Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
35 Cards in this Set
- Front
- Back
|
In animals, sleep is usually characterized by... (5) |
• behavioral quiescence, with the exception of aquatic mammals and migratory birds • species‐specific posture and location • elevated arousal threshold (=reduced responsiveness to stimuli) • rapid reversibility (contrary to other quiescent states, like hybernation) • homeostatic regulation (a compensatory increase in duration/intensity following sleep loss) |
|
|
Of 30+ animal phyla, sleep info is only known for... |
Chordata (includes vertebrates) and Arthropoda (includes insects) |
|
|
Mammals: Placental and Marsupial mammals show...... |
SWS and REMS, with the EEG characteristics like humans, cats, rodents |
|
|
What are the two species of Monotremes (egg-laying mammals) ? How does sleep happen in each? Implications? |
Echidna: - early study showed SWS but not REMS - later looking at brainstem showed that during SWS reticular neurons fire in irregular patterns similar to REMS - combination of SWS and REMS-like aspects in single sleep state Platypus: - similar findings. REMs and twitching of head seen while cortex shows slow waves - spend 8 hours a day in this REMS-like state WHAT DOES THIS SAY? since they represent an earliest branch of mammalian evolution, the characteristics of their sleep suggests that REMS and NREMS evolved as a differentiation of a phylogenetically older sleep state which showed mixed characteristics. (so the common ancestor with the placentals and marsupials mammals prob had these traits) (these monotremes are probably more similar to this ancestor) |
|
|
What is the most studied class of aquatic mammals? Describe their sleep. |
cetacean (dolphin and porpoises) they show: - uni-hemispheric SWS (USWS) where one hemisphere has EEG of SWS and other is W - during USWS, they will swim and surface to breath, their posture is symmetrical! - Lighter stages of SWS can occur concurrently in both hemi. - they also show twitching and REMs but REMS has not been recorded - Killer whales and dolphins dont show sleep signs for several months after birth- so it cant really be for development... |
|
|
Sleep in manatees.... Sleep in seals... |
• Manatees exhibit USWS and small amount of REMS • Some seals (Phocidae family) sleep normally on land and hold their breath during periods of bilateral SWS (BSWS) and REMS underwater • Other seals (Otariidae family) sleep normally on land, where they show BSWS and long REMS episodes (up to 15 min). When they sleep on the surface of the water, they show USWS with very short REMS episodes (< 5 sec). UNLIKE dolphin, they have unsymmetrical posture during this, but rather the contralateral flipper is active |
|
|
Why has unequivocal REMS not been recorded in cetaceans? |
• Possible explanations:‐ cetacean may have lost REMS secondarily ‐ current electrophysiological techniques are not adequate ‐ REMS could occur in very small amounts ‐ REMS could occur in a modified form in cetaceans |
|
|
USWS in dolphins seems to be... |
homeostatically regulated independently in the 2 hemis. similar to the use-dependent SWS in humans, the SWs seem to have higher power in the hemisphere that has been awake. |
|
|
How is the brain of a bird organized? |
• Birds have brains comparable in relative size to mammals. Like mammals, they show cognitive abilities like vocal learning and tool making • However, their brain is organized quite differently from mammals • The dorsal 2/3 of the avian forebrain (originally thought to be striatal) derives embryonically form the pallium, the same tissue that gives rise in mammals to the NeoCx. The avian pallium is instead organized in a nuclear manner and lacks the laminar organization of the NeoCx |
|
|
Despite a difference in brain structure in humans and birds ... |
birds are the only non‐mammalian group to show unequivocal SWS and REMS!! • Since SWS and REMS have been recorded in all avian species investigated, both sleep states were probably present in the most recent common dinosaur ancestor to birds |
|
|
Describe SWS in birds (avian) (4) |
- same as in mammals, low frequency, high voltage - SWA is greatst early and then declines - after SD, there is a compensatory increase in the SWA like mammals - Often also have USWS, especially when perceived dagner. Birds can direct the open eye towards the potential danger and can respond to it
|
|
|
Describe REMs in birds (5) |
- short REM episodes (2-10 sec) which occur in clusters - only about 8% time spent in REMS compared to 17% in mammals -REMS increase during the night like mammals - EEG pattern is similar to wake, REMs occur, twicthing, reducion in thermoregulatory response, reduction in muscle tone (but complete atonis in neck only if they can rest head on back)- REMS increases after SD - Unlike SWS, REMS is bi- hemi ONLY |
|
|
The presence of SWs during sleep seems to be due to the connections within the neocortex. How do mammals, birds, and reptiles differ? |
