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Single rodent mesohabenular axons release glutamate and GABA


The lateral habenula (LHb) is involved in reward, aversion, addiction and depression through descending interactions with several brain structures, including the ventral tegmental area (VTA). The VTA provides reciprocal inputs to LHb, but their actions are unclear. Here we show that the majority of rat and mouse VTA neurons innervating LHb coexpress markers for both glutamate signaling (vesicular glutamate transporter 2; VGluT2) and GABA signaling (glutamic acid decarboxylase; GAD, and vesicular GABA transporter; VGaT). A single axon from these mesohabenular neurons coexpresses VGluT2 protein and VGaT protein and, surprisingly, establishes symmetric and asymmetric synapses on LHb neurons. In LHb slices, light activation of mesohabenular fibers expressing channelrhodopsin2 driven by VGluT2 (Slc17a6) or VGaT (Slc32a1) promoters elicits release of both glutamate and GABA onto single LHb neurons. In vivo light activation of mesohabenular terminals inhibits or excites LHb neurons. Our findings reveal an unanticipated type of VTA neuron that cotransmits glutamate and GABA and provides the majority of mesohabenular inputs.

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Figure 1: Most VTA neurons projecting to LHb coexpress VGluT2 and GAD.
Figure 2: Most mesohabenular axon terminals (ATs) coexpress VGluT2 and VGaT, and a single terminal simultaneously establishes symmetric and asymmetric synapses.
Figure 3: Presence of both glutamatergic and GABAergic receptors postsynaptic to single mesohabenular axon terminals.
Figure 4: Selective stimulation of mesohabenular terminals evokes both GABAA-mediated outward and AMPA-mediated inward currents in LHb neurons.
Figure 5: In vivo optical stimulation of mesohabenular inputs evokes inhibition in most LHb neurons and evokes excitation in some.
Figure 6: Mesohabenular light-evoked inhibition is sensitive to GABAA antagonists in vivo.
Figure 7: Mesohabenular light-evoked excitation is sensitive to glutamate receptor antagonists in vivo.

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  1. Matsumoto, M. & Hikosaka, O. Lateral habenula as a source of negative reward signals in dopamine neurons. Nature 447, 1111–1115 (2007).

    Article  CAS  Google Scholar 

  2. Friedman, A. et al. Electrical stimulation of the lateral habenula produces enduring inhibitory effect on cocaine seeking behavior. Neuropharmacology 59, 452–459 (2010).

    Article  CAS  Google Scholar 

  3. Bromberg-Martin, E.S. et al. Distinct tonic and phasic anticipatory activity in lateral habenula and dopamine neurons. Neuron 67, 144–155 (2010a).

    Article  CAS  Google Scholar 

  4. Bromberg-Martin, E.S., Matsumoto, M., Hong, S. & Hikosaka, O. A pallidus-habenula-dopamine pathway signals inferred stimulus values. J. Neurophysiol. 104, 1068–1076 (2010b).

    Article  Google Scholar 

  5. Li, B. et al. Synaptic potentiation onto habenula neurons in the learned helplessness model of depression. Nature 470, 535–539 (2011).

    Article  CAS  Google Scholar 

  6. Jhou, T.C. et al. The rostromedial tegmental nucleus (RMTg), a GABAergic afferent to midbrain dopamine neurons, encodes aversive stimuli and inhibits motor responses. Neuron 61, 786–800 (2009).

    Article  CAS  Google Scholar 

  7. Jhou, T.C. et al. Cocaine drives aversive conditioning via delayed activation of dopamine-responsive habenular and midbrain pathways. J. Neurosci. 33, 7501–7512 (2013).

    Article  CAS  Google Scholar 

  8. Hong, S. et al. Negative reward signals from the lateral habenula to dopamine neurons are mediated by rostromedial tegmental nucleus in primates. J. Neurosci. 31, 11457–11471 (2011).

    Article  CAS  Google Scholar 

  9. Stamatakis, A.M. & Stuber, G.D. Activation of lateral habenula inputs to the ventral midbrain promotes behavioral avoidance. Nat. Neurosci. 15, 1105–1107 (2012).

    Article  CAS  Google Scholar 

  10. Lammel, S. et al. Input-specific control of reward and aversion in the ventral tegmental area. Nature 491, 212–217 (2012).

