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Via dopaminergica

Viae dopaminergicae vel itinera dopaminergica sive proiectiones dopaminergicae sunt cerebri greges fibrarum projectionis, quae neurotransmissorem dopaminum generant liberantque[1][2]. Viarum singulares neurones vocitantur neurona dopaminergica. Neuronis dopaminergicis sunt axona, quae proiectionum dopaminergicarum toto longitudine perveniunt. Perikarya cellularum generant enzyma, quae secundum axona transportata, in synapsibus chemicis neurotransmissorem synthesem biologicam dopamini perficiunt. Haec perikarya, ut cellularum substantiae nigrae partis compactae (SNc), colorationem obscuram pigmento melanino causa solent.

Viae cerebri dopaminergicae principales (caerulee)

Perbene itinera dopaminergica se habent functionibus multis, ut functionibus executivis, discere, remunerationibus, motivatione, gubernationibus endocrineis[3]. Suspicatur itinerum horum cum nucleis dysfunctiones cum morbis multis ut morbo Parkinsoniano[4], conturbatione hypercinetica cum attentionis defecto[5] (CHAD), dependentia[6], syndromate pedum inquietorum (SPI)[7] coniunctas esse.

Itinera singularia

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Itineris nomen Descriptio Res sociatae Mala sociata
Proiectiones
mesocorticolimbicae
Via
mesolimbica
 Iter mesolimbicum signa dopaminergica ab area tegmentali ventrali (ATV) mesencephali in striatum ventrale transmittit, ambos et nucleum accumbentem atque tuberculum olfactorium includens[8][9]. Praefixum "meso" verbi "mesolimbici" ad mesencephalon valet (seu "cerebrum medium"), quia Graecum μέσος medium significat.
Via
mesocorticalis
 Iter mesocorticale signa dopaminergica ab ATV in corticem praefrontalem transmittit. Praefixum "meso" "mesocorticalis" ad ATV mesencephali, at "corticale" ad cerebri cortices respicit.
Via nigrostriatalis
 Iter nigrostriatale signa dopaminergica ab substantia nigra parte compacta (SNc) in nucleum caudatum atque putamen transmittit. Substantia nigra in mesencephalo locata est, at et nucleus caudatus et putamen in striato dorsali locata sunt.
Via tuberoinfundibularis
 Iter tuberoinfundibulare signa dopaminergica ab nucleo arcuato (seu nc. infundibulari noto) hypothalami in glandulam pituitariam ope liberationis dopamini in eminentiam medianam et postea circulationem trans venas portales hypophysiales transmittit. Iter hoc secretionem varium hormontum gubernat, ut prolactini ex glandula pituitaria liberati. "Infundibularis" verbi "tuberoinfundibularis" ad infundibulum pediculum hypophysis respicit, ex quo glandula pituitaria emanat.
  • Itineris actio liberationem prolactini inhibet.
Proiectio hypothalamospinalis
 Iter hoc et trunci encephali et medullae spinalis retia neuralia locomotoria amovet.
  • Functio motoria
Via incertohypothalamica
 Iter hoc, ex zona incerta oriens, hypothalamum atque centra locomotoria trunci encephali amovet.
  • Actiones viscerales et sensorimotoriae

Itinera momenti maioris[8][9][10] (eadem ut supra descripta)

Mesocorticolimbica
Nigrostriatalis
Tuberoinfundibularis
Hypothalamospinalis
Incertohypothalamica

Aliae viae

Viae mesocorticalis et mesolimbica interdum communiter proiectio mesocorticolimbica, systema mesocorticolimbicum, sive iter mesocorticolimbicum nominantur[2][12].