• Mammals: corticortical connections in layers 2‐3 play arole in synchronizing slow neuron oscillations andgenerate slow waves • Birds: they lack a true neocortex, but their hyperpallium (wulst) shows extensive interconnectivity • Reptiles: their three‐layered dorsal cortex lacks the equivalent of the mammalian layers 2‐3 and shows limited corticocortical connectivity SO mammals and birds, but NOT reptiles have SWs |
|
|
Sleep in amphibians |
• Amphibians gave rise to land vertebrates • Modern amphibians are interesting because their sleep may be more similar to that of the ancestor animals than ours • Detailed sleep studies are sparse and variable and contradictory. However, they support the existence of behavioral sleep with possible electrophysiological correlates (slow waves in the South American toad; spike‐like activity in the frog Rana Temporaria; decreased EEG frequencies in the salamander) |
|
|
Sleep in fish |
- few studies done -behavioural sleep seen, and homeostatic regulation - Zebrafish only shows sleep rebound after SD if the fish is released into darkness. In the light, constant suppression of sleep is seen. Once in regular environment, sleep is gradually seen after several days - might be similar to migrating birds |
|
|
Sleep in invertebrates (research focus, vs mammals, Honey bees, Drosophila) |
- research focused on Anthropods (honey bee) and Drosophila (fruit fly) - there are major dif between mammals and invertabrates, for ex. orexins are not found in invertebrates, and octopamine (major sleep transmittor in Drosophila) is not seen in mammals. - Honeybees: periods of quiescence with increased arousal threshold and antenna immobility, neurons have lowered sensitivity and sleep is homostatically regulated Drisiohila: response threshold increases, but will rapidly awaken to stimuli. They have a sleep rebound after sleep deprivation |
|
|
Other phyla that may show sleep: |
Nematods (like C. elegans), Mollusca (i.e. cephalopods like octopus and sepia) and Cnidaria (like box jellyfish) |
|
|
What is the Drosophila Monitoring system? |
|
|
|
Why are sleep studies not exhaustive? |
- more is known about mammals that other animals, but even still we only know about 200/5,000 mammals. - the ones we can study in the lab or non invasively (these animals have artificial light available food, neutral temp.) - only about 60 of the 100 have been sufficiently studied for REM/NREMS, and very few for things like arousal threshold and rebound |
|
|
Correlational studies in mammals have been able to find some small correlations, what are they for sleep cycle duration, sleep time, REMS time? |
A) DURATION OF SLEEP CYCLE: - strongest correlation seen - Brain weight + duration of cycle= positive corr - Metabolic rate/ body temp= negative corr - accounts for 80% of variance in sleep B) TOTAL SLEEP DURATION: - negatively correlated with boy weight - positively correlated with metabolic rate/temp - this seems to support the energy conservation hypothesis of sleep, but it was later found that the neg correlation between total sleep time and body weight was only seen in herbivores. C) REMS TIME: - negative correlation with brain weight and encephalization (brain/ body weight) - this only accounts for 4% of the variance in REMS - One study found that higher encephalization actually meant more REMS, which would support neurophysological role of REMS - no such correlation seen in SWS, but SWA might be different |
|
|
Correlational studies in mammals have been able to find some small correlations, what are they for predatorial risk, and immaturity? |
D) PREDATORIAL RISK - high risk, less sleep - sleeping in risky places may result in less REMS, but the SWS time is largely independent from this - intensity of SWS may correlate with this, but measurements are needed E) IMMATURITY AT BIRTH - more altricial (immature) species at birth show more REMS as adults - this is not dependent on predation risks, but may effect an extension of ontogenetic changes in REMS - this would support the idea that REMS is particularly more important in brain development, but we dont know why it persists to adulthood |
|
|
What are CNS stimulants? |
- drugs that have an altering effect, improve the mood and quicken the intellect - their action implies an increase in neuronal activity due to increased excitation, decreased inhibition, or both - generic term used to all wake-promoting compounds of potential use in the treatment of Excessive Daytime Sleepiness EDS (common to patients with sleep disorders) |
|
|
What are the main CNS Stimulants? |
• Modafinil/Armodafinil • Amphetamines • Caffeine |
|
|
MODAFINIL/ARMODAFINIL: names, type of drug, what is it for? |
NAMES: • Modafinil commercial names: Provigil, Alertec, Modavigil, Modalertec • Armodafinil commercial name: Nuvigil TYPE: • Modafinil is a racemic drug, while Armodafinil represents just the active (‐)‐(R)‐enantiomer - both are sched 4 drugs with lower potential for abuse than amphetamines WHAT FOR? - developed for narcolepsy - has FDA approval for narcolepsy, residual sleepiness in apnea, shift work - effective for Jet lag, ADHD, depression and schiz bit no approval - drug abusers dont like it |
