Download Reticular formation

Brain stem
Reticular formation
Definition
Mass of neurons and nerve fibers extending from the
caudal medulla to the rostral midbrain and continuous
with the zona incerta of the subthalamus and midline,
intralaminar and reticular nuclei of the thalamus
Organized into definite nuclear groups with known
afferent and efferent connections
As a whole, the reticular formation comprises a neural
system with multiple inputs and multisynaptic system of
impulse conduction
Organization of reticular formation
Median raphe nuclear group
Paramedian reticular nuclear group
Medial reticular nuclear group
Lateral reticular nuclear group
Each nuclear group is represented at the level of
midbrain
pons
medulla
Reticular nuclei
(MCP)
Reticular nuclei
Median Raphe
Medulla
Raphe obscurus
Raphe pallidus
Rostral medulla
caudal pons
Raphe magnus
Pons
Raphe pontis
Dorsal Raphe
(nucleus
supratrochlearis)
Superior central
(Bekhterew)
Medial
Lateral
Reticularis giganto
cellularis
Reticularis
parvocellular
is
Reticularis
lateralis
Reticularis pontis
caudalis
Reticularis
pontis oralis
Reticularis
parvocellular
is
Paramedian
reticular
Reticulotegm
ental
Rostral pons–
caudal
midbrain
Midbrain
Paramedian
Parabrachial
Pedunculop
ontine
Cuneiform
Subcuneifor
m
Reticular formation – summary of functions
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
Purves, et al, Neuroscience, 3rd ed.
Kandel, Schwartz, Jessell; Principles of
Neural Science, 4th ed.
Descending analgesic pathways activate enkephalincontaining 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
Premotor cortex regulates posture via the
reticular formation
Purves, et al, Neuroscience, 3rd ed.
Integration of direct and indirect
neocortical pathways to spinal cord
Cortex
Limb fine
movements
Brainstem
Spinal cord
Postural
adjustments
to movements
Paramedian reticular (precerebellar) nuclei
Cortex
control of
movements
Paramedian
reticular nuclei
Spinal cord/vestibular nuclei
Cerebellum
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
Reticular formation – summary of functions
Purves, et al, Neuroscience, 3rd ed.
Reticular formation – summary of major pathways
Noradrenergic neurons
Reticulospinal tract
Serotonergic neurons
Chemically specified systems of the reticular
formation
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 schizophrenia
mesocortical – to prefrontal cortex → cognitive deficits in PD
Direct (aminergic) and indirect (cholinergic)
cortical arousal system regulate sleep
Monoaminergic nuclei promote wakefulness via facilitation of the
cerebral cortex and inhibition of sleep-promoting neurons
(hypothalamus)
Coma
Damage to the reticular formation at the level of
the rostral pons and caudal medulla may lead to
coma or akinetic mutism (coma vigil). An EEG
similar to the slow phase of the sleep
characterizes this condition, with no appreciable
change in the autonomic and somatomotor
reflexes or eye movement
Coma might be reversible
Brain death
State of irreversible brain damage so severe that normal
respiration and cardiovascular function can no longer
be maintained
In modern clinical medicine, cessation of life is equated
with brain death rather than with cessation of heart beat
Criteria (comatose patients fulfilling these 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
Reticular formation in midbrain
Reticular formation in pons
Reticular formation in medulla
Development of reticular formation
Modified from Bayer SA et al. Neurotoxicology 14:83–144, 1993