Chapter 8
Lecture Overview
Circadian rhythms
Stages of sleep
Sleep function
Neural control of sleep
Sleep Disorders
Biological Rhythms
Behaviors display rhythmic variation
90 minute rest-activity cycle
Circadian: "about a day"
e.g. sleep/waking cycle, temperature
Monthly rhythms
Menstrual cycle
Seasonal rhythms
e.g. aggression, sexual activity in deer
SCN and Circadian Rhythms
Suprachiasmatic Nucleus (SCN) contains a biological clock that governs circadian rhythms
SCN receives input from retina (light resets clock)
SCN lesions disrupt circadian rhythms
SCN clock cells do not require direct neural connections to control circadian rhythms
SCN Biological Clock
SCN cells exhibit circadian rhythms
Involves glucose metabolism
Appears to be synchronized by SCN chemicals
Nature of clock
Fruit fly analogy
Activity of PER and TIM genes
Light pulses inhibit TIM gene
Resets circadian cycle
EEG Studies of Sleep
Sleep/waking cycle is experienced each day
Physiological changes that occur during sleep
Muscle tone (EMG)
Brain wave activity
Synchrony vs desynchrony
Eye movements
Genital activity
EEG Waveforms During Sleep
Non-REM Sleep
Alpha, delta, theta activity in the EEG
Stages 1 and 2
Stages 3 and 4: delta activity (synchronized)
Termed slow-wave sleep (SWS)
Light, even respiration
Muscle control is present (toss and turn)
Dreaming (cold, rational)
Difficult to rouse from stage 4 SWS (resting brain?)
REM sleep
Presence of beta activity (desynchronized)
Enhanced respiration and blood pressure
Rapid eye movements (REM)
PGO waves
Loss of muscle tone (paralysis)
Vivid, emotional dreams
Signs of sexual arousal
Assess impotence: stamps versus the sleep lab
Cycling of SWS and REM
What is the Function of Sleep?
Sleep as an adaptive response?
Found in all vertebrates (REM in mammals)
Kept our ancestors our of predators way?
Restoration and repair?
- Reduced brain activity during SWS
- Changes in sleep during:
- Prolonged bed rest (no real changes in SWS)
- Exercise (temperature inc. => inc. SWS)
- Mental activity increases SWS
Sleep Deprivation Studies
Human Sleep Deprivation
Peter Tripp: 200 hrs sleep deprivation produces psychosis
Randy Gardner: sleep deprivation does not induce psychosis
Perhaps drugs taken by Tripp contributed to psychosis
Sleep deprivation impairs cognitive functions
Perceptual distortions and hallucinations
Animal Sleep Deprivation Studies
Rats forced to walk lose sleep
Eat more, increased activity, illness and then death
Sleep Functions
SWS may reflect restoration
REM sleep may reflect:
Vigilance: alertness to the environment
Consolidation of learning/memory
Species-typical reprogramming
Facilitation of brain development
Chemical Modulation of Sleep/waking?
Notion of sleep-promoting or wakefulness-promoting factors?
Unlikely given:
Severed head study: two brains slept independently
Siamese twins share circulatory system but sleep independently
Bottle-nose dolphins: two hemispheres sleep independently
Sleep in Bottle-Nose Dolphins
Neural Regulation of Arousal
Electrical stimulation of brainstem induces arousal
Dorsal path: RF--> to medial thalamus --> cortex
Ventral path: RF --> to LH, basal ganglia, forebrain
Neurotransmitters involved in arousal:
NE: high activity when wake, low during sleep (LC)
ACh: agonists increase arousal, antagonists decrease arousal
5-HT: raphe nuclei: activity is low during sleep
5-HT neurons were most active during wakefulness, activity declined during SWS, and reached 0 during REM sleep
Locus Coeruleus and Arousal
NE secretion inhibits sleep (amphetamine) (Peter Tripp)
Lesions of ascending LC fibers: increase REM, slow wave sleep
Correlation of LC NE neurons with sleep-waking cycle
LC firing rate declines during REM sleep
LC firing rates increases on awakening
Dorsolateral Pons and REM Sleep
Pontine neurons initiate REM sleep
PGO waves are first predictor of REM sleep
ACh levels elicit PGO waves
Increased ACh increases REM sleep
Decreased ACh decreases REM sleep (kainic acid lesions)
Pontine lesions decrease REM sleep (Israeli soldier)
Pontine cells project via magnocellular cells within medulla to the spinal cord: release glycine to inhibit alpha-motoneurons (induce paralysis or atonia)
Sleep Disorders
Insomnia: Difficulty in sleeping
Many causes: situational, drug-induced
Sleeping pills: drug-dependence insomnia
Narcolepsy: Sleep at odd times
Sleep attack: urge to sleep
Cataplexy: REM paralysis
Sleep paralysis
Hypnagogic hallucinations
Muscles
Muscles
Smooth, cardiac, and skeletal
Movement Reflexes
Mono- and poly-synaptic reflexes
Brain Control of Movement
Cortex
Extrapyramidal systems
Muscle Fibers
Smooth Muscle
Multiunit: normally inactive
Located in large arteries, around hair
Responds to neural or hormonal stimulation
Single unit: rhythmic contraction
Located in gi tract, uterus, small blood vessels
Cardiac: rhythmic contraction
Responds to neural and hormonal stimulation
Muscle Fibers, continued
Skeletal muscle (striated appearance)
Composed of two fiber types:
Extrafusal: innervated by alpha-motoneurons from spinal cord: exert force
Intrafusal: no real force: are sensory fibers
Afferent fibers: report length of intrafusal: when stretched, the fibers stimulates the alpha-neuron that innervates the muscle fiber: maintains muscle tone
Efferent fibers: contraction adjusts sensitivity of afferent fibers.