Functiones

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Viae dopaminergicae, quarum proiectiones ab substantia nigra pars compacta et area tegmentali ventrali in striatum (i.e., itinera nigrostriatalia et mesolimbica) inveniuntur, vero una pars sequentiae multorum itinerum circulus gangliothalamocorticalis corticobasalis nominatae, formant[13][14] Iste classificationis methodus in multorum morborum mentis inquirendo adhibetur. Circuli antea dicti pars nigrostriatalis ex substantia nigra parte compacta consistit, initium et inhibentium et incitantium itinerum, quae ex striato in globum pallidum currunt, protractura adversus thalamum; aut currunt in nucleum subthalamicum, protractura adversus thalamus. Istius circuitus neurona dopaminergica phasium magnitudinem, numerum potentialium actionum icentium ope, responsum erroris remunerationis positivi, augent, quod est cum primum remuneratio vera remunerationi expectatae emineat. Neuronae haec minime incentium phases, praedictionis remunerationis negativae causa (minus remunerationis quam praedictum), minuunt. Hac de re hypothesis, plus enim serotonergica, quam dopaminergica neurona remunerationis spoliationem indicare, evolvebat. Dopaminergicorum quoque actionum phases, stimulis negativos eventus indicantibus, incrementum ostendunt, quamvis dopaminergicorum neuronorum stimulatio constanter praeferentiam loco condicionalem exorsa sit, ita ipsum momentum principale in stimulorum positivorum calculando indicans. Istis de investigationibus hypotheses duo elucebantur, quoad et nucleorum basalium et circuituum nigrostriatalium dopaminergicorum momentum selectionis actionum. Exemplum primum cum criticum valorem imprimentem, dum auctor stimulis valore percepto elictis responsa imprimentem, poscit. Secundum tamen exemplum actiones non in ganglionibus basalibus oriri, sed verisimiliter in cerebri corticibus generari atque omnino ganglionibus basalibus seligi, proponit. Itaque retur exemplum hoc pariter iter et directe pariter mores congruentes gubernare et indirecte actiones condicioni non congruentes supprimere. Proponit quoque id exemplum incentes potentiales actiones dopaminergicas tonicae directi itineris augere, ita inclinationem obliquam actiones celerius faciendi elucidare[15].

Putatur quoque exempla nucleorum basalium haec CHAD, syndromatis Tourette, morbi Parkinsoniani, schizophreniarum, mali obsessivi et compulsivi[16][17] atque dependentiae indagationum necesse esse. Per exemplum, morbum Parkinsonianum putatur effectus actionum itineris inhibentis excessivarum, quibus explicentur motus tardos et mala cognitiva; at syndroma Tourette actionum incitantium, quibus syndromatis impulsus characteristicos interpretatur[15].

Mesocorticolimbica itinera, ut supra dictum, nucleorum basalium relatione, discere componendum consideratur. Proponebantur varia exempla; inter ea tamen principale discentia differentiae temporalis causa: Praedictio, primum remuneratio deinde gubernatio facturae, factore discendi cum remunerationis effectu contra exspectationem in curvam discendi resolveat[18].

Mesocorticale iter imprimis ad functionas executivas gubernandas (e.g., attentionem, memoriam laborantem, gubernationem inhibentem, proponenda, et cetera) relatum, ita illud praecipue ad CHAD spectat[19][20]. Iter mesolimbicum salientiam incensivam, motivationem, apprehensionem incrementi ope, atque timorem, velut alias res cognitivas, gubernat.[9][20][21]. Praeterea ad motivatione cognitionem relatum est. huius itineris dopamini inopia, aut laesionibus loco originis sui, voluntatis magnitudinem cuiusque animalis praemium accipiendi minuit (e.g., aut numerum vectem nicotini deprimentem aut vitam nutrimentum quaerendi). Dopaminergicae drogae etiam animalis magnitudinem voluntatis approprinquandi praemo dein praemium recipiendi augere queant; supra itineris mesolimbici neuronorum potentiales actiones anticipatione remunerationis ineunte numerus augent[22]. Putabatur olim dopamini liberationem mesolimbicam voluptatis mediatorem primarium esse, hodiernis autem temporibus illae modo momentum minus voluptatis perceptionis habere[23][24]. Duo status hypothesis actionum corticis praefrontalis, ope actionis itinerum D1 ac D2, propositi sunt: alter itinere D1 iussus quo cancelli melius informationem tenendi, alter D2 iussus quo mutationes faciliores melius informationem ingenerandi permittent [25][26].

