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number of different receptors are distributed in glutamatergic neurons of the lateral habenula (LHb). These glutamatergic neurons are involved in different neural pathways, which may identify how the LHb regulates various physiological functions. However, the role of dopamine D1 receptor (D1R)-expressing habenular neurons projecting to the ventral tegmental area (VTA) (LHbD1R–VTA) remains not well understood. In the current study, to determine the activity of D1R-expressing neurons in LHb, D1R-Cre mice were used to establish the chronic restraint stress (CRS) depression model. Adeno-associated virus was injected into bilateral LHb in D1R-Cre mice to examine whether optogenetic activation of the LHb D1R-expressing neurons and their projections could induce depression-like behavior. Optical fibers were implanted in the LHb and VTA, respectively. To investigate whether optogenetic inhibition of the LHbD1R–VTA circuit could produce antidepressant-like effects, the adeno-associated virus was injected into the bilateral LHb in the D1R-Cre CRS model, and optical fibers were implanted in the bilateral VTA. The D1R-expressing neuronal activity in the LHb was increased in the CRS depression model. Optogenetic activation of the D1R-expressing neurons in LHb induced behavioral despair and anhedonia, which could also be induced by activation of the LHbD1R–VTA axons. Conversely, optogenetic inhibition of the LHbD1R–VTA circuit improved behavioral despair and anhedonia in the CRS depression model. D1R-expressing glutamatergic neurons in the LHb and their projections to the VTA are involved in the occurrence and regulation of depressive-like behavior.",{"EN":381,"VI":382},"Optogenetic activation of the lateral habenulaD1R–ventral tegmental area circuit induces depression-like behavior in mice","Kích hoạt quang di truyền mạch habenulaD1R bên–vùng trần bụng gây hành vi giống trầm cảm ở chuột nhắt",{"VOID":384},"Abi-Dargham A, Mawlawi O, Lombardo I, Gil R, Martinez D, Huang Y, Hwang DR, Keilp J, Kochan L, Van Heertum R, Gorman JM, Laruelle M (2002) Prefrontal dopamine d1 receptors and working memory in schizophrenia. J Neurosci 22:3708–3719\nAizawa H, Kobayashi M, Tanaka S, Fukai T, Okamoto H (2012) Molecular characterization of the subnuclei in rat habenula. J Comp Neurol 520:4051–4066\nBaño-Otálora B, Piggins HD (2017) Contributions of the lateral habenula to circadian timekeeping. 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Science 341:1016–1020\nLiu H, Rastogi A, Narain P, Xu Q, Sabanovic M, Alhammadi AD, Guo L, Cao JL, Zhang H, Aqel H, Mlambo V, Rezgui R, Radwan B, Chaudhury D (2021) Blunted diurnal firing in lateral habenula projections to dorsal raphe nucleus and delayed photoentrainment in stress-susceptible mice. PLoS Biol 19:e3000709\nMa Z, Zhong Y, Hines CS, Wu Y, Li Y, Pang M, Li J, Wang C, Fox PT, Zhang N, Wang C (2020) Identifying generalized anxiety disorder using resting state habenular circuitry. Brain Imaging Behav 14:1406–1418\nMcNab F, Varrone A, Farde L, Jucaite A, Bystritsky P, Forssberg H, Klingberg T (2009) Changes in cortical dopamine d1 receptor binding associated with cognitive training. Science 323:800–802\nMorales M, Root DH (2014) Glutamate neurons within the midbrain dopamine regions. Neuroscience 282:60–68\nPark H, Rhee J, Park K, Han JS, Malinow R, Chung C (2017) Exposure to stressors facilitates long-term synaptic potentiation in the lateral habenula. 