Hoorcolleges
Premotor cortex = voorbereiden beweging
Primaire motor cortex = aansturen specifieke delen lichaam
Signalen (uit secundaire motor cortex) van verschillende regionen uit
brein die corresponderen met bijv duim, vingers, hand, pols etc moeten in
goede volgorde plaatsvinden
Supplementaire motor cortex = organiseren van sequenties van
bewegingen in specifieke volgorde door verschillende sterkte van signalen
te sturen naar respectievelijke delen in primaire motor cortex / neuronen
coördineren activiteit van neuronen in primaire motor cortex
Primaire visuele cortex = signalen uit oog via thalamus komen binnen
Secundaire visuele cortex = zetten die elementaire zaken in elkaar
zodat je hele vorm waarneemt
Basale ganglia: Motoriek regulatie (directe input/output van/naar motor
cortex)
Ontvangt signalen, stuurt signaal terug dat remmend is, als signaal uit
motor cortex drempel overschrijdt haalt de rem weg signaal naar
ruggenmerg. Niet kiezen tussen responsen. Betrokken bij hevigheid van
beweging. Signaal m.b.t. vooruitzicht van beloning uit nucleus accumbens.
Als basale ganglia reageert op vooruitzicht dan echt verslaafd. Zelf
geïnitieerde bewegingen
Schade BG: moeite initiëren beweging, tremor (secundair symptoom)
Parkinson: wat te doen?:
- Celdood (substantia nigra) stoppen, niemand weet hoe
- L-dopa als medicatie
- Overmatige rem van globus pallidus op thalamus remmen
- Elektrische stimulatie in buurt van globus pallidus
Langdurige onderstimulatie van putamen door gebrek aan dopamine
heftige reactie op medicatie die kunstmatige dopamine toevoegt.
Chronische onderstimulatie leidt tot overgevoeligheid
Cerebellum: timing van beweging
Locked-in syndrome (LIS): hersenen formuleren wel signalen maar
geen signalen naar lichaam, hooguit ja en nee antwoorden. Cognitief
intact, alleen geen beweging. Oorzaak: motor-neuron degenerate disease,
trauma, beroerte
Bij epilepsie soms hersengebied verwijderen die epilepsie veroorzaakt
Bci = braincomputerinterface: elektroden op specifieke plek (in dit
geval hand region left motor cortex) hersenen connected to amplifier at
torso that emits to receiver/tablet.
,Hoofdstuk 8
8.1
Internal mechanism drive inner rhythms, not only external stimuli.
Endogenous circannual rhythm = rhythm that prepares for seasonal
changes
Circadian rhythm = daily rhythms for sleep/wake, mood, body temp, etc.
Zeitgeber = stimulus to reset/influence circadian rhythm:
- Light, tides, meals, temperature, arousal, exercise
Social interaction per se is not a zeitgeber
Blind people often sleep problems because CR not determined by light.
Phase-delay: going west, staying up longer, waking up later
Phase-advance: going east, sleep earlier, waking up earlier
Jet-lag prolonged stress/cortisol damage in hippocampus (memory)
Prolonged shift-work decreased cognition.
Bluish (short wavelength) light better at resetting circadian rhythm.
Preferred bedtime gets later until 20, then gradually reverses due to sex
hormones.
Early start of school problem for especially evening people other
problems: eating disorders/depressions etc.
Biological clock is hardy & robust because not easily disturbed by drugs,
radiation, food/water deprivation, brain damage etc.
SCN = suprachiasmatic nucleus (part of hypothalamus just above optic
chiasm): main driver of sleep/temp rhythms. Single isolated SCN cell
maintains rhythm, although interactions among cells sharpen accuracy.
Mutation could cause different length rhythms. Donor of SCN determines
rhythm, so rhythm inherent to SCN cells.
Retinohypothalamic path = small branch of optic nerve from retina to
SCN alters SCN’s settings. This path comes from special population of
retinal ganglion cells that have own photopigment = melanopsin, unlike
rods & cones. These special ganglion cells some input from rods & cones
but also direct input from light, located close to nose. If rods & cones
damaged, circadian rhythm still intact. Slow response to overall light,
respond mainly to bluish light.
Two genes period & timeless produce proteins PER & TIM in flies. [PER]
& [TIM] promote sleep & inactivity. mRNA levels responsible for PER & TIM
production rise gradually over day, few hours lag due to protein synthesis.
Negative feedback from these proteins inhibits mRNA, which lacks 24
hours. Light breaks down TIM protein. Mammals 3 versions of PER and
several related to TIM.
PER mutation rhythm < 24 hours, as if moving east depression.
