVT: fentanyl effect
F
(1,29)
= 48.72,
P
< 0.001, naloxone effect
F
(1,28)
= 0.47,
P
> 0.05, interaction
F
(1,29)
= 1.65,
P
> 0.05; BLA: fentanyl effect
F
(1,29)
= 13.73,
P
< 0.001, naloxone effect
F
(1,29)
= 0.39,
P
> 0.05, interaction
F
(1,29)
= 0.73,
P
> 0.05; CeA: fentanyl effect
F
(1,29)
= 51.86,
P
< 0.001, naloxone effect
F
(1,29)
= 60.56,
P
< 0.001, interaction
F
(1,29)
= 18.54,
P
< 0.001; vHYP: fentanyl effect
F
(1,25)
= 42.72,
P
< 0.001, naloxone effect
F
(1,25)
= 1.37,
P
> 0.05, interaction
F
(1,25)
= 0.13,
P
> 0.05; VTA: fentanyl effect
F
(1,29)
= 51.48,
P
< 0.001, naloxone effect
F
(1,29)
= 2.00,
P
> 0.05, interaction
F
(1,29)
= 2.44,
P
> 0.05, Bonferoni’s multiple comparisons test. *
P
< 0.05, **
P
< 0.01, ***
P
< 0.001). Data are mean ± s.e.m.
f
, Schematic of mouse preparation to induce µOR knockdown in various brain regions (control (CTL),
n
= 12; VTA,
n
= 13; NAc,
n
= 13; BLA,
n
= 12; CeA,
n
= 14; PVT,
n
= 13).
g
, Left, schedule of experiment to induce fentanyl dependence. Right, behavioural test to evaluate precipitated withdrawal induced by intraperitoneal injection of 5 mg kg
−1
naloxone.
h
,
i
, Left, box plot of precipitated jump (
h
) and immobility (
i
) withdrawal symptoms after µOR deletion in indicated brain areas (CTL,
n
= 12; VTA,
n
= 13; NAc,
n
= 13; BLA,
n
= 12; CeA,
n
= 14; PVT,
n
= 13). Right, proportion of mice showing the presence of at least one precipitated jump (
h
) and at least 5 min of immobility (
i
) withdrawal symptoms. Kruskal–Wallis test: jumps,
H
(6) = 15.39,
P
< 0.01; immobility,
H
(6) = 8.774,
P
= 0.12; Dunn’s multiple comparisons test, *
P
= 0.0218. In box plots, the centre line is the median, box edges delineate first and third quartiles, and whiskers extend to maximum and minimum values. Source Data
a
, Left, representative example of CeA imaged by single-molecule fluorescent in situ hybridization (smFISH) for
Oprm1
(blue), somatostatin (
Sst
) (green) and
Prkcd
(red) mRNA. Right, quantification of co-localization between
Sst
- and
Prkcd
-positive neurons (
n
= 7 mice). Scale bar, 100 μm.
b
, Left, representative example of CeA imaged by smFISH for µOR (
Oprm1
) (white),
Sst
(green) and
Prkcd
(red). Right, quantification of
Oprm1
-positive neurons among the
Sst
+
and
Prkcd
+
populations. Data are mean ± s.e.m. (
n
= 7 mice). Two-sided Mann–Whitney test, ***
P
= 0.0006. Scale bar, 20 μm.
c
, Schematic of mouse preparation to visualize the µOR-expressing CeA efferent pathway (top) and representative image showing injection (bottom). Scale bar, 100 µm.
d
, Projection site of µOR-expressing CeA neurons in the parabrachial lateral nucleus (PBL) and the ventral bed nucleus of the stria terminalis (BNSTv) and dorsal bed nucleus of the stria terminalis (BNSTd). Scale bars, 1 mm. Source Data
a
, Top, schematic of mouse preparation for recording Ca
2+
activity of VTA neurons expressing dopamine and GABA. Bottom, schedule of the recording experiment in fentanyl-dependent mice. Withdrawal is precipitated by naloxone on day 7 (intraperitoneal injection, 5 mg kg
−1
).
