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Lecture 20

BIL 268 Lecture Notes - Lecture 20: Volt, Pyramidal Cell, Electroencephalography

Course Code
BIL 268
Lu Zhongmin(john)

of 3
Lecture 20: Brain Rhythms
Brain activity recorded from scalp
I. Auditory Evoked Potential (slide not posted) detects less than 1 microvolt.
II. Repeat recoding many times and you obtain an average. By reducing the background
noise, you increase the signal.
EEG results from synaptic excitation in the cerebral cortex: EEG- signals are large; average is not
calculated. (10-20 microvolts)
Non-invasive recording.
Synchronous activity of many pyramidal neurons: This is the sum of response of many neurons;
excitation and inhibition are locked together.
III. Two pairs of electrodes detecting potential difference.
IV. Synchronous activity must be present for EEG.
V. Electrode is far away from neurons. One or two cells are too small for the EEG to detect.
VI. Pyramidal cells have greater potential to detect.
VII. In the irregular, the neurons are irregular and the sum is irregular too.
VIII. Blink – mechanical artifact recorded in the EEG. What is the real signal compared to
background noise?
How are synchronous EEG waves generated?
Mutual excitation and inhibition
IX. Types of neural network:
One neuron is a leader
Neurons are working together
X. Right- rhythm
XI. Cells receive excitatory input- The E cell will excite I cell and will inhibit (locomotion
behavior- alternating pattern of excitation)
XII. Where can you find an oscillator? You can find in the thalamus- sensory gateway. Inside
the thalamus, you find two cells.
EEG waves
XIII. Based on frequency and amplitude.
Beta wave- activated cortex- you can record when you are awake and sleep
Sleep state- can detect brain activity not necessarily passive.
XIV. Beta: fastest (> 14 Hz), activated cortex
XV. Alpha: 8-13 Hz, waking states
XVI. Theta: 4-7 Hz, sleep states
XVII. Delta: < 4 Hz, deep sleep, large amplitude
Functions of brain rhythms
Disconnect the cortex from sensory input
Coordinate activity between regions of NS
No function
Functions of the brain waves- hypotheses
Take a rest- disconnecting from sensory input
For any task, you need to have so many neurons in your brain to wok together. Recruiting
neurons to work together between regions.
Not important to brain function
Seizures and epilepsy
Seizures result from extremely synchronous brain activity
Generalized/partial seizure
Epilepsy: repeated seizures
What happens when your brain waves go wrong?
Seizures and epilepsy
Periodic seizures– become epilepsy
Why is this bad to the brain? This is over excitation- exitoxicity- from too much neuron
activity- and will kill postsynaptic neurons and produce brain damage.
Generalized seizure- covers the whole brain
Universal among higher vertebrates
Sleep deprivation, devastating.
One-third of lives in sleep state
Defined: “Sleep is a readily reversible state of reduced responsiveness to, and interaction
with, the environment.”
Do fish sleep?
How to tell that fish is asleep?
Sleep deprivation by electrical shock and constant light
Hypocretin (orexin), hypothalamus, narcolepsy
Zebra fish sleep is quite similar to mammalian sleep
How to tell fish is asleep? Stop swimming, immobilized at bottom or on the surface,
increased threshold for electric shock
Sleep deprivation by electrical shockà sleep more after that
Constant light almost suppress zf sleep completely (different from humans) and no
compensatory increase in sleep. This might result from light suppression of melatonin
Both humans and zf have hypocretin, one of the most important sleep-regulating
molecules. In Humans death of hypocretin-producing neurons or mutation of hypocretin
receptors à narcolepsy (excessive sleep during the day). But mutation of hypocretin
receptors in zf à no increase in sleep during the day. Human hypocretin-producing
neurons project to DA and 5-HT neurons while zf HPNs project to GABA neurons.
Insomnia: cannot fall in asleep at night.
Article from Mike Locher: Orexin, a neuropeptide that stimulates eating and regulates
wakefulness, also fosters animal’s seeking and craving (intense or abnormal desire)
It promotes drug-seeking and craving in rats.
Two states of sleep
Dreams – REM
Somnambulism – Non-REM
What’s PET imaging? Positron emission tomography
Inject radioactively labeled 2-DG called FDG, fludeoxyglocose with radioactive
isotope fluorine-18 (18F)
Neurons pick up FDG à correlation between neural activity and amount of FDG taken by
Red (+4) means more activity in REM, green and dark blue (between +1 and -1) mean
similar activity, white (-4) means less activity in REM!
The sleep cycle:
Stage 1: non-REM, Theta
Stage 2: non-REM, spindle & K complex
Stage 3: non-REM, Delta
Stage 4: non-REM, Delta
Stage 5: REM, Beta
Repeat every 90 min
Why do we sleep?
Synaptic homeostasis hypothesis: Sleeping to reset overstimulated synapses. “One major
function of sleep is to reduce synaptic connection in the brain.” (Sci. 2009 324:109)
“Synaptic communication can grow stronger during sleep.”
Mechanisms of sleep
Sleep is an active process
DMS à thalamus à control EEG & block sensory input
REM-on cells: ACh in pons
REM-off cells: NE and serotonin in locus coeruleus and raphe nuclei
Circadian Rhythms
Ultradian rhythms: < 24 h, sleep cycle, heartbeat
Circadian rhythms: 24 h, sleep-wake cycle
Infradian rhythms: > 24 h, menstrual cycle
Circadian rhythms: rhythms with a period of one day
Zeitgebers: environmental time cues
Primary zeitgeber: light-dark cycle
Internal biological clocks
Suprachiasmatic nuclei (SCN): luminance
Blocker-TTX does not disrupt their rhythmicity
Lesions of SCN disrupt the clock
Light sensors (retinal GCs)à clocks à output
Benson and colleagues: Discovered specialized type of ganglion cell in retina
Photoreceptor, but not rod or cone cell
Contains melanopsin, slowly excited by light
Synapses directly onto SCN neurons
Molecular clocks similar in humans, mice, flies, mold
Clock genes: Period (Per), Timeless (Tim), Clock
Takahashi: Regulation of transcription and translation, negative feedback loop
per à mRNA à PER protein
tim à mRNA à TIM protein
Increase in [PER/TIM dimers] à dissociated à PER transported into nucleus à PER
binding to CLK/CYC transcription factor à removal of CLK/CYC from promoter of per