SCN regulated sleep/wake by controlling pineal gland, which releases
melatonin (posterior to thalamus). Melatonin increases sleepiness in
diurnal animals but increases wakefulness in nocturnal animals. Pineal
gland also involved in puberty & adjustments to seasons.
8.2
, Stages in order from unconscious to more conscious:
Coma = extended unconsciousness by trauma/stroke/disease.
Vegetative state: alternating sleep & moderate arousal yet no
awareness of surroundings and no purposeful behavior. Pain does cause
autonomous response.
Minimally conscious: brief period of purposeful actions and limited
amount of speech & comprehension. Veg & MC state can last for years.
Brain death no sign of brain activity & no response to any stimulus. Often
wait for 24 hours of no activity before pronouncing brain death ethical
to remove life support.
EEG to record brain activity.
Polysomnograph = combination of EEG & eye-movement records.
Wake/sleep-stages:
- Awake: neurons out of phase with one another just like
stage 1
- Stage 1 sleep
- Stage 2 sleep
- Slow-wave (stage 3 – fewer slow waves):
heart/breathing/brain-activity decrease, whereas large-
amplitude waves more common, synchronized neural
activity because input to cerebral cortex inhibited
- slow-wave (stage 4 – more slow waves)
- REM
Alpha waves = 8-12Hz: relaxation, awake.
K-complex = sharp wave associated with temporary inhibition of
neuronal firing.
Sleep spindle = burst 12-14Hz waves for at least 0,5s: result from
oscillations between cells thalamus & cortex.
Amount of spindle activity correlates more than 0.7 with nonverbal tests of
IQ.
K-complex & sleep spindle (increase in number after learning/related to
consolidation of memory) characteristics of stage 2 sleep.
Learning ability of cat after removal cerebral cortex tested: high brain
activity during particular sleeping phase = paradoxical sleep = REM
sleep: irregular low-voltage fast waves (in that regard light sleep similar
to stage 1, except for eye movement, yet postural muscles more relaxed:
deep sleep). Also erections in REM sleep, other autonomous responses
fluctuate more as well.
Other stages are NREM sleep.
Cycle (90 min): First stage 1, then 2, then slow-wave. After hours of
sleep back to stage 2, then REM.
Early night slow-wave sleep predominates, later on more REM. Amount of
REM depends more on time of day than how long you’ve been asleep.
Loss of cells hypothalamus frequent awakenings. Dreaming more likely
during REM, yet also in NREM.
Tables P212.
Premotor cortex = voorbereiden beweging
Primaire motor cortex = aansturen specifieke delen lichaam
Signalen (uit secundaire motor cortex) van verschillende regionen uit
brein die corresponderen met bijv duim, vingers, hand, pols etc moeten in
goede volgorde plaatsvinden
Supplementaire motor cortex = organiseren van sequenties van
bewegingen in specifieke volgorde door verschillende sterkte van signalen
te sturen naar respectievelijke delen in primaire motor cortex / neuronen
coördineren activiteit van neuronen in primaire motor cortex
Primaire visuele cortex = signalen uit oog via thalamus komen binnen
Secundaire visuele cortex = zetten die elementaire zaken in elkaar
zodat je hele vorm waarneemt
Basale ganglia: Motoriek regulatie (directe input/output van/naar motor
cortex)
Ontvangt signalen, stuurt signaal terug dat remmend is, als signaal uit
motor cortex drempel overschrijdt haalt de rem weg signaal naar
ruggenmerg. Niet kiezen tussen responsen. Betrokken bij hevigheid van
beweging. Signaal m.b.t. vooruitzicht van beloning uit nucleus accumbens.
Als basale ganglia reageert op vooruitzicht dan echt verslaafd. Zelf
geïnitieerde bewegingen
Schade BG: moeite initiëren beweging, tremor (secundair symptoom)
Parkinson: wat te doen?:
- Celdood (substantia nigra) stoppen, niemand weet hoe
- L-dopa als medicatie
- Overmatige rem van globus pallidus op thalamus remmen
- Elektrische stimulatie in buurt van globus pallidus
Langdurige onderstimulatie van putamen door gebrek aan dopamine
heftige reactie op medicatie die kunstmatige dopamine toevoegt.
Chronische onderstimulatie leidt tot overgevoeligheid
Cerebellum: timing van beweging
Locked-in syndrome (LIS): hersenen formuleren wel signalen maar
geen signalen naar lichaam, hooguit ja en nee antwoorden. Cognitief
intact, alleen geen beweging. Oorzaak: motor-neuron degenerate disease,
trauma, beroerte
Bij epilepsie soms hersengebied verwijderen die epilepsie veroorzaakt
Bci = braincomputerinterface: elektroden op specifieke plek (in dit
geval hand region left motor cortex) hersenen connected to amplifier at
torso that emits to receiver/tablet.