    Article  CAS  Google Scholar 

  11. Stamatakis, A.M. et al. A unique population of ventral tegmental area neurons inhibits the lateral habenula to promote reward. Neuron 80, 1039–1053 (2013).

    Article  CAS  Google Scholar 

  12. Swanson, L.W. The projections of the ventral tegmental area and adjacent regions: a combined fluorescent retrograde tracer and immunofluorescence study in the rat. Brain Res. Bull. 9, 321–353 (1982).

    Article  CAS  Google Scholar 

  13. Phillipson, O.T. & Pycock, C.J. Dopamine neurons of the ventral tegmentum project to both medial and lateral habenula. Some implications for Habenular function. Exp. Brain Res. 45, 89–94 (1982).

    CAS  PubMed  Google Scholar 

  14. Skagerberg, G., Lindvall, O. & Björklund, A. Origin, course and termination of the mesohabenular dopamine pathway in the rat. Brain Res. 307, 99–108 (1984).

    Article  CAS  Google Scholar 

  15. Gruber, C. et al. Dopaminergic projections from the VTA substantially contribute to the mesohabenular pathway in the rat. Neurosci. Lett. 427, 165–170 (2007).

    Article  CAS  Google Scholar 

  16. Hnasko, T.S. et al. Ventral tegmental area glutamate neurons: electrophysiological properties and projections. J. Neurosci. 32, 15076–15085 (2012).

    Article  CAS  Google Scholar 

  17. Taylor, S.R. et al. GABAergic and glutamatergic efferents of the mouse ventral tegmental area. J. Comp. Neurol. 522, 3308–3334 (2014).

    Article  CAS  Google Scholar 

  18. Yamaguchi, T. et al. Mesocorticolimbic glutamatergic pathway. J. Neurosci. 31, 8476–8490 (2011).

    Article  CAS  Google Scholar 

  19. Peters, A. & Palay, S.L. The morphology of synapses. J. Neurocytol. 25, 687–700 (1996).

    Article  CAS  Google Scholar 

  20. Peters, A., Palay, S. & Webster, H.D.F. The Fine Structure of the Nervous System (Oxford Univ. Press, New York, 1991).

  21. Boulland, J.L. et al. Vesicular glutamate and GABA transporters sort to distinct sets of vesicles in a population of presynaptic terminals. Cereb. Cortex 19, 241–248 (2009).

    Article  Google Scholar 

  22. Foss, S.M. et al. Multiple dileucine-like motifs direct VGLUT1 trafficking. J. Neurosci. 33, 10647–10660 (2013).

    Article  CAS  Google Scholar 

  23. Petreanu, L., Mao, T., Sternson, S.M. & Svoboda, K. The subcellular organization of neocortical excitatory connections. Nature 457, 1142–1145 (2009).

    Article  CAS  Google Scholar 

  24. Cruikshank, S.J., Urabe, H., Nurmikko, A.V. & Connors, B.W. Pathway-specific feedforward circuits between thalamus and neocortex revealed by selective optical stimulation of axons. Neuron 65, 230–245 (2010).

    Article  CAS  Google Scholar 

  25. Tritsch, N.X., Ding, J.B. & Sabatini, B.L. Dopaminergic neurons inhibit striatal output through non-canonical release of GABA. Nature 490, 262–266 (2012).

    Article  CAS  Google Scholar 

  26. Münster-Wandowski, A., Gómez-Lira, G. & Gutiérrez, R. Mixed neurotransmission in the hippocampal mossy fibers. Front. Cell. Neurosci. 7, 10.3389/fncel.2013.00210 (2013).

  27. Cohen, J.Y. et al. Neuron-type-specific signals for reward and punishment in the ventral tegmental area. Nature 482, 85–88 (2012).

    Article  CAS  Google Scholar 

  28. Tan, K.R. et al. GABA neurons of the VTA drive conditioned place aversion. Neuron 73, 1173–1183 (2012).

    Article  CAS  Google Scholar 

  29. Johnston, G.A.R. Advantages of an antagonist: bicuculline and other GABA antagonists. Br. J. Pharmacol. 169, 328–336 (2013).