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Nat Commun 13:4039\nTye KM, Mirzabekov JJ, Warden MR, Ferenczi EA, Tsai HC, Finkelstein J, Kim SY, Adhikari A, Thompson KR, Andalman AS, Gunaydin LA, Witten IB, Deisseroth K (2013) Dopamine neurons modulate neural encoding and expression of depression-related behaviour. Nature 493:537–541\nWallace ML, Huang KW, Hochbaum D, Hyun M, Radeljic G, Sabatini BL (2020) Anatomical and single-cell transcriptional profiling of the murine habenular complex. Elife 9:e51271\nWang D, Li Y, Feng Q, Guo Q, Zhou J, Luo M (2017) Learning shapes the aversion and reward responses of lateral habenula neurons. Elife 6:e23045\nWinter C, von Rumohr A, Mundt A, Petrus D, Klein J, Lee T, Morgenstern R, Kupsch A, Juckel G (2007) Lesions of dopaminergic neurons in the substantia nigra pars compacta and in the ventral tegmental area enhance depressive-like behavior in rats. Behav Brain Res 184:133–141\nWirtshafter D, Krebs JC (1997) Interactive effects of stimulation of d1 and d2 dopamine receptors on Fos expression in the lateral habenula. Brain Res 750:245–250\nYang Y, Wang H, Hu J, Hu H (2018) Lateral habenula in the pathophysiology of depression. Curr Opin Neurobiol 48:90–96\nZhao H, Zhang BL, Yang SJ, Rusak B (2015) The role of lateral habenula-dorsal raphe nucleus circuits in higher brain functions and psychiatric illness. Behav Brain Res 277:89–98\nZhou L, Liu MZ, Li Q, Deng J, Mu D, Sun YG (2017) Organization of functional long-range circuits controlling the activity of serotonergic neurons in the dorsal raphe nucleus. 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9 Patienten, die wegen eines Alkoholdelirs zur Aufnahme kamen, wurden die Parameter des Säure-Basen-Haushaltes, Lactat, Pyruvat und Elektrolyte in Liquor cerebrospinalis und Blut 1. im Vollbild, 2. im Verlauf von 3 Tagen und 3. nach abgeklungenem Delirium tremens bestimmt. Der deutliche Lactat-, Pyruvat-Anstieg bzw. der erhöhte Lactat-Pyruvat-Quotient im Liquor cerebrospinalis weisen auf eine Störung der energieliefernden Prozesse des Gehirnparenchyms hin. Die metabolische Liquoracidose spiegelt hierbei die zugrundeliegende cerebrale Gewebshypoxie wider. Als Ursache einer solchen wird eine cerebrale Durchblutungsminderung im Delir, etwa im Rahmen eines sich entwickelnden Ödems, diskutiert. Die Liquoracidose löst eine Steigerung des Atemantriebes aus und läßt so eine respiratorische Blutalkalose entstehen. Der pCO2-Abfall im Blut beeinflußt rückläufig den Säure-Basen-Zustand des Liquor cerebrospinalis. — Die klinische Schwere des Krankheitsbildes geht mit der Schwere der Stoffwechselveränderungen im Liquor cerebrospinalis parallel, die so als Maß für die cerebrale Gewebsstörung aufzufassen sind. Verlaufsuntersuchungen lassen dies besonders deutlich erkennen und ermöglichen eine prognostische Aussage. Das gegensätzliche Verhalten des Kalium im Liquor cerebrospinalis und Blut findet in Beziehung zum Säure-Basen-Haushalt seine Erklärung. Schließlich wird auch auf korrelationsstatistisch faßbare Zusammenhänge eingegangen.",{"EN":609},"Entgleisung des Säure-Basen-Gleichgewichtes im Liquor Cerebrospinalis beim Delirium Tremens",{"VOID":611},"[\"12559702285549512237\"]",{"VOID":613},"Allgén, L. G., Izikowitz, S., Ordelli, J. B., Salum, J.: Clinical and chemical studies in delirium tremens and predelirious states. Nord. Med. 58, 1921 (1957).