b
, Ca
2+
signal (Δ
F
/
F
0
) of dopamine (
n
= 8 mice) and GABA (
n
= 8 mice) neurons after intraperitoneal injection of naloxone (5 mg kg
−1
), fentanyl (0.3 mg kg
−1
) and fentanyl plus naloxone.
c
, Top, schematic representation of NAc dLight recordings after µOR deletion in VTA. Bottom, schedule of intraperitoneal injections for dLight recordings after saline, fentanyl (0.3 mg kg
−1
) and apomorphine (10 mg kg
−1
) treatments.
d
, Accumbal dLight signal (Δ
F
/
F
0
) in mice with deletion of µORs in VTA (
n
= 8 mice) versus control mice (
n
= 7 mice).
e
, Quantification of the area under the curve (AUC) after intraperitoneal injection of saline or fentanyl in mice with deletion of µORs in VTA (
n
= 8 mice) versus control mice (
n
= 7 mice). Two-way repeated measures ANOVA: group effect,
F
(1,26)
= 4.371,
P
< 0.05; injection effect,
F
(1,26)
= 23.95,
P
< 0.0001; group × injection,
F
(1,26)
= 5.777,
P
< 0.05; Bonferroni post hoc analysis, **
P
= 0.0076. Data are mean ± s.e.m.
f
, Top, schematic of mice preparation to label µOR-expressing neurons in CeA. Bottom, schedule of the experiment to induce fentanyl dependence and precipitation of withdrawal on the challenge day (day 6).
g
, Box plot representation of jumps and immobility time withdrawal symptoms quantified in
Oprm1
-
cre
(
n
= 8 mice) and
Sst
-
cre
(
n
= 8) mice. The centre line is the median, box edges delineate first and third quartiles, and whiskers extend to maximum and minimum values.
h
, Left, representative example of CeA µOR-expressing neurons co-localizing with cFOS (white arrows) after precipitated withdrawal. Right, fraction of cFOS-expressing neurons among CeA µOR or SST-expressing neurons (
n
= 8 mice for SST and
n
= 8 mice for µOR; two-sided unpaired
t
-test, ***
P
< 0.0001). Scale bar, 20 μm.
i
, Schematic of mouse preparation for Ca
2+
recording of CeA µOR-expressing neurons during precipitation of withdrawal.
j
, Average Ca
2+
signal (Δ
F
/
F
0
) of CeA µOR-expressing neurons in naive mice after intraperitoneal injection of naloxone (left) and independent mice after intraperitoneal injection of fentanyl (0.3 mg kg
−1
) plus saline or fentanyl (0.3 mg kg
−1
) plus naloxone (5 mg kg
−1
) (
n
= 7 mice).
k
, Quantification of AUC after intraperitoneal injection of saline or naloxone in naive and dependent mice (
n
= 7 mice; Kruskal–Wallis test for AUC
H
(3) = 7.577,
P
< 0.05; Dunn’s multiple comparisons test, *
P
= 0.0258). Data are mean ± s.e.m.
l
, Bottom, average Ca
2+
traces align to different behavioural events during precipitation of withdrawal. Top, trials activity map of each behavioural parameter during precipitation of withdrawal. Source Data
a
, Schematics for oGABAsi experiments (top) and histological validation (bottom). Scale bar, 1 mm.
b
, Fentanyl occlusion schedule during oGABAsi experiment.
c
, Active lever presses (ALP), inactive lever presses (ILP) and laser stimulations (LS) per minute during operant conditioning (
n
= 9 mice; LP: two-way repeated measures ANOVA, LP effect
F
(1,8)
= 203, ***
P
< 0.001; session effect
F
(16,128)
= 12.12, ***
P
< 0.001; LP × time interaction
F
(16,128)
= 11.23, ***
P
< 0.001). Data are mean ± s.e.m.