    Article  CAS  Google Scholar 

  30. Morales, M. & Root, D.H. Glutamate neurons within the midbrain dopamine regions. Neuroscience 282C, 60–68 (2014).

    Article  Google Scholar 

  31. Sulzer, D. et al. Dopamine neurons make glutamatergic synapses in vitro. J. Neurosci. 18, 4588–4602 (1998).

    Article  CAS  Google Scholar 

  32. Dal Bo, G. et al. Dopamine neurons in culture express VGLUT2 explaining their capacity to release glutamate at synapses in addition to dopamine. J. Neurochem. 88, 1398–1405 (2004).

    Article  CAS  Google Scholar 

  33. Li, X. et al. Heterogeneous composition of dopamine neurons of the rat A10 region: molecular evidence for diverse signaling properties. Brain Struct. Funct. 218, 1159–1176 (2013).

    Article  CAS  Google Scholar 

  34. Weiss, T. & Veh, R.W. Morphological and electrophysiological characteristics of neurons within identified subnuclei of the lateral habenula in rat brain slices. Neuroscience 172, 74–93 (2011).

    Article  CAS  Google Scholar 

  35. Maroteaux, M. & Mameli, M. Cocaine evokes projection-specific synaptic plasticity of lateral habenula neurons. J. Neurosci. 32, 12641–12646 (2012).

    Article  CAS  Google Scholar 

  36. Shabel, S.J. et al. Input to the lateral habenula from the basal ganglia is excitatory, aversive, and suppressed by serotonin. Neuron 74, 475–481 (2012).

    Article  CAS  Google Scholar 

  37. Tye, K.M. et al. Dopamine neurons modulate neural encoding and expression of depression-related behaviour. Nature 493, 537–541 (2013).

    Article  CAS  Google Scholar 

  38. Chaudhury, D. et al. Rapid regulation of depression-related behaviours by control of midbrain dopamine neurons. Nature 493, 532–536 (2013).

    Article  CAS  Google Scholar 

  39. Nair, S.G., Strand, N.S. & Neumaier, J.F. DREADDing the lateral habenula: a review of methodological approaches for studying lateral habenula function. Brain Res. 1511, 93–101 (2013).

    Article  CAS  Google Scholar 

  40. Yamaguchi, T., Sheen, W. & Morales, M. Glutamatergic neurons are present in the rat ventral tegmental area. Eur. J. Neurosci. 25, 106–118 (2007).

    Article  Google Scholar 

  41. Tagliaferro, P. & Morales, M. Synapses between corticotropin-releasing factor-containing axon terminals and dopaminergic neurons in the ventral tegmental area are predominantly glutamatergic. J. Comp. Neurol. 506, 616–626 (2008).

    Article  CAS  Google Scholar 

  42. Miyazaki, T., Fukaya, M., Shimizu, H. & Watanabe, M. Subtype switching of vesicular glutamate transporters at parallel fibre-Purkinjec cell synapses in developing mouse cerebellum. Eur. J. Neurosci. 17, 2563–2572 (2003).

    Article  Google Scholar 

  43. Watanabe, M. et al. Selective scarcity of NMDA receptor channel subunits in the stratum lucidum (mossy fibre-recipient layer) of the mouse hippocampal CA3 subfield. Eur. J. Neurosci. 10, 478–487 (1998).

    Article  CAS  Google Scholar 

  44. Ichikawa, R. et al. Developmental switching of perisomatic innervation from climbing fibers to basket cell fibers in cerebellar Purkinje cells. J. Neurosci. 31, 16916–16927 (2011).

    Article  CAS  Google Scholar 

  45. Dobi, A., Margolis, E.B., Wang, H.L., Harvey, B.K. & Morales, M. Glutamatergic and nonglutamatergic neurons of the ventral tegmental area establish local synaptic contacts with dopaminergic and nondopaminergic neurons. J. Neurosci. 30, 218–229 (2010).

    Article  CAS  Google Scholar 

  46. Piñol, R.A., Bateman, R. & Mendelowitz, D. Optogenetic approaches to characterize the long-range synaptic pathways from the hypothalamus to brain stem autonomic nuclei. J. Neurosci. Methods 210, 238–246 (2012).

    Article  Google Scholar 

  47. Cardin, J.A. et al. Targeted optogenetic stimulation and recording of neurons in vivo using cell-type-specific expression of channelrhodopsin-2. Nat. Protoc. 5, 247–254 (2010).