\nAstrup, P.: A simple electrometric technique for the determination of carbon dioxide tension in blood and plasma. Scand. J. Lab. Invest. 8, 33–43 (1956).\nBauer, H.: Die Cerebrospinalflüssigkeit. Internist 2, 85–94 (1961).\nBischof, H. L.: Zur Pathogenese des Alkoholdelirs. Nervenarzt 40, 318–325 (1969).\nBostroem, A.: Über Leberfunktionsstörungen bei symptomatischen Psychosen, insbesondere bei Alkoholdelirien. Z. ges. Neurol. Psychiat. 68, 48 (1921).\nBüchler, P.: Leberfunktionsstörungen bei Geistes- und Nervenkrankheiten. Arch. Psychiat. Nervenkr. 73, 610 (1925).\nBühlmann, A. A., Rossier, H. P.: Klinische Pathophysiologie der Atmung, 1. Aufl. Berlin-Heidelberg-New York: Springer 1970.\nBumke, O., Kant, F.: Rausch und Genußgifte. In: Bumke, O., O. Foerster (Hrsg.): Handbuch der Neurologie, Bd. XIII, S. 828. Berlin: Springer 1936.\nDavson, H.: Physiology of the cerebrospinalfluid. London: Churchill 1967.\nFahr, H.: zitiert in: Hallen, O., B. Neundörfer u. M. v. Rad: Neurologische Erkrankungen bei chronischen Alkoholismus. Nervenarzt 42, 57–65 (1971).\nFeuerlein, W.: Neuere Ergebnisse der Alkoholdelir-Forschung. Nervenarzt 38, 492–500 (1967).\nGänshirt, H.: Der Sauerstoffdruck der Cerebrospinalflüssigkeit des Menschen. Klin. Wschr. 46, 771–779 (1968).\nHallen, O., Neundörfer, B., v. Rad, M.: Neurologische Erkrankungen bei chronischem Alkoholismus. Nervenarzt 42, 57–65 (1971).\nIrsigler, K., Kryspin-Exner, K., Mildschuh, W., Pointner, H., Schmidt, P.: Lebermorphologie und Leberfunktion. Dtsch. med. Wschr. 96, 9–12 (1971).\nKaasik, A. E., Zupping, R.: Correlations between Brain Gas Exchange and CSF Acis-Base-Status in Patients with Cerebral Hemorrhage. In: Cerebral Blood Flow. M. Brock, C. Fieschi, D. H. Ingvar, N. A. Lassen, K. Schürmann, eds. Berlin-Heidelberg-New York: Springer 1969.\nKalant, H.: zit. in: Bischof, H. L.: Zur Pathogenese des Alkoholdelirs. Nervenarzt 40, 318–325 (1969).\nKienle, G.: Methodische Hinweise für die Untersuchungen des Säure-Basen-Haushaltes im Liquor cerebrospinalis. Klin. Wschr. 47, 545–549 (1969a).\n—: The Acid-Base-Equilibrium of the CSF and the Respiration in Cerebral Vascular Diseases. In: Cerebral Blood Flow. M. Brock, C. Fieschi, D. H. Ingvar, N. A. Lassen, K. Schürmann, eds. Berlin-Heidelberg-New York: Springer 1969b.\nKrück, F.: Säure-Basen-Haushalt. In: Siegenthaler, W.: Klinische Pathophysiologie. Stuttgart: Thieme 1970.\nLassen, N. A.: The luxury perfusion syndrome of the brain. Lancet 1966 II, 1113.\nLeusen, J. R.: Chemosensitivity of the respiratory center. Influence of changes in the H+ and total buffer concentration in the cerebral ventricles on respiration. Amer. J. Physiol. 176, 45–51 (1954).\nLoeschke, H. H.: A concept of the role of intracranial chemosensitivity in respiratory control. In: Cerebrospinal fluid and the regulation of ventilation, pp. 183 to 207. C. M. Brooks, F. F. Kao and B. B. Lloyd, eds. Oxford: Blackwell 1965.\nMartin, H. E., McCuskey, Ch., Tupikova, N.: Electrolyte disturbance in acute alcoholism with particular reference to magnesium. Amer. J. clin. Nutr. 7, 191 (1959).\nMitchell, R. A., Loeschke, H. H., Severinghaus, J. W., Richardson, B. W., Massion, W. H.: Region of the respiratory chemosensitivity on the medulla. Ann. N. Y. Acad. 