PSY 4127 Lecture Notes - Lecture 8: Orexin, Preoptic Area, Monoaminergic
Two components of wake-fullness.
i. Cortical Arousal (Basal Forebrain Pathway): there is a system of pathways within the
brain, arising from the brainstem (ARAS/AAS), that stimulate the forebrain and cause it
to remain awake. These wakefulness pathways consistent of nerve cells that communicate
using as neurotransmitters group of chemicals, called monoamines: the monoamines
include norepinephrine, dopamine, serotonin, and histamine.
ii. Sensory and motor transmission (thalamic pathways): ACh is the major arousing input to
the thalamus, a way station in the brainstem (PPT) that controlled the transmission of
sensory and motor information to the cerebral cortex.
Wake
• during wakefulness, both cholinergic and monoaminergic pathways are firing at full speed
• injury to these pathways results in a coma
• unjustly to the hypothalamus in the preoptic area (VLPO) can produce long lasting
insomnia
• GABAergic neurons from the VLPO wrap around the monoamine/ACh activating
pathways
• during sleep GABA activity represses wake, suppressing waves
The Sleep-Wake Switch: Neurons of the ventrolateral prep-tic nucleus (VLPO) are active in
sleep. The loss of VLPO neurons leads to sleep fragmentation and insomnia. The VLPO
projects to brainstem areas are mutually inhibitory, meaning as one goes up the other goes
down (a flip-flop switch). The lateral hypothalamic (LH) orexin neurons probably play a
stabilizing role in the switch.
i. Orexin neurons are active and VLPO is inhibited (wake).
ii. Orexin neurons are inhibited and VLPO.
This is how the different brain areas work together to produce sleep but does not explain
REM sleep.
Hobson and McCarley’s (1975) Reciprocal Activation Model of REM Sleep
Reciprocal interaction between brainstem REM-ON neurons of LDT/PPT null and REM-
OFF neurons of the locus corrileus.
Locus Correlius: REM-OFF 5HT and NA inhibits LDT and PPT.
LDT + PPT: REM-ON Ach inhibits locus corrileus.
find more resources at oneclass.com
find more resources at oneclass.com
Document Summary
Two components of wake-fullness: cortical arousal (basal forebrain pathway): there is a system of pathways within the brain, arising from the brainstem (aras/aas), that stimulate the forebrain and cause it to remain awake. The sleep-wake switch: neurons of the ventrolateral prep-tic nucleus (vlpo) are active in sleep. The loss of vlpo neurons leads to sleep fragmentation and insomnia. The vlpo projects to brainstem areas are mutually inhibitory, meaning as one goes up the other goes down (a flip-flop switch). The lateral hypothalamic (lh) orexin neurons probably play a stabilizing role in the switch: orexin neurons are active and vlpo is inhibited (wake), orexin neurons are inhibited and vlpo. This is how the different brain areas work together to produce sleep but does not explain. Hobson and mccarley"s (1975) reciprocal activation model of rem sleep. Reciprocal interaction between brainstem rem-on neurons of ldt/ppt null and rem- Locus correlius: rem-off 5ht and na inhibits ldt and ppt.