    Article  CAS  Google Scholar 

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We thank R. Wise, J. Qi and J. Aceves for comments and J. Qi for assistance with viral injections used in ultrastructural experiments. Viruses were packaged by the NIDA IRP Optogenetics and Transgenic Technology Core. The Intramural Research Program of the National Institute on Drug Abuse, US National Institutes of Health (IRP/NIDA/NIH) supported this work.

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Authors and Affiliations



M.M., D.H.R. and C.A.M.-A. conceived this project. H.-L.W. and D.H.R. performed retrograde tract tracing and in situ hybridization experiments. Cellular characterization and analysis were done by M.M., H.-L.W., C.A.M.-A. and D.H.R. S.Z. performed confocal and electron microscopy experiments, the result of which were analyzed by M.M. and S.Z. C.R.L. and A.F.H. designed the whole-cell electrophysiological experiments. A.F.H. performed these experiments and A.F.H. and C.R.L. analyzed them. C.A.M.-A. and D.H.R. performed and analyzed in vivo electrophysiological recording experiments. M.M., C.A.M.-A. and D.H.R. wrote the manuscript with the contribution of all authors.

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Correspondence to Marisela Morales.

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The authors declare no competing financial interests.

Integrated supplementary information

Supplementary Figure 1 Most mesohabenular neurons are VGluT2+.

(a) Representative FluoroGold (FG) injection site within the LHb. MHb - medial habenula. (b) Outlines of injection sites corresponding to 5 rats. Numbers refer to bregma level. Green = rat 1, purple = rat 2, blue = rat 3, orange = rat 4, red = rat 5. (c,d) VTA coronal section showing FG-labeled neurons (c, brown neurons under brightfield) and TH immunolabeled neurons (d, green fluorescence). (e-i) Higher magnification of boxed area in c. Mesohabenular neurons analyzed for VGluT2 mRNA and TH-immunofluorescent expression are indicated by different outlines: VGluT2+ TH expression (solid green), VGluT2+ TH+ dual expression (dotted green), or lack of both VGluT2 and TH expression (solid white). The majority of FG-labeled mesohabenular neurons (white in e, brown in g) lacks TH (green in f), but expresses VGluT2+ mRNA (clusters of green grains in h, clusters of white grains in i). The second largest population of FG-labeled mesohabenular neurons co-expresses TH immunofluorescence and VGluT2 mRNA. (j) Frequency of mesohabenular neurons expressing VGluT2 mRNA or TH immunoreactivity (mean ± s.e.m). FG-VTA cell counting was made in 9 or 10 sections, each from rats #1, #2, and #3 (n = 3 rats), between bregma –4.9 mm and –6.1 mm.

Supplementary Figure 2 Most mesohabenular neurons are GAD+.

(a,b) VTA coronal section showing FG-labeled neurons (a, brown neurons under brightfield) and GAD-expressing neurons (b, GAD mRNA expression; clusters of green grains). (c–e, f–h). Higher magnification of boxed areas in a. Mesohabenular neurons analyzed for GAD mRNA expression are indicated by different outlines: GAD expressing neurons [GAD+, solid red] and neurons lacking GAD expression [GAD, solid white]. The majority of FG-labeled mesohabenular neurons (brown in c and f) express GAD mRNA (clusters of green grains in d and g, clusters of white grains in e and h). (i). Frequency of mesohabenular neurons expressing GAD mRNA (mean ± s.e.m). FG-VTA cell counting was made in 10 sections, each from rats #2, #3, and #4 (n = 3 rats), between bregma –4.9 mm and –6.1 mm.

Supplementary Figure 3 Minor mesohabenular phenotypes projecting to LHb.

