 dolphins  whales

sperm whale (off the coast of Chilé)

 multimedia/news mov multimedia/news mov

 135,000 hours of your life asleep (1/3)  How do we study sleep?  What do we know about it?  What are some sleep disorders  What do we know about brain regions and neurotransmitters involved in sleep?

 typically in a sleep lab….  EEG – electroencephalogram  EPSPs of cortical neurons ◦ EMG – electromyelogram  looking at muscle tone (usually electrodes on jaw) ◦ EOG – electrooculogram  looking at eye movements (electrodes around eye)

 look at 2 components of the EEG 1.the frequency of the wave (n of peaks/unit time) –tells you about the number of cortical neurons generating EPSPs 2.the amplitude of the wave (height of wave) –tells us about the n of EPSPs that occur at the same point in time –n of neurons firing in synchrony

high frequency, low amplitude beta waves

start seeing higher amplitude, lower frequency alpha waves

1 st sleep stage – still fairly high frequency low amplitude but clear difference from alert and awake state often will deny being asleep

15 min later (if not disturbed) stage 2 – characterized by high frequency low amplitude sleep spindles and high amp low f k complexes role of these wave forms?–

15 min later if not disturbed stage 3 – first of the slow wave sleep stages characterized by delta waves high amplitude, low frequency waves less than 50% delta waves is stage 3; more than 50% stage 4 (15 min later)

 during SWS, parasympathetic NS activity seems to predominate (hr and bp decrease, respiration decreases, gastric motility increases)  person relaxed but still motor activity; normal sleeper changes position every 20 min or so  stage 4 deepest stage ?

 typical 90 min sleep cycles goes from ◦ stage 1 (15 min) to stage 2 (15 min) to stage 3 (15 min) to stage 4 (15 min) to stage 3 (15 min) to stage 2 (15 min) to  first bout of REM sleep

 low amplitude, high frequency desynchronous EEG

 rapid eye movement (REM)  narrative dreams  muscle atonia ◦ look at motor cortex – extremely active but descending motor pathways paralyzed ◦ REM without atonia  penile erections and vaginal secretions  deepest stage? ◦ incorporate things into our dreams ◦ more likely to spontaneously awaken

 changes in amount of time spent in REM over the night

 maturational changes in pattern ◦ species with underdeveloped CNS – spend more time in REM

 changes in amount of time spent in REM over the night  maturational changes in pattern ◦ species with underdeveloped CNS – spend more time in REM ◦ human newborns ~ 50% sleep time in REM ◦ human premies ~ 80% sleep time in REM

 evolutionary theory ◦ predictions……  restoration and repair

 Sleep more if: ◦ No predators ◦ Safe place for sleeping ◦ Dangerous to yourself in the dark  Sleep less if: ◦ Fear of predation ◦ Food of low nutritional value

 evolutionary theory  restoration and repair ◦ marathon runner studies

1. Insomnia

-primary cause - sleep medications

1. Insomnia -primary cause - sleep medications -develop tolerance; REM rebound

 short-acting benzodiazepenes ◦ triazolam (Halcion®)

 short-acting benzodiazepenes ◦ triazolam (Halcion®)  problems with BZ  tolerance  REM suppression (and REM rebound)  WD

 Zolpidem- (Ambien) ◦ non hypnotic sedative ◦ Also a muscle relaxant and anticonvulsant ◦ Still works on GABA A receptors ◦ Works quickly (15 min) and with a short ½ life (how quickly it clears out of the body

 releases hormone melatonin at night

 Ramelteon (Rozerem) ◦ First in a new class of sleep medications ◦ non BZ ◦ non sedative ◦ melatonin agonist

1. Insomnia -primary cause - sleep medications -develop tolerance; REM rebound -we are often poor estimators of how much sleep we get

-sleep apnea – difficulty sleeping and breathing at the same time -two types -1. CNS mediated – very rare -2. obstructive sleep apnea- main cause

weight loss, reducing alcohol consumption (or other muscle relaxants), elevated sleeping, CPAP machine – continuous postive airway pressure surgical procedures to remove or tighten tissue

 SIDS – sudden infant death syndrome ◦ possible link

 Nocturnal myoclonus – twitching of the body, usually the legs, during sleep – most are not aware of why they don’t feel rested (now called periodic limb movement disorder); involuntary  Restless legs – sufferers complain of legs being uncomfortable that prevents sleep- can occur when awake or asleep  Txt can include DA agonists; anticonvulsants Copyright © 2006 by Allyn and Bacon

 ~ 250,000 people in US ◦ symptoms: uncontrollable recurring sleep during daytime (usually during mundane tasks) ◦ subcategories  cataplexy-  hypnagogic hallucinations  REM sleep behavior disorder

 often (not always) older males  often (not always) associated with other neurodegenerative diseases

 brainstem structures – pons, medulla  abnormalities in noradrenergic, cholinergic, and serotonergic systems, seems to exist in the pathogenesis of RBD  clonazepam (Klonopin) ◦ anticonvulsant – ◦ benzodiazpene

 unusual sleep characteristics ◦ short latency to REM ◦ persistent muscle tone ◦ excessive muscle twitching  Treatment for narcolepsy ◦ stimulants; caffeine, ◦ GHB – gamma hydroxy butyrate**

 genetics of narcolepsy ◦ people with family history + are 50X more likely to have disorder than families without history + ◦ animal species

 Non-REM sleep disorders ◦ Enuresis ◦ Sleep walking

 locus coerulus- in hindbrain (NE transmitter) ◦ important for arousal  What does it do during sleep?

 locus coerulus- in hindbrain (NE transmitter) ◦ important for arousal  What does it do during sleep? ◦ active when awake; inhibited during sleep – particularly REM

 Acetylcholine – in pons – important for REM onset ◦ AChE poisoning (mustard gas or pesticides)  people go into REM immediately after falling asleep- very vivid dreams and nightmares!  PGO waves –

 Increases in tryptophan – increases in 5HT  Increases in 5HT – increases in drowsiness (?)