Spinal Cord: Alpha-Motoneurons
Spinal cord is organized into dorsal and ventral aspects
Dorsal horn receives incoming sensory information
Ventral horn issues efferent fibers (alpha-motoneurons) that innervate extrafusal fibers
Neuromuscular Junction
Neuromuscular junction is the synapse formed between an axon and a muscle fiber
ACh is the transmitter at the junction
Release produces a large endplate potential
Potential opens CA++ channels
CA++ entry triggers myosin-actin interaction
Shortens muscle fiber
Intrafusal Spindle Fibers
Intrafusal fibers are in parallel with extrafusal fibers
Intrafusal receptors fire when:
Muscle relaxes and lengthens-
Loads stretch muscle
Activate agonist muscle fibers
Inhibit antagonist muscle fibers
Extrafusal contraction eliminates intrafusal firing
Gamma Motoneurons
Golgi Tendon Organs
GTO receptors are located within tendons
Sense degree of stretch on muscle
GTO activation inhibits the agonist muscle (via release of glycine onto alpha-motoneuron
Functions to prevent overcontraction of muscle
Spinal Cord Reflexes
Monosynaptic reflexes:
Incoming afferent --> synapse onto alpha-motoneuron
Examples:
- Patellar reflex
- Monosynaptic stretch stretch (posture)
Polysynaptic reflexes:
Incoming afferent --> synapse onto
Alpha motoneuron serving the agonist muscle
An inhibitory interneuron that serves the antagonist muscle
Motor Cortex
Primary Motor Cortex:
Receives input from
Frontal association cortex
Premotor cortex
Supplemental motor area
Primary somatosensory cortex
Motor Control: Descending Pathways
Lateral group: controls independent limb movements
Corticospinal tract: hand/finger movements
Corticobulbar tract: movements of face, neck, tongue, eye
Rubrospinal tract: fore- and hind-limb muscles
Ventromedial group: gross limb movements
Vestibulospinal tract: control of posture
Tectospinal tract: coordinate eye and head/trunk movements
Reticulospinal tract: walking, sneezing, muscle tone
Ventral corticospinal tract: muscles of upper leg/trunk
Corticospinal Tract
Starts in layer 5 of primary motor cortex
Passes through the internal capsule
Decussates in the pyramids (75-80% cross)
80% become the lat. corticospinal tract
20% become the ventral corticospinal tract
Terminate onto internuncial neurons or alpha-motoneurons of ventral horn
Corticospinal tract controls fine movements
Destruction: loss of muscle strength, reduced dexterity of hands and fingers
No effect on posture or use of limbs for reaching
Connections of the Basal Ganglia
Basal Ganglia and Movement Disorders
Parkinson’s disease
Muscle rigidity, resting tremor, slow movement
Damage to dopamine neurons within nigrostriatal bundle accounts for slow movement and postural problems
Neurological treatments for PD:
Fetal tissue transplants
Stereotaxic lesions of the globus pallidus alleviates some symptoms of Parkinson’s disease
Huntington’s chorea
Uncontrollable jerky movements
Loss of inhibitory cells in putamen
Brainstem Motor Structures
Cerebellum
Damage produces jerky, erratic, uncoordinated movements
Interconnects with all major motor nuclei
Involved in coordinating motor sequences
Reticular formation
Controls the activity of the gamma motoneurons
Involved in control of posture and locomotion