(a) VTA coronal section from a rat injected with FG (see in Figure 1b,c). TH-immunofluorescence (green). Dotted yellow lines indicate VTA subregional boundaries. (bg, hm, and ns). Higher power of boxed areas in a. Distinct phenotypes of FG-labeled mesohabenular neurons are indicated by different outlines: VGluT2+ GAD+ TH (solid pink), VGluT2+ GAD TH+ (dotted green), VGluT2 GAD+ TH (solid red), VGluT2 GAD+ TH+ (dotted brown). In each panel, the most encountered mesohabenular neuronal phenotype, VGluT2+ GAD+ TH, is displayed. (bg) A FG-labeled VGluT2+ GAD TH+ mesohabenular neuron (white in b, brown in e) expresses TH (green in c), lacks GAD mRNA (purple in d), but expresses VGluT2 mRNA (clusters of green grains in f, clusters of white grains in g). (hm) A FG-labeled VGluT2 GAD+ TH mesohabenular neuron (white in h, brown in k) lacks TH (green in i), expresses GAD mRNA (purple in j) and lacks VGluT2 mRNA (clusters of green grains in l, clusters of white grains in m). (ns) A FG-labeled VGluT2 GAD+ TH+ mesohabenular neuron (white in n, brown in q) expresses TH (green in o), expresses GAD mRNA (purple in p) but lacks VGluT2 mRNA (clusters of green grains in r, clusters of white grains in s).

Supplementary Figure 4 Phenotype map of mesohabenular neurons in four anteroposterior planes.

Circles represent one mesohabenular neuron from rats #2, #3, and #5 within sections between bregma –5.16 mm and –5.52 mm. Mesohabenular neurons were typically intermingled within a specific location of the anteromedial VTA (medial to the fasciculus retroflexus and around the borders of the rostral linear, interfascicular, medial paranigral, and medial parabrachial pigmented nuclei). (ad) Left: Major phenotypes of mesohabenular neurons. The most frequently encountered mesohabenular neuronal phenotype dually co-expressed VGluT2 mRNA and GAD mRNA without TH immunoreactivity (pink). The second most frequently encountered mesohabenular neuronal phenotype triple co-expresses VGluT2 mRNA, GAD mRNA and TH immunoreactivity (purple). Right: Minor phenotypes of mesohabenular neurons. Small numbers of FG-labeled mesohabenular neurons express single VGluT2 mRNA (light green), dual VGluT2 and TH signals (dark green), single GAD mRNA (light red), dual GAD and TH signals (brown), single TH (blue), or were undetected with VGluT2, GAD, and TH (white). PIF = parainterfascicular nucleus; mp = mammillary peduncle; mtg = mammillotegmental tract.

Supplementary Figure 5 Phenotypes of axon terminals in rat lateral habenula.

Lateral habenula samples were processed for detection of VGluT2 by immunoperoxidase labeling (scattered dark material) and for detection of VGaT by immunogold (punctate dark circles, blue arrowhead in b). Experiments were repeated successfully three times. (a) At low magnification, three phenotypes of axon terminals (AT) are seen in the LHb. (b) A single AT co-expressing VGluT2 and VGaT forming both asymmetric (black arrow) and symmetric synapses (blue arrow) with dendrites. (c) AT expressing only VGluT2 without VGaT forming an asymmetric synapse (black arrow). (d) AT expressing only VGaT without VGluT2 forming two symmetric synapses (blue arrows). Axon terminals are outlined by pink, green, or blue dots. LHb dendrites are outlined by white dots. (e) Frequency of lateral habenula axon terminal phenotypes expressing VGluT2 alone, VGaT alone, or co-expressing VGluT2 and VGaT (mean ± s.e.m). Axon terminal counting was made from four Sprague-Dawley rats between bregma –3.0 mm and –4.2 mm.

Supplementary Figure 6 A single presynaptic mesohabenular terminal containing VGluT2 establishes multiple synapses.

(ad) Four sequential serial sections of LHb from a VGluT2::Cre mouse expressing Cre-inducible mCherry following injection of an AAV-DIO-ChR2-mCherry vector in VTA. Detection of mCherry by immunoperoxidase labeling (scattered dark material) and detection of VGluT2 by immunogold (black dots indicated by black arrowhead in a). AT co-expressing mCherry and VGluT2 that establishes multiple asymmetric synapses (black arrows) with dendrite (De) or spine (sp). Mesohabenular axon terminals are outlined by green dots. LHb dendrites or spines are outlined by white dots. Experiments were repeated successfully three times.

Supplementary Figure 7 Single presynaptic mesohabenular terminals dually establish asymmetric and symmetric synapses.