Gubernatio

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Recipiunt area tegmentalis ventralis et substantia nigra pars compacta informationem de aliis systematibus neurotransmissoribus, ut de glutamatergicis , GABAergicis, cholinergicis inditis velut de aliis nucleis monoaminergicis. Continet ATV receptoria 5-HT1A, quae effectus biphasicos ad potentialium actionum generationem exercent, cum dosibus exiguis agonistatum receptorii 5-HT1A potentialium actionum numerum augentibus, at dosibus maioribus actiones reducentibus. Expresserunt receptoria 5-HT2A neuronibus dopaminergicis incrementum actionum, vice versa receptoria 5-HT2C decrementum[27]. Mesolimbicum iter, quod ab ATV in nucleum accumbentem profertur, acetylcholini receptoriis quoque gubernatur. Praecipue et receptoriorum M2 et M4 agentia liberationem dopamini inhibent, sed receptorioriis M1 mediantibus liberationem dopamini auget.[28] Indita GABAergica ab striato orientia actiones neuronales dopaminergicas minuunt, insuper indita glutaminergica ab multis areis et corticalibus et subcorticalibus multitudinem agentis electrici neuronorum dopaminergicorum augent. Praeterea endocannabinoida habere effectus gubernantes in liberationem dopamini ab neuronibus ex ATV ac SN transcurrentibus videtur.[29] Noradrenergicis inditis ab loco caeruleo derivatis effectus et excitantes et inhibentes in neurona dopaminergica, quae ex ATGV et SNc egrediuntur, sunt.[30][31] Indita excitantes orexinergia in ATV in hypothalamo laterali oriuntur; ea lineam basales potentialium actionum ATV neuronorum dopaminergicorum gubernent[32][33].

Indita in aream tegmentalem ventralem (ATV) atque substantiam nigram partem compactam (SNc)
Neurotransmissor Origo Type of Connection Fontes
Glutamatum Incitantes projectiones in ATV et SNc [30]
GABA Inhibentes proiectiones in ATV et SNc [30]
Serotoninum Effectus gubernantes, receptorii sybtypo pendentes
Generat effectum biphasicos in ATV neurona 		[30]
Noradrenalinum Effectus gubernantes, receptorii sybtypo pendentes
Effectus et excitantes et inhibentes loci caerulei in ATV et SN partem compactam tempori pendentes sunt 		[30][31]
Endocannabinoida
  • ATV neurona dopamini
  • SNc neurona dopamini
 Effectus excitantes in neurona dopaminergica, ab inditis GABAergicis inhibentibus
Effectus inhibentes in neurona dopaminergica, ab inditis glutamatergicis inhibentibus
Interagat cum orexino per CB1–OX1 receptoriorum heterodimera ad actiones neuronales electricos gubernandos 		[29][30][32][34]
Acetylcholinum Effectus gubernantes, receptiorii sybtypo pendentes [30]
Orexinum Effectus excitantes in dopaminergica neurona ope signa dantium receptoriis orexini (OX1 atque OX2)
Auget et tonicas et phasicas actiones neuronorum dopaminergicorum in ATV
Interagat cum endocannabinoidis per CB1–OX1 receptoriorum heterodimera ad actiones neuronales electricos gubernandos 		[32][33][34]