d
, ALP and ILP during the pre-session (top) and during the session (bottom) after injection of fentanyl at different doses (
n
= 9 mice; LP pre-session: two-way repeated measures ANOVA, LP effect
F
(1,8)
= 198.3, ***
P
< 0.001; time effect
F
(13,104)
= 2.263, *
P
< 0.05; LP × time interaction
F
(13,104)
= 2.586, *
P
< 0.05) Data are mean ± s.e.m.
e
, Laser stimulations per minute during the pre-session and post-session following intraperitoneal injection of saline or fentanyl at increasing doses (
n
= 9 mice). Data are mean ± s.e.m.
f
, Dose–response curve for fentanyl occlusion of oGABAsi (
n
= 9 mice). Sigmoid fit yielding an IC
50
of 187.2 μg kg
−1
and a Hill coefficient of −2.33. Data are mean ± s.e.m.
g
, Schematic of mouse preparation for optogenetic manipulation of CeA µOR-expressing neurons during an operant negative reinforcement task.
h
, Fentanyl occlusion schedule during the operant negative reinforcement task.
i
, ALP and ILP (top) and laser stop (bottom) rates during the FR1 and FR3 operant conditioning phases in control (
n
= 7 mice) or ChR2 (
n
= 8 mice) mice (ALP: two-way repeated measures ANOVA, group effect
F
(1,13)
= 6.671, *
P
< 0.05; time effect
F
(19,247)
= 4.64, ***
P
< 0.001; LP × time interaction
F
(19,247)
= 2.59, ***
P
< 0.001; rate: two-way repeated measures ANOVA, group effect
F
(1,13)
= 12.74, *
P
< 0.05; time effect
F
(19,247)
= 6.059, ***
P
< 0.001; LP × time interaction
F
(19,247)
= 3.801, ***
P
< 0.001). Data are mean ± s.e.m.
j
, ALP and ILP (left) and laser stop (right) after injection of fentanyl at different doses (
n
= 7 mice). Data are mean ± s.e.m.
k
, Dose–response curve for fentanyl occlusion of optogenetically manipulating CeA µOR-expressing neurons in an operant negative reinforcement task (
n
= 7 mice). Sigmoid fit yielding an IC
50
of 70 μg kg
−1
and a Hill coefficient of −1.94. Data are mean ± s.e.m. Source Data
(
A
) Representative example of occupancy (left) and distance traveled (Right) after i.p. injection of fentanyl (Reward, left panel) or during precipitation of withdrawal by an i.p. injection of naloxone (Withdrawal, right panel). (
B
) Box Plot representation (Quartils and median, whiskers min to max) of the seven withdrawal symptoms quantified in dependent animal with no precipitation (grey,
n
= 14), in dependent animal with precipitation (red,
n
= 13) and in non-dependent animal with naloxone injection (white,
n
= 13). (During fentanyl: Kruskal-Wallis test: Rearing, H(3) = 31.72, P < 0.001, Jump, H(3) = 2.077, Defecation, H(3) = 26.32, P < 0.001, Wet Dog Shake, H(3) = 33.37, P < 0.001, Body Licking, H(3) = 37.14, P < 0.001, Immobility Time, H(3) = 20.47, P < 0.001, Distance, H(3) = 25.84, P < 0.001; During Naloxone: Kruskal-Wallis test: Rearing, H(3) = 27.67, Jump, H(3) = 26.79, P < 0.001, Defecation, H(3) = 21.65, P < 0.001, Wet Dog Shake, H(3) = 25.83, P < 0.001, Body Licking, H(3) = 30.14, P < 0.001, Immobility Time, H(3) = 28.94, P < 0.001, Distance, H(3) = 26.70; P < 0.001; Dunn’s multiple comparisons test, *p < 0.05, **p < 0.01, ***p < 0.001). (
C
) Heat-map representation of the different precipitated withdrawal symptoms normalized individually from min to max (respectively 0 and 1). (
D
) Correlation matrix of the individual precipitated withdrawal symptoms. Superimposed are annotated the Spearman correlation coefficient. Source Data