|
|
MODAFINIL/ARMODAFINIL: what are the main effects? |
- improve daytime sleepiness without interfering with sleep - 100-300mg in morning - less agitated than amphetamines, no rebound hypersomnolence once you stop - only limited efficacy for cataplexy and abnormal REM symptoms Side effects: - well tolerated - headache, nausea - does not increase BP, HR or pupil size |
|
|
MODAFINIL/ARMODAFINIL: Mechanism of action (where does it act and where does it not?) |
- involves DAT Dopamine transporter- to which it binds with low affinity. It would thus inhibit dopamine reuptake by the dopaminergic terminals leading to increased extracellular dopamine levels - it activates the orexin neurons of the LH, and histamine neurons of the TMN - also appears to inhibit the VLPO, which would disinhibit orexin and histaminergic neurons, further promoting W - At therapeutic doses, Modafinil has no effect on the serotonin transporter (SERT) and serotonin receptors - Modafinil does not seem to act on the noradrenergic system. It does not bind to the noradrenergic transporter (NET) or to noradrenergic receptors. For this reason, it does not affect blood pressure, heart rate, pupil size |
|
|
Why might Modafinil, unlike unlike other DAT inhibitors (ex. amphetamines), have a low potential for abuse? |
low solubility (can be taken only orally and NOT iv) , low potency (it is impossible to greatly increase the effects), slowabsorption (no rapid brain effects), atypical interactions with DAT |
|
|
AMPhETAMINES: types of drugs and structure |
‐ D‐ and L‐ Amphetamine (Adderal, Dexedrine) ‐ Methamphetamine (Desoxyn) ‐ Methylphenidate (MPH; Ritalin) * structure similar to dopamine * they are all schedule 2 drugs |
|
|
AMPHETAMINES: Mechanism of action |
• They increase synaptic concentration of monoamines (especially noradrenaline and dopamine) 1) transported to terminals by plasma membrane transporters (esp DAT, NET), where they decrease monoamine reabsorption with a competition mechanism 2) once in terminal, they are transported into the synaptic vesicles by the vesicular monoamine transporter (VMAT)With a competition mechanism, they decrease monoamine transport in the vesicles. They also displace monoamines from the vesicles. These 2 actions cause increased monoamine concentration inside cell and also their reversed transport through the plasma membrane transporters |
|
|
AMPHETAMINES: what are they for? |
-Amphetamines and methylphenidate primarily for the treatment of narcolepsy, idiopathic hypersomnia and ADHD - methamphetamine ADHD and obesity - can help with fatigue form MS and HIV, small effect on depression - during sleep deprivation healthy individuals report subjective feeling of improved attention, memory, concentration and fatigue and they show improvedperformance on a variety of tests |
|
|
AMPHETAMINES: What are the main effects? |
- increase W, decrease S duration with a decrease in all stages but an increase in stage N1 - decrease fatigue and appetite - In narcoleptic patients, they also decrease the occurrence of cataplexy and all abnormal REMS related symptoms Side effects: - cardio, sweating, pupil, dryness of mouth - mood, agitation, headache, psychosis, anorexia - sleep disruption - addiction potential |
|
|
CAFFEINE: what type of drug is it? |
- most commonly used CNS stimulant ‐ Caffeine belongs to the methylxantine class ‐ Xantine is a purine base similar to adenine and guanine ‐ Theophilline (found in tea) and theobromine (found in chocolate) also belong to themethylxantine and have action similar to caffeine |
|
|
CAFFEINE: Mechanism of action |
- antagonist of adenosine A1, A2 receptors - Endogenous Adenosine has been shown to suppresse the TMN histaminergic system via A1 receptors and to promote NREM sleep. The TMN could be one of the site of action of caffeine as a stimulant - Caffeine also inhibits phosphodiesterase (degrades cAMP into AMP), thus resulting in increased cAMP levels and increased activation of protein kinase A. This action is at the basis of an antinflammatory and diuretic effect of caffeine |
|
|
CAFFEINE: Main effects |
• Increased mental alertness • Faster and clearer flow of thought • Reduced fatigue • Wakefulness • Delayed sleep onset • Restlessness • Cardiovascular effects: palpitations and hypertension • Increased gastric acid secretion • Increased urine production - 4+ cups per day can give caffenism syndrome- tachycardia, insomnia lethal dose= 5-10 gr. |
|
|
What are some future developments of CNS Stimulants? |
• Orexin receptor agonists: low‐molecular‐weight agonists need to be developed. They are expected to be beneficial in narcolepsy and excessive daytime sleepiness(EDS). They are also predicted to be useful for treating migraine and cluster headache (Ox modulate pain) • Histaminergic H3 receptor antagonists (H3 receptors are located presynaptically on histaminergic fibers and inhibit histamine release) They are inhibitory. so if you inhibit the inhibition= increased wakefullness |