Notae

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  1. ↑ "Beyond the Reward Pathway" 
  2. ↑ 2.0 2.1 Le Moal, Michel. "Mesocorticolimbic Dopaminergic Neurons". Neuropsychopharmacology: The Fifth Generation of Progress 
  3. ↑ Alcaro A., Huber R., Panksepp J. (Dec 2007). "Behavioral functions of the mesolimbic dopaminergic system: an affective neuroethological perspective". Brain research reviews 56 (2): 283-321 
  4. ↑ Galvan A., Wichmann T. (Iul 2008). "Pathophysiology of parkinsonism". Clinical neurophysiology 119 (7): 1459-74 
  5. ↑ Blum K., Chen A. L.-C., et al. (Oct 2008). "Attention-deficit-hyperactivity disorder and reward deficiency syndrome". Neuropsychiatric disease and treatment 4 (5): 893-918 
  6. ↑ Volkow N. D., Wang G.-J., et al. (Sep 2010). "Addiction: decreased reward sensitivity and increased expectation sensitivity conspire to overwhelm the brain's control circuit". BioEssays 32 (9): 748-55 
  7. ↑ Guo S., Huang J., et al. (Iun 2017). "Restless Legs Syndrome: From Pathophysiology to Clinical Diagnosis and Management". Frontiers in aging neuroscience 9: 171 
  8. ↑ 8.0 8.1 Ikemoto S. (2010). "Brain reward circuitry beyond the mesolimbic dopamine system: a neurobiological theory". Neuroscience and Biobehav. Review 35 (2): 129–50 
    Figure 3: The ventral striatum and self-administration of amphetamine
  9. ↑ 9.0 9.1 9.2 9.3 9.4 9.5 9.6 Malenka R. C., Nestler E. J., Hyman S. E. (2009). "Chapter 6: Widely Projecting Systems: Monoamines, Acetylcholine, and Orexin". In Sydor A., Brown R. Y.. Molecular Neuropharmacology: A Foundation for Clinical Neuroscience (2nd ed.). New York: McGraw-Hill Medical. pp. 147–148, 154–157. ISBN 9780071481274 
  10. ↑ Malenka R. C., Nestler E. J., Hyman S. E. (2009). "Chapter 10: Neural and Neuroendocrine Control of the Internal Milieu". In Sydor A., Brown R. Y.. Molecular Neuropharmacology: A Foundation for Clinical Neuroscience (2nd ed.). New York: McGraw-Hill Medical. p. 249. ISBN 9780071481274 
  11. ↑ Cragg S. J., Baufreton J., Xue Y., Bolam J. P., Bevan M. D . (2004). "Synaptic release of dopamine in the subthalamic nucleus". Eur. J. Neurosci. 20 (7): 1788–802 
  12. ↑ Doyon WM, Thomas AM, Ostroumov A, Dong Y, Dani JA (October 2013). "Potential substrates for nicotine and alcohol interactions: a focus on the mesocorticolimbic dopamine system". Biochem. Pharmacol. 86 (8): 1181–93 
  13. ↑ Taylor S. B., Lewis C. R., Olive M. F. (2013). "The neurocircuitry of illicit psychostimulant addiction: acute and chronic effects in humans". Subst Abuse Rehabil 4: 29–43 
  14. ↑ Yager LM, Garcia AF, Wunsch AM, Ferguson SM (August 2015). "The ins and outs of the striatum: Role in drug addiction". Neuroscience 301: 529–541 
  15. ↑ 15.0 15.1 Maia T. V., Frank M. J. (2011). "From reinforcement learning models to psychiatric and neurological disorders". Nat. Neurosci. 14 (2): 154–62 
  16. ↑ Beucke, Jan C.; Sepulcre, Jorge; Talukdar, Tanveer; Linnman, Clas; Zschenderlein, Katja; Endrass, Tanja; Kaufmann, Christian; Kathmann, Norbert (1 June 2013). "Abnormally High Degree Connectivity of the Orbitofrontal Cortex in Obsessive-Compulsive Disorder". JAMA Psychiatry 70 (6): 619–29 
  17. ↑ Maia, Tiago V.; Cooney, Rebecca E.; Peterson, Bradley S. (1 January 2008). "The Neural Bases of Obsessive-Compulsive Disorder in Children and Adults". Development and Psychopathology 20 (4): 1251–1283 
  18. ↑ Schultz W. (2015). "Neuronal Reward and Decision Signals: From Theories to Data". Physiol. Rev. 95 (3): 853–951 