(
A
) Schematic of the mice preparation to induce VTA µORs deletion. (
B
) Fluorescent in situ hybridization (RNAscope) for
Oprm1
(µORs, red) and DAPI (blue) in VTA (Left) or CeA (Right) without (Top) or with µORs deletion (Bottom) (
C
) Quantification of mRNA puncta (Mean ± SEM) per images in control (black) vs KD animals (red) respectively in VTA (Left) and CeA (Right). For VTA,
n
(images) = 14 and
n
(images) = 10, respectively for KD animals (
n
= 3 mice) and control animals (
n
= 3 mice). For CeA,
n
(images) = 16 and
n
(images) = 16, (
n
= 7 mice) (unilateral injection). Mann-Whitney test, two-sided, ***p < 0.001. Source Data
(
A
) Top: Representative example of the injection site in the different brain regions. Bottom: Localization of the injection centre in the different mice (CTL (
n
= 12); VTA (
n
= 13); NAc (
n
= 13); BLA (
n
= 12); CeA (
n
= 14); PVT (
n
= 13)). (
B
) Names of the variable extracted for DLC tracking. (
C
-
D
) Top: Spider plot representing the multidimensional distance between each experimental groups (µORs KD in different brain regions) vs control group (non-KD) of each time-series quantified after precipitation of withdrawal. Bottom: SVM classification of the 15 variables extracted from DLC in the different experimental groups (µORs KD) vs control group after precipitation of withdrawal. Color code used to evaluate the accuracy of prediction of each variables extract. (estimated p value with permutation test; *p < 0.05, **p < 0.01, ***p < 0.001).
(
A
) Left: Low VTA magnification representative example of fluorescent in situ hybridization for opioid receptor mu 1 (
Oprm1
, Blue), solute carrier family 32 member 1 (
Slc32a1
, green) and solute carrier family 6 member 3 (
Slc6a3
, red) mRNAs (Scale bars: 100 µm). Right: Quantification of colocalization between
Slc32a1
(DAT) and
Slc6a3
(GABA) positive neurons (
n
= 5 mice). (
B
) Left: Fluorescent in situ hybridization representative example of VTA molecular marker for
Oprm1
(µORs, White),
Slc32a1
(GABA, green) and
Slc6a3
(DA, red). Right: Proportion of GABA and DA neurons (Mean ± SEM) within the µORs-expressing neurons (
n
= 5 mice). Mann-Whitney test, two-sided, **p = 0.0079. Source Data
(
A
) Localization of the recording site in DAT-cre (
n
= 8) and GAD-cre (
n
= 8) animals. (
B
) Representative histological example of virus infection and fibre implantation in VTA. (
C
,
F
) Raw signal recording example (470 and 405 nm) of GCaMP6m after i.p. injection of Naloxone in naïve mice (Left), after i.p. injection of fentanyl (middle) and after fentanyl plus naloxone i.p. injection (right) in dopaminergic neurons (Pink) and GABAergic neurons (Green). (
D
,
G
) Example Ca
2+
signal (ΔF/F0) of dopamine (Pink) and GABA (green) VTA neurons and its associated transients identification (Blue). (
E
,
F
) Average transients rate (Mean ± SEM) after i.p. injection of Naloxone in naïve mice, after i.p. injection of fentanyl and after fentanyl plus naloxone i.p. injection in dopaminergic neurons (pink) and GABAergic neurons (green) (For DAT transients, Kruskal-Wallis test H(7) = 21.66, P < 0.01, For GAD transients, Kruskal-Wallis test H(7) = 6.788, P > 0.05, Dunn’s multiple comparisons test, *p < 0.01). Source Data
(
A
) Localization of the NAc recording site in VTA µORs KD (
n
= 8 mice) and CTL (
n