,Hoofdstuk 8
8.1
Internal mechanism drive inner rhythms, not only external stimuli.
Endogenous circannual rhythm = rhythm that prepares for seasonal
changes
Circadian rhythm = daily rhythms for sleep/wake, mood, body temp, etc.
Zeitgeber = stimulus to reset/influence circadian rhythm:
- Light, tides, meals, temperature, arousal, exercise
Social interaction per se is not a zeitgeber
Blind people often sleep problems because CR not determined by light.
Phase-delay: going west, staying up longer, waking up later
Phase-advance: going east, sleep earlier, waking up earlier
Jet-lag prolonged stress/cortisol damage in hippocampus (memory)
Prolonged shift-work decreased cognition.
Bluish (short wavelength) light better at resetting circadian rhythm.
Preferred bedtime gets later until 20, then gradually reverses due to sex
hormones.
Early start of school problem for especially evening people other
problems: eating disorders/depressions etc.
Biological clock is hardy & robust because not easily disturbed by drugs,
radiation, food/water deprivation, brain damage etc.
SCN = suprachiasmatic nucleus (part of hypothalamus just above optic
chiasm): main driver of sleep/temp rhythms. Single isolated SCN cell
maintains rhythm, although interactions among cells sharpen accuracy.
Mutation could cause different length rhythms. Donor of SCN determines
rhythm, so rhythm inherent to SCN cells.
Retinohypothalamic path = small branch of optic nerve from retina to
SCN alters SCN’s settings. This path comes from special population of
retinal ganglion cells that have own photopigment = melanopsin, unlike
rods & cones. These special ganglion cells some input from rods & cones
but also direct input from light, located close to nose. If rods & cones
damaged, circadian rhythm still intact. Slow response to overall light,
respond mainly to bluish light.
Two genes period & timeless produce proteins PER & TIM in flies. [PER]
& [TIM] promote sleep & inactivity. mRNA levels responsible for PER & TIM
production rise gradually over day, few hours lag due to protein synthesis.
Negative feedback from these proteins inhibits mRNA, which lacks 24
hours. Light breaks down TIM protein. Mammals 3 versions of PER and
several related to TIM.
PER mutation rhythm < 24 hours, as if moving east depression.
SCN regulated sleep/wake by controlling pineal gland, which releases
melatonin (posterior to thalamus). Melatonin increases sleepiness in
diurnal animals but increases wakefulness in nocturnal animals. Pineal
gland also involved in puberty & adjustments to seasons.
8.2
, Stages in order from unconscious to more conscious:
Coma = extended unconsciousness by trauma/stroke/disease.
Vegetative state: alternating sleep & moderate arousal yet no
awareness of surroundings and no purposeful behavior. Pain does cause
autonomous response.
Minimally conscious: brief period of purposeful actions and limited
amount of speech & comprehension. Veg & MC state can last for years.
Brain death no sign of brain activity & no response to any stimulus. Often
wait for 24 hours of no activity before pronouncing brain death ethical
to remove life support.
EEG to record brain activity.
Polysomnograph = combination of EEG & eye-movement records.
Wake/sleep-stages:
- Awake: neurons out of phase with one another just like
stage 1
- Stage 1 sleep
- Stage 2 sleep
- Slow-wave (stage 3 – fewer slow waves):
heart/breathing/brain-activity decrease, whereas large-
amplitude waves more common, synchronized neural
activity because input to cerebral cortex inhibited
- slow-wave (stage 4 – more slow waves)
- REM
Alpha waves = 8-12Hz: relaxation, awake.
K-complex = sharp wave associated with temporary inhibition of
neuronal firing.
Sleep spindle = burst 12-14Hz waves for at least 0,5s: result from
oscillations between cells thalamus & cortex.
Amount of spindle activity correlates more than 0.7 with nonverbal tests of
IQ.
K-complex & sleep spindle (increase in number after learning/related to
consolidation of memory) characteristics of stage 2 sleep.
Learning ability of cat after removal cerebral cortex tested: high brain
activity during particular sleeping phase = paradoxical sleep = REM
sleep: irregular low-voltage fast waves (in that regard light sleep similar
to stage 1, except for eye movement, yet postural muscles more relaxed:
deep sleep). Also erections in REM sleep, other autonomous responses
fluctuate more as well.
Other stages are NREM sleep.
Cycle (90 min): First stage 1, then 2, then slow-wave. After hours of
sleep back to stage 2, then REM.
Early night slow-wave sleep predominates, later on more REM. Amount of
REM depends more on time of day than how long you’ve been asleep.
Loss of cells hypothalamus frequent awakenings. Dreaming more likely
during REM, yet also in NREM.
Tables P212.
