Biological basis of behavior 2

How do we measure sleep?

EEG, EMG, EOG

What does a EEG do

Measures Brain activity

What does a EMG do?

Measures muscle activity

What does an EOG do?

measures eye movement

Synchronized EEG

Neurons fire more together, Lower frequency, higher amplitude, larger, clearer waves

Desynchronized EEG

neurons fire in more independent or irregular patterns, higher frequency and lower amplitude, smaller irregular waves

Waking EEG patterns: Alpha

Occurs during relaxed waking; regular, medium-frequency waves; frequency: 8 - 12 Hz

Waking EEG patterns: Beta

Occurs during alert/ attentive waking; irregular, low-amplitude waves, frequency: 13 - 3 0 _ Hz

Waking

EEG: alpha/beta activity, generally higher frequency + Lower amplitude; EMG: muscle tone present, brain is relatively activated

Slow-wave sleep

EEG: delta activity, low frequency + high amplitude EMG: muscle tone reduced, deepest stage of sleep

REM sleep

EEG: desynchronized, resembles waking

EEG, EMG: profound loss of muscle tone, rapid eye movements, vivid dreaming, activated brain + muscle atonia

Acetylcholine (ACh)

Origin: pons, basal forebrain, medial septum; projects to the cortex and

hippocampus; agonists increase EEG signs of arousal; activity: high during waking

and REM, low during SWS

Norepinephrine (NE)

Origin: Locus; projects widely throughout the brain; increases Vigilance/ alert behavior; activity: high during waking, decreases during SWS, essentially absent during REM

Serotonin (5-HT)

Origin: raphe nuclei; projects widely throughout the brain; raphe stimulation produces cortical arousal; activity is greatest during waking, decreases during SWS, and is minimal

during REM

Histamine

origin: tubero-mammillary nucleus (TMN), directly increases cortical arousal, antagonists (e.g., diphenhydramine), increase Sleep; activity: high during waking, low during SWS and REM

Orexin (Hypocretin)

Origin: lateral hypothalamus, projects to almost every part of the brain; especially active during alert / exploratory waking, degeneration of these neurons causes narcolepsy.

5 arousal systems

Most arousal systems are active/high during waking and decrease during sleep; an important exception is that ACh becomes active again during REM

vIPOA-sleep-promoting region

Activity increases during sleep, releases GABA which has an inhibitory effect which projects to dorsal raphe, basal forbrain, locous coeruleus, orexin neurons.

evidence for vIPOA

Damage causes insomnia, and sleep is suppressed. Stimulation causes drowsiness; neurons are more active during sleep

Adenosine

Released by astrocytes during neural metabolic activity, accumulates during prolonged waking. produces drowsiness/ sleepiness; activates vIPOA; caffeine blocks adenosine receptors.

Sleep/ wake flip-flop

Based on reciprocal inhibition, WAKE: arousal systems are active; vIPOA is inhibited. SLEEP: vIPOA is active; arousal systems are inhibited; transitions are rapid; orexin stabilizes the waking state

REM flip-flop

REM-ON region= (SLD) sublaterodorsal nucleus; REM-OFF region= (vIPAG) ventrolateral periaqueductal gray, connected by inhibitory GABA neurons. During waking, orexin activates REM-OFF during sleep. vIPOA inhibits VIPAG. REM can occur.

sublaterodorsal nucleus (SLD)

REM-ON region, contributes to muscle paralysis/ atonia

ventrolateral periaqueductal gray (vIPAG)

REM-OFF region, when active suppresses REM

Magnocellular Nucleus of the medulla

Part of the pathway producing muscle paralysis/ atonia, helps suppress skeletal motor output during REM

Tectum

controls Rapid eye movements, receives input from pontine acetylcholine cholinergic neurons

Lateral Geniculate Nucleus

involved in PGO waves, participates in REM-related visual system activity

Light input to the SCN

Light acts as a zeitgeber that resets/ synchronizes the clock, special retinal ganglion cells detect ambient light, photopigment= melanopsin pathway: retina —> retinohypothalamic pathway —> SCN = primary biological clock in the hypothalamus, constant light —> normal circadian sleep patterns become disrupted.

Daytime

DMH inhibits the vIPOA activates orexin neuron/ arousal systems, favors wakefulness

Nighttime

DMH activates the vIPOA, favors sleep

SCN output to the sleep/wake system

SCN —> SP2 —> DMH projects to vIPOA lateral hypothalamic orexin neurons.

NIGHTLY PATTERN & BRAIN ACTIVITY

As the night goes on, the relative length of REM sleep increases in each successive

sleep cycle; during slow-wave sleep, activation in the visual and auditory cortices decreases, whereas activity in the thalamus and cerebellum decreases. Dolphins can sleep with one hemisphere at a time (hemispheres sleep independently)

CIRCADIAN & SEASONAL RHYTHMS

Circadian rhythms are endogenous cycles of activity that occur over ~24 hours, the hormone melatonin is secreted by the pineal gland and helps regulate seasonal rhythms (especially in response to changes in daylight)

FUNCTIONS, DEPRIVATION & LEARNING

One important function of slow-wave sleep is to allow the brain to rest and recover from the demands of waking activity. After prolonged sleep deprivation, the stage that shows a strong rebound (increased amount) is Slow-wave sleep; REM sleep is especially associated with nondeclarative learning (e.g., skills, habits, procedures)