= 7 mice) animals plus viral infection in VTA. Bottom: (
B
) Representative histological example of fibre implantation in NAc and virus infection in VTA. (
C
) Representative example of NAc raw dLight signal (470 and 405 nm) in control (Top) and VTA µORs KD (Bottom) animals after i.p. injection of saline, Fentanyl (0.3 mg/kg) and apomorphine (10 mg/kg). (
D
) Accumbal dLight signal (ΔF/F0) in VTA µORs KD (red,
n
= 8 mice) vs CTL mice (grey,
n
= 7 mice) after i.p. injection of apomorphine at 10 mg/kg. (
E
) Mean ± SEM of the area under the curve after pharmacological i.p. injection of apomorphine in VTA µORs KD (
n
= 8 mice) and CTL (
n
= 7 mice). (
F
) Normalization of AUC (Mean ± SEM) evoked by fentanyl 0.3 mg/kg i.p. injection compared to the AUC of the partial agonist D1/D2 dLight apomorphine in VTA µORs KD (
n
= 8 mice) and CTL (
n
= 7 mice) (Mann-Whitney test, two-sided, p > 0.05). Source Data
(
A
) i.p. protocol fentanyl injection. (
B
) Average speed locomotion induced by fentanyl at different doses in 1 h open field test (
n
= 7 mice). (
C
) Correlation matrix of the different behavioral parameters during oGABAsi occlusion. Superimposed are annotated the Spearman correlation coefficient (
n
= 7 mice). (
D
) Active lever press number (ALP, Mean ± SEM) through the session of oGABAsi occlusion after different dose of fentanyl i.p. injected (
n
= 7 mice). (
E
) Frequency distribution of latency between ALP during oGABAsi occlusion experiment after different dose of fentanyl i.p. injected (
n
= 7 mice). (
F
) Schematic of the mice preparation to induce VTA µORs deletion. (
G
) Distance travelled (Mean ± SEM) after i.p. injection of saline (sal) or Fentanyl 0.2 mg/kg in mice with VTA µORs KD (
n
= 4 mice, red), control animal (
n
= 4 mice, grey) or control saline animal (
n
= 4 mice, black).
(
A
) Schedule of the experiment to induce Place preference with i.p. injection of fentanyl 0.3 mg/kg. (
B
) Representative example of occupancy plot for control mice (Left) and VTA µORs KD mice (Right), before (top) and after (Bottom) conditioning. (
C
) Left: Average preference score (Mean ± SEM) for the fentanyl compartment before and after conditioning in CTL mice (Black,
n
= 11) and VTA µORs KD mice (red,
n
= 10) (Two way RM ANOVA, Session, F
(1,38)
= 10.91, p < 0.01, Genotype, F
(1,38)
= 0.8352, p > 0.05, Session x Genotype, F
(16,38)
= 2.046, p > 0.05; Bonferroni post hoc analysis, **p = 0.029). Right: Average difference of time (in seconds, Mean ± SEM) spent in the fentanyl compartment for CTL mice vs VTA µOR KD mice (Right, Mann-whitney test, two-sided, p > 0.05). Source Data
(
A
) Schematic of the mice preparation for optogenetically manipulating CeA µORs-expressing neurons during a real-time place aversion task. (
B
) Schedule of the experiment to induce real-time place aversion with 20 Hz stimulation, consisting of a pre-session (20 min), three sessions of conditioning (30 min) and a post-conditioning session (20 min) (
C
) Relative time spent in the stimulating chamber (Mean ± SEM) during the behavioral task (
n
= 9 for ChR2 group and
n
= 15 for the GFP group). (
D
) Average (Mean ± SEM) relative time spent in the conditioning chamber over the 3 conditioning days (
n
= 9 for ChR2 group and
n
= 15 for the GFP group; Unpaired t test, two-sided, *p = 0.028). Source Data
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