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wird eine sporadische Encephalitis bei einem 32jährigen Mann mitgeteilt, die im Anschluß an eine Angina innerhalb von 8 Tagen zum Tode führte. Neuropathologisch fand sich ein ausgeprägter intracerebraler Entzündungsprozeß, der sich in diffus-fleckförmiger, panencephaler Ausbreitung über die Großhirnrinde und das Mark unter Beteiligung der Stammganglien erstreckt, nach occipital zu an Intensität abnimmt und die Mittelhirnregion nur schwach einbezieht, während er im Kleinhirn, Brücke und Medulla oblongata örtlich akzentuiert ist. Die besondere Eigenart des Falles besteht in einer Kombination sehr vielseitiger, gliöser Reaktionsweisen sowie der Merkmale einer Virus- und einer parainfektiösen Encephalitis und wird deshalb zu der von Jacob als „polioleukencephale Kombinationsencephalitiden“ bezeichneten Gruppe gerechnet.",{"EN":793},"Über eine atypische Kombinationsencephalitis",{"VOID":795},"[\"8704594871086302399\"]",{"VOID":797},"Amler, G., u. H. J. Colmant: Beitrag zur „einheimischen sporadischen Panencephalitis“ (Pette-Döring). Arch. Psychiat. Nervenkr. 193, 161 (1955).\nBieling, R., u. G. Poetschke: Allgemeine Pathogenese der Viruskrankheiten des Zentralnervensystems. In Hdb. d. spez. pathol. Anat. u. Histol. (Lubarsch- Henke-Rössle), Bd.XIII, Nervensystem, 2.Teil, Bandteil A, S. 101. Berlin, Göttingen, Heidelberg: Springer 1958.\nBogaert, L. van: Postinfektiöse Encephalomyelitis und Multiple Sklerose. J. Neuropath. exp. Neurol. 9, 219 (1950).\n—: Une Encephalomyélite du type périveineuse au cours d'une gingivostomatite aigue infectieuse. Rev. neurol. 95, 431 (1956).\n—: Encéphalites d'origine inconnue. In Hdb. d. spez. pathol. Anat. u. Histol. (Lubarsch-Henke-Rössle), Bd. XIII, Nervensystem, 2. Teil, Bandteil A, S. 394. Berlin, Göttingen, Heidelberg: Springer 1958.\n—, et J. Radermecker: Neuropathologie de quelques encéphalites humaines à virus. Rev. neurol. 108, 361 (1963).\nBonhoff, G.: Über atypische Encephalitisfälle mit Gliaknötchenbildung. Arch. Psychiat. Nervenkr. 181, 421 (1948).\nDöring, G.: Zur Pathologie und Klinik der Entmarkungsencephalomyelitis. Dtsch. Z. Nervenheilk. 152, 73 (1941).\nDraganesco, St., et A. Petresco: L'encéphalite periveneuse gliogène démyelinisante primitive. Acta neurol. belg. 58, 8 (1958).\nEicke, W. J., u. W. Ziegler: Ein Beitrag zur Frage der atypischen Encephalitis. Nervenarzt 1950, 312.\nGrinschgl, G.: Zur Neuropathologie der zentraleuropäischen Encephalomyelitis unter Berücksichtigung der Differentialdiagnose zu den Virusmeningoencephalomyelitiden anderer Ätiologie. Wien. klin. Wschr. 69, 761 (1957).\nHöra, J.: Encephalitis japonica. Beitr. path. Anat. 103, 280 (1939).\nJacob, H.: Die postinfektiösen sekundären Encephalitiden und Encephalopathien. Fortschr. Neurol. Psychiat. 24, 244 (1956).\n—: Masernencephalitis-Masernencephalopathie. Fortschr. Neurol. Psychiat. 24, 635 (1956).\n—: Postvaccinale Encephalitis und Encephalopathie. Fortschr. Neurol. Psychiat. 24, 651 (1956).\n—: Zur klinisch-neuropathologischen Differentialdiagnose zwischen parainfektiösen (und postvaccinalen) Encephalitiden und akuten sporadischen Panleukoencephalitiden. Arch. Psychiat. Nervenkr. 197, 507 (1958).