SLEEP DISORDERS

narcoleptic sleep attacks can be treated with stimulant drugs that act as catecholamine agonists (e.g., amphetamines). A sudden loss of muscle tone while the person is fully conscious is called Cataplexy; pavor nocturnus is another name for night terror (s)

Schizophrenia POSITIVE SYMPTOMS

Represents an excess of normal functioning, associated mainly with the mesolimbic pathway; it is a thought disorder with delusions and hallucinations

Schizophrenia

Represents a decrease/absence of normal behavior associated mainly with the mesocortical pathway: leads to reduced emotional response, reduced speech, lack of motivation/initiative, anhedonia, and social withdrawal

Schizophrenia COGNITIVE SYMPTOMS

Associated mainly with the mesocortical pathway: characterized by difficulty sustaining attention, low psychomotor speed, deficits in learning + memory, poor abstract thinking, and poor problem solving

Schizophrenia EVIDENCE FOR HERITABILITY

Genes increase susceptibility rather than determining the disorder; concordance is higher in identical twins; monochorionic twins show higher concordance than dichorionic twins; genetics interact with environmental/ prenatal factors

Schizophrenia DOPAMINE HYPOTHESIS

Positive symptoms reflect increased dopaminergic activity, mainly in the mesolimbic pathway, caused by hyperactivity of dopaminergic synapses

Schizophrenia drug evidence

Dopamine agonists: positive symptoms; example: amphetamine. Dopamine antagonists act as antipsychotics; a classic antipsychotic example: chlorpromazine blocks D2 and D3 receptors

Schizophrenia DIRECT DOPAMINE FINDINGS

Patients show greater dopamine release after amphetamine, especially in the striatum; greater dopamine release correlates with more severe positive symptoms. D2 receptors may be slightly increased, but this is unlikely to be the primary cause

Schizophrenia key takeaways

Too much dopamine in the mesolimbic pathway → positive symptoms

reducing dopamine signaling → reduces positive symptoms

Schizophrenia BRAIN-DAMAGE EVIDENCE

Enlarged lateral Ventricles, enlargement reflects loss of brain tissue; patients show greater loss of gray matter, affected twin may show: larger ventricles, smaller anterior hippocampus, and reduced left frontal gray matter

Schizophrenia EARLY / DEVELOPMENTAL CLUES

Children who later develop schizophrenia may show deficits in facial expression; they may also show abnormal movement. Symptoms usually emerge after puberty in adolescence

Schizophrenia SEASONALITY & ENVIRONMENT

Increased risk for births during February - May; one proposed contributor = low vitamin D, prenatal infection / obstetric factors can increase risk

Schizophrenia QUICK FACTS

Affects approximately 1 % of the population; DISC1 mutations can greatly increase

susceptibility; belief that others are plotting against you = delusion of persecution

MAJOR DEPRESSIVE DISORDER (MDD)

Feelings of unworthiness and guilt, little energy + slowed movement; diminished ability to feel pleasure, sleep and eating may be disturbed.

Bipolar Disorder

Alternates between Mania and depression: mania involves pathological energy and may include intense euphoria; the depressive phase resembles MDD. Close relatives show increased risk. Concordance is higher in Monozygotic twins MZ concordance ~69 % DZ concordance = 13 %

GENES + CIRCADIAN RHYTHMS

Affective disorders are partly heritable/genetic RORA / RORB are candidate genes involved in circadian regulation; genetics increase susceptibility rather than guaranteeing the disorder.

MONOAMINE HYPOTHESIS

depression is caused by insufficient activity of monoaminergic neurons. Research focuses mainly on serotonin (5-HT) and norepinephrine (NE). Monoamine agonists can reduce/alleviare depressive; therapeutic effects usually take several weeks

Brain evidence for antidepressents

depressed patients show increased activity in the subgenual ACC; successful antidepressant treatment decreases sgACC activation. Other PFC regions may show decreased activity; DBS of the sgACC can reduce depressive symptoms

ANTIDEPRESSANTS

Tricyclics block reuptake of serotonin and norepinephrine

• fluoxetine (Prozac) is an SSRI • Prozac blocks serotonin reuptake

• used to treat depression and OCD

• therapeutic lag may involve desensitization of

presynaptic autoreceptors

NEUROGENESIS & TREATMENT

stress/depression inhibits hippocampal neurogenesis; antidepressants increase neurogenesis; this increase occurs with the same 2-3 week delay as therapeutic effects; exercise can produce antidepressant effects.

SLEEP IN DEPRESSION

Sleep cycle is more fragmented; patients awaken more frequently, Slow-wave sleep is reduced, REM begins earlier and makes up more of the first half of sleep

SLEEP DEPRIVATION

REM deprivation can alleviate depression. Effects of REM deprivation may persist after deprivation ends. Slow-wave sleep deprivation can have immediate effects; total sleep deprivation can reduce depression, but symptoms return after normal sleep

ANTIDEPRESSANTS & REM

Most antidepressant drugs suppress REM sleep This connects antidepressant treatment

with altered REM regulation

SEASONAL AFFECTIVE DISORDER (SAD)

a unique type of depression; reduced light can disrupt circadian rhythms. Perry discusses decreased sensitivity of the photopigment melanopsin. can be treated with phototherapy/bright-light exposure