(af) Six sequential serial sections in LHb from a VGluT2::Cre mouse delivered with a Cre-inducible AAV-DIO-ChR2-mCherry vector into the VTA. Tissue were processed for detection of mCherry by immunoperoxidase labeling (scattered dark material) and for detection of VGaT by immunogold (punctate dark circles, blue arrowhead in a). This axon terminal (AT) co-expresses mCherry and VGaT, establishes dual asymmetric (black arrows) and symmetric synapses (blue arrows) with dendrites (De), and puncta adhaerentia (white arrow). Mesohabenular axon terminals are outlined by red dots. LHb dendrites are outlined by white dots. Experiments were repeated successfully three times.

Supplementary Figure 8 Monosynaptic release of glutamate and GABA from mesohabenular terminals.

(a) Individual trials obtained from a VGluT2-ChR2 mouse. Upper traces show light-evoked inward currents obtained at –70 mV, lower traces show light-evoked outward currents obtained at –50 mV. Individual responses are shown in gray, averaged responses are shown in color. Dashed line indicates the onset of the laser pulse (5 ms). (b) Latencies and jitter (mean ± s.e.m) for all recorded neurons from rats and mice (n = 23 neurons). No significant differences in latency (paired t-test, t(22) = 1.733, p = 0.0971) or jitter were observed (paired t-test, t(22) = 0.3061, p = 0.7624). (c) Traces and time course from a single LHb neuron from a rat injected with a AAV-CAMKIIα-ChR2-eYFP vector in the VTA. Light-evoked inward and outward currents were observed at –70 mV and –50 mV, respectively. Application of TTX (1µM) eliminated both currents; subsequent application of 4-AP (200 µM) restored both inward and outward responses. (d) Summary of effects of TTX and TTX/4AP on percent of light-evoked responses. Left: CAMKIIα-ChR2 rats (F(1,6) = 46.2, p = 0.0005; *p = 0.0231, **p = 0.0013 versus TTX, two-way repeated measures ANOVA and Sidak’s multiple comparison test, n = 6 from 3 rats). Right: VGluT2-ChR2 mice (F(1,8) = 43.54, p = 0.0002; **p = 0.0014, ***p=0.00095 versus TTX, two-way repeated measures ANOVA and Sidak’s multiple comparison test, n = 8 from 3 mice). Data are mean ± s.e.m.

Supplementary Figure 9 Single 10-ms light stimulation of VTA VGluT2-ChR2 neurons evokes burst firing.

(a) Delivery of a Cre-inducible AAV-DIO-ChR2-eYFP vector into the VTA of VGluT2::Cre mice. Transfected VTA VGluT2 neurons and processes expressing ChR2-eYFP are indicated by dark blue signal. (b) VTA VGluT2-ChR2 neurons were recorded in vivo. A glass electrode was glued to an optical fiber and single 1 or 10 ms light pulses (473 nm) were delivered every 2 sec. c, Light-evoked action potentials were detected by the peak of their rising waveforms. (df) Light-evoked responses of VTA VGluT2-ChR2 neurons. Neurons responding to 1 ms light pulse with a firing fidelity over 90% were considered to be VGluT2-ChR2 neurons. (d) Top: Representative VTA VGluT2-ChR2 neuron exhibiting one or two spikes following each 1 ms light pulse. Bottom: The same neuron showed burst firing (3-6 spikes) in response to light pulses of 10 ms duration. (e) Single 1 or 10 ms light pulses evoked spiking with high fidelity in VTA VGluT2-ChR2 neurons. (f) Single 10 ms light stimulation reliably evoked burst firing in VTA VGluT2-ChR2 neurons (y-axis mean number of spikes).

Supplementary Figure 10 Localization of recorded LHb neurons in mice and rats.

(a) LHb neurons responding to light stimulation of mesohabenular ChR2-eYFP fibers from VGluT2-ChR2 mice or VGaT-ChR2 mice are represented as circles or triangles, respectively. Initially inhibited neurons are shown in red and initially excited neurons are shown in black. (b) LHb optical activation of mesohabenular fibers in CaMKIIα-ChR2 rats initially inhibited some LHb neurons (red squares), and initially excited others (black squares).

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Root, D., Mejias-Aponte, C., Zhang, S. et al. Single rodent mesohabenular axons release glutamate and GABA. Nat Neurosci 17, 1543–1551 (2014).

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