\n—: Das Zentralnervensystem bei Infektionen, Intoxikationen und anderen Allgemein- und Organerkrankungen. Allgemeines über seine Anteilnahme mit degenerativen Veränderungen, entzündlichen und zirkulatorischen Reaktionen. Hdb. d. spez. pathol. Anat. u. Histol. (Lubarsch-Henke-Rössle), Bd. XIII, Nervensystem, 2. Teil, Bandteil A, S. 688. Berlin, Göttingen, Heidelberg: Springer 1958.\n—: Sporadische atypische, „primäre“ Encephalitiden, Encephalitis japonica B und parainfektiöse Encephalitiden. Psychiat. Neurol. jap. 61, 311 (1959).\n—: Neuropathologie der Viruserkrankungen des Zentralnervensystems. Dtsch. Z. Nervenheilk. 182, 472 (1961).\n—: Postvaccinal Encephalitis. In: Encephalitides. Proceedings of a Symposium on the Neuropathology, Elektroencephalography and Biochemistry of Encephalitides, S. 100. Amsterdam, London, New York, Princeton: Elsevier Publishing Company 1961.\nJacob, H.: Review of the Pathology of the Enoephalitic-Encephalopathic Processes. In: Encephalitides. Proceedings of a Symposium on the Neuropathology, Elektroencephalography and Biochemistry of Encephalitides, p. 702. Amsterdam, London, New York, Princeton: Elsevier Publishing Company 1961.\nJellinger, K., u. F. Seitelberger: „Encephalitis“ bei Grippe. Wien. med. Wschr. 109, 1 (1959).\nKersting, G.: Beitrag zur Frage der Panencephalitis. Dtsch. Z. Nervenheilk. 168, 464 (1952).\nKrücke, W.: Über eine besondere Form der spontanen Encephalitis. Nervenarzt 28, 289 (1957).\nKufs, H.: Atypische Encephalitis epidemica mit lyssaähnlichem Verlauf, starker Beteiligung des Großhirns und relativer Verschonung wichtiger praedilektiver Stellen im Zwischen- und Mittelhirn. Mschr. Psychiat. 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There is evidence that the allegiance of a researcher to a given school of thought may influence the results of studies comparing different psychotherapeutic techniques, thus colliding with the primary interest represented by the progress of science. Political commitment is also emerging as a source of conflicts of interests. Financial and non-financial conflicts of interests are widespread in psychiatric practice and research. They cannot be eradicated, but must be managed more effectively than is currently the case.",{"EN":1595},"Financial and non-financial conflicts of interests in psychiatry",{"VOID":1597},"[\"1609507283950182403\"]",{"VOID":1599},"Thompson DF (1993) Understanding financial conflicts of interest. N Engl J Med 329:573–576\nMaj M (2005) Conflicts of interests in psychiatric practice and research. Psychiatrie 3:138–140\nMaj M (2008) Non-financial conflicts of interests in psychiatric research and practice (editorial). Br J Psychiatry 193:91–92\nSen P, Gordon H, Adshead G, Irons A (2007) Ethical dilemmas in forensic psychiatry: two illustrative cases. J Med Ethics 33:337–341\nWarner TD, Gluck JP (2003) What do we really know about conflicts of interest in biomedical research? Psychopharmacology 171:36–46\nFava GA (2007) Financial conflicts of interest in psychiatry. World Psychiatry 6:19–24\nCialdini RB, Trost MR (1998) Influence, social norms, conformity, and compliance. In: Gilbert DT, Fiske ST, Lindzey G (eds) The handbook of social psychology, 4th edn. Oxford University Press, New York\nWazana A (2000) Physicians and the pharmaceutical industry. Is a gift ever just a gift? JAMA 283:373–380\nLexchin J, Bero LA, Djulbegovic B, Clarke O (2003) Pharmaceutical industry sponsorship and research