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Reticular Formationformation Definitiondefinition BrainBrain stemstem ReticularReticular formationformation DefinitionDefinition MMassass ofof neuronsneurons andand nervenerve fibersfibers extendingextending fromfrom thethe caudalcaudal medullamedulla toto thethe rostralrostral midbrainmidbrain andand continuocontinuousus withwith thethe zonazona incertaincerta ofof thethe subthalamussubthalamus andand midlinmidline,e, intralaminarintralaminar andand reticularreticular nucleinuclei ofof thethe thalamusthalamus OOrganizedrganized intointo definitedefinite nuclearnuclear groupsgroups withwith knownknown afferentafferent andand efferentefferent connectionsconnections AsAs aa whole,whole, thethe reticularreticular formationformation comprisescomprises aa neurneuralal systemsystem withwith multiplemultiple inputsinputs andand multisynapticmultisynaptic systesystemm ofof impulseimpulse conductionconduction OrganizationOrganization ofof reticularreticular formationformation MedianMedian rapheraphe nuclearnuclear groupgroup ParamedianParamedian reticularreticular nuclearnuclear groupgroup MedialMedial reticularreticular nuclearnuclear groupgroup LateralLateral reticularreticular nuclearnuclear groupgroup Each nuclear group is represented at the level of midbrain pons medulla ReticularReticular nnucleiuclei (MCP) ReticularReticular nnucleiuclei Median Raphe Paramedian Medial Lateral Medulla Raphe obscurus Reticularis giganto Reticularis Raphe pallidus cellularis parvocellular is Reticularis lateralis Rostral medulla Raphe magnus Paramedian caudal pons reticular Pons Raphe pontis Reticularis pontis Reticularis caudalis parvocellular Reticularis is pontis oralis Rostral pons– Reticulotegm Parabrachial caudal ental Pedunculop midbrain ontine Midbrain Dorsal Raphe Cuneiform (nucleus Subcuneifor supratrochlearis) m Superior central (Bekhterew) ReticularReticular formationformation –– summarysummary ofof functionsfunctions Purves, et al, Neuroscience, 3rd ed. Median raphe nuclei rostral raphe nuclei → reticular activating system (wakefulness, alertness, and sleep) caudal raphe nuclei → pain mechanisms Pain control pathways & reticular formation Ascending pain pathways Descending systems modulate the transmission of ascending pain signals Kandel, Schwartz, Jessell; Principles of Purves, et al, Neuroscience, 3rd ed. Neural Science, 4 th ed. Descending analgesic pathways activate enkephalin- containing local circuit neurons SER, NA morphine acts here Glu, NP Purves, et al, Neuroscience, 3rd ed. Medial reticular nuclei cuneiform & subcuneiform nuclei ascending projections → consciousness and alertness Gigantocellular nucleus descending projections → motor control PremotorPremotor cortexcortex regulatesregulates postureposture viavia thethe reticularreticular formationformation Purves, et al, Neuroscience, 3rd ed. IntegrationIntegration ofof directdirect andand indirectindirect neocorticalneocortical pathwayspathways toto spinalspinal cordcord Cortex Limb fine Postural movements Brainstem adjustments to movements Spinal cord Paramedian reticular (precerebellar) nuclei Cortex control of movements Paramedian Cerebellum reticular nuclei Spinal cord/vestibular nuclei Lateral reticular nuclei Pedunculopontine – connections with cortex & substantia nigra → locomotor center Parabrachial nucleus – connections with amygdala, nucleus solitarius , hypothalamus → autonomic function N. parvocellularis and lateralis constitute the receptive component of reticular nuclei – receive from ascending sensory systems, project to cortex & medial reticular group ReticularReticular formationformation –– summarysummary ofof functionsfunctions Purves, et al, Neuroscience, 3rd ed. ReticularReticular formationformation –– summarysummary ofof majormajor pathwayspathways Noradrenergic neurons Reticulospinal tract Serotonergic neurons CChemicallyhemically specifiedspecified systemssystems ofof thethe reticularreticular formationformation Cholinergic system (groups Ch1 -Ch6) - Ach Locations pontomesencephalic junction – e.g. pedunculopontine nucleus basal forebrain - nucleus basalis of Meynert Function - cortical arousal - wakefulness and REM sleep Monoaminergic System – NE, E, Ser, Dop Serotonergic neurons (groups B1 to B9 ) – most median raphe nuclei → destruction of these neurons leads to insomnia ; mood regulation Noradrenergic neurons - attention, sleep -wake state and mood locus ceruleus (group A6 ); (Latin, “dark blue place ”) lateral tegmental norepinephrine system (groups A1 to A7) Adrenergic neurons (groups C1 -C2) - a minor component of the monoaminergic system Dopaminergic neurons – most are in the midbran (ventral tegmental area ) mesostriatal ( = nigrostriatal) pathway – to substantia nigra → PD!!! mesolimbic pathway – to the limbic system → overactivity in schizophreni a mesocortical – to prefrontal cortex → cognitive deficits in PD DDirectirect (aminergic)(aminergic) andand indirectindirect (cholinergic)(cholinergic) corticalcortical arousalarousal systemsystem regulateregulate sleepsleep Mono aminergic nuclei promote wakefulness via facilitation of the cerebral cortex and inhibition of sleep -promoting neurons (hypothalamus) ComaComa DamageDamage toto thethe reticularreticular formationformation atat thethe levellevel ofof thethe rostralrostral ponspons andand caudalcaudal medullamedulla maymay leadlead toto comacoma oror akineticakinetic mutismmutism (coma(coma vigil).vigil). AnAn EEGEEG similarsimilar toto thethe slowslow phasephase ofof thethe sleepsleep characterizescharacterizes thisthis condition,condition, withwith nono appreciableappreciable changechange inin thethe autonomicautonomic andand somatomotorsomatomotor reflexesreflexes oror eyeeye movemenmovemen tt ComaComa mightmight bebe reversiblereversible BrainBrain deathdeath SStatetate ofof irreversibleirreversible brainbrain damagedamage soso severesevere thatthat nonormalrmal respirationrespiration andand cardiovascularcardiovascular functionfunction cancan nono longlongerer bebe maintainedmaintained InIn modernmodern clinicalclinical medicine,medicine, cessationcessation ofof lifelife isis eqequateduated withwith brainbrain deathdeath ratherrather thanthan withwith cessationcessation ofof hearheartt beatbeat CCriteriariteria ((comatose patients fulfill ing the se criteria are considered dead ) Unresponsiveness to external stimuli Absence of spontaneous breathing Dilated fixed pupils Absence of brain stem reflexes (corneal, gag, vestibuloocular) No recognizable reversible cause for the coma Flat electroencephalogram (absence of electrical activity) Nonfilling of cerebral vessels in arteriography or radioisotope imaging ReticularReticular formationformation inin midbrainmidbrain ReticularReticular formationformation inin ponspons ReticularReticular formationformation inin medullamedulla DevelopmentDevelopment ofof reticularreticular formationformation Modified from Bayer SA et al. Neurotoxicology 14:83–144, 1993 .
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