  19. ↑ Malenka R. C., Nestler E. J., Hyman S. E. (2009). "Chapter 13: Higher Cognitive Function and Behavioral Control". In Sydor A., Brown R. Y.. Molecular Neuropharmacology: A Foundation for Clinical Neuroscience (2nd ed.). New York: McGraw-Hill Medical. pp. 313–321. ISBN 9780071481274 
  20. ↑ 20.0 20.1 Engert, Veronika; Pruessner, Jens C (9 January 2017). "Dopaminergic and Noradrenergic Contributions to Functionality in ADHD: The Role of Methylphenidate". Current Neuropharmacology 6 (4): 322–328 
  21. ↑ Pezze, Marie A.; Feldon, Joram (1 December 2004). "Mesolimbic dopaminergic pathways in fear conditioning". Progress in Neurobiology 74 (5): 301–20 
  22. ↑ Salamone, John D.; Correa, Mercè (2012). "The Mysterious Motivational Functions of Mesolimbic Dopamine". Neuron 76 (3): 470–485 
  23. ↑ Berridge KC, Kringelbach ML (May 2015). "Pleasure systems in the brain". Neuron 86 (3): 646–664 
  24. ↑ Berridge, Kent C; Kringelbach, Morten L (1 June 2013). "Neuroscience of affect: brain mechanisms of pleasure and displeasure". Current Opinion in Neurobiology 23 (3): 294–303 
  25. ↑ Durstewitz, Daniel; Seamans, Jeremy K. (1 November 2008). "The dual-state theory of prefrontal cortex dopamine function with relevance to catechol-o-methyltransferase genotypes and schizophrenia". Biological Psychiatry 64 (9): 739–749 
  26. ↑ Seamans, Jeremy K.; Yang, Charles R. (1 September 2004). "The principal features and mechanisms of dopamine modulation in the prefrontal cortex". Progress in Neurobiology 74 (1): 1–58 
  27. ↑ Jacobs, edited by Christian P. Müller, Barry (2009). Handbook of the behavioral neurobiology of serotonin (1st ed.). London: Academic. pp. 262–264. ISBN 978-0-12-374634-4 
  28. ↑ Shin, Jung Hoon; Adrover, Martín F.; Wess, Jürgen; Alvarez, Veronica A. (30 June 2015). "Muscarinic regulation of dopamine and glutamate transmission in the nucleus accumbens". Proceedings of the National Academy of Sciences of the United States of America 112 (26): 8124–8129 
  29. ↑ 29.0 29.1 "Endocannabinoid signaling in midbrain dopamine neurons: more than physiology?". Curr. Neuropharmacol. 5 (4): 268–277. December 2007 
  30. ↑ 30.0 30.1 30.2 30.3 30.4 30.5 30.6 Morikawa, Hitoshi; Paladini, Carlos A. (15 December 2011). "Dynamic Regulation of Midbrain Dopamine Neuron Activity: Intrinsic, Synaptic, and Plasticity Mechanisms". Neuroscience 198: 95–111 
  31. ↑ 31.0 31.1 "New perspectives on catecholaminergic regulation of executive circuits: evidence for independent modulation of prefrontal functions by midbrain dopaminergic and noradrenergic neurons". Front Neural Circuits 8: 53. 2014 
  32. ↑ 32.0 32.1 32.2 "Cannabinoid-hypocretin cross-talk in the central nervous system: what we know so far". Front. Neurosci. 7: 256. 2013 
     • Imago 1: Schematic of brain CB1 expression and orexinergic neurons expressing OX1 (HcrtR1) or OX2 (HcrtR2)
     • Imago 2: Synaptic signaling mechanisms in cannabinoid and orexin systems
     • Imago 3: Schematic of brain pathways involved in food intake
  33. ↑ 33.0 33.1 "Lateral hypothalamic orexin/hypocretin neurons: A role in reward-seeking and addiction". Brain Res. 1314: 74–90. February 2010 
  34. ↑ 34.0 34.1 "Human orexin/hypocretin receptors form constitutive homo- and heteromeric complexes with each other and with human CB1 cannabinoid receptors". Biochem. Biophys. Res. Commun. 445 (2): 486–90. 2014 

Nexus externi

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  • learn.genetics.utah.edu: de itineris cerebri (Anglice)
  • www.acnp.org: de via mesolimbica (Anglice)
 
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