outcome and quality: systematic review. BMJ 326:1167–1170\nHeres S, Davis J, Maino K, Jetzinger E, Kissling W, Leucht S (2006) Why olanzapine beats risperidone, risperidone beats quetiapine, and quetiapine beats olanzapine: an exploratory analysis of head-to-head comparison studies of second-generation antipsychotics. Am J Psychiatry 163:185–194\nPerlis RG, Perlis CS, Wu Y, Hwang C, Joseph M, Nierenberg AA (2005) Industry sponsorship and financial conflict of interest in the reporting of clinical trials in psychiatry. Am J Psychiatry 162:1957–1960\nSafer DJ (2002) Design and reporting modifications in industry-sponsored comparative psychopharmacology trials. J Nerv Ment Dis 190:583–592\nFava GA (2001) Conflict of interest and special interest groups. Psychother Psychosom 70:1–5\nChoudhry NK, Stelfox HT, Detsky AS (2002) Relationships between authors of clinical practice guidelines and the pharmaceutical industry. JAMA 287:612–617\nRelman AS (2001) Separating continuing medical education from pharmaceutical marketing. JAMA 285:2009–2012\nRoss JS, Lurie P, Wolfe SM (2000) Medical education services suppliers: a threat to physician education. Public Citizen’s Health Research Group, Washington, DC\nHussain A, Smith R (2001) Declaring financial competing interests: survey of five general medical journals. BMJ 323:263–264\nInternational Committee of Medical Journals Editors. Uniform requirements for manuscripts submitted to biomedical journals: writing and editing for biomedical publication. http:\u002F\u002Fwww.icmje.org\u002Findex.html\nFoster RS (2003) Conflicts of interest: recognition, disclosure, and management. J Am Coll Surg 196:505–517\nAmerican College of Surgeons (1987) Statements on principles. http:\u002F\u002Fwww.org\u002Ffellows_info\u002Fstatements\u002Fstonprin.html\nFrancis L (1996) IRBs and conflicts of interest. In: Spece RG, Shimm DS, Buchanan AE (eds) Conflicts of interest in clinical practice and research. Oxford University Press, New York\nWorld Health Organization (2006) International clinical trials registry platform. World Health Organization, Geneva\nWager E, Field EA, Grossman L (2003) Good publication practice for pharmaceutical companies. Curr Med Res Opin 19:149–154\nGoodwin G (2007) Conflicting interests and doing right. World Psychiatry 6:25–26\nVieta E (2007) Psychiatry: from interest in conflicts to conflicts of interest. World Psychiatry 6:27–29\nThase ME (2007) On the property of collaborations between academicians and the pharmaceutical industry: an alternate viewpoint. World Psychiatry 6:29–31\nPaul SM, Tohen M (2007) Conflicts of interests and the credibility of psychiatric research. World Psychiatry 6:33–34\nNierenberg AA (2007) A counter proposal to manage financial conflicts of interests in academic psychiatry. World Psychiatry 6:34–36\nRodwin MA (1993) Medicine, money, and morals: physicians’ conflicts of interest. Oxford University Press, New York\nLuborsky L, Diguer L, Seligman DA, Rosenthal R, Krause ED, Johnson S, Halperin G, Bishop M, Berman JS, Schweizer E (1999) The researcher’s own therapy allegiance: a “wild card” in comparisons of treatment efficacy. Clin Psychol Sci Pract 6:95–106\nPaley G, Shapiro DA (2002) Lessons from psychotherapy research for psychological interventions for people with schizophrenia. 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