essay plans Flashcards

Question

the neural basis of sleep

Answer 1

- neurochemical and hormones cause sleep-wake cycles - melatonin secreted by pineal gland during dark promotes sleepiness Adenosine: accumulates during the day after prolonged wakeness --> promotes sleep - caffeine antagonises its effects observations: patients with encephalitis: - some = constant sleepiness - base of brain damage - some = insomnia - anterior hypothalamus damage - anterior hypothalamus contains inhibitory neurotransmitters such as gaba - damage in rats = insomnia and death - electrical stimulation = sleep Reticular activating system - RAS: nuclei in the brainstem that extend to the forebrain and promote arousal orexin/hypocretin --> peptide released from lateral hypothalamus - responsible for maintenance of wakefulness - implicated in narcolepsy

Answer 2

- associated with 24h cycle such as day or night - endogenous cycles = generated from within - our brain and body spontaneously generate its own rhythms based on the earth's rotation - endogenous rhythms can be annual - migration or seasonal - breeding - humans = diurnal - 24hr rhythm controls sleep, wakefulness, eating, drinking, body temp, hormones, urinations, sensitivity to drugs Aschoff: - humans placed in underground bunker - no external cues - allowed to select light-dark cycle by turning lights on and off - showed daily sleep-activity rhythms that drifted to more than 24hrs - have an endogenous biological clock which governs sleep-wake behaviour - Zeitgebers - cues that serve to set our biological clock - most important = light - others = meals, activity, temperature - zeitgeber resets biorhythm = untrained Jet-lag - disruption in circadian rhythm due to crossing of time zone - stemps from mismatch of internal circadian clokc and external time - sleepines and impaired concentration west = phase-delays east = phase-advances chronotypes = different patterns of wakefulness and alertness --> individual differences morning people = larks evening people = owls genetic basis but also change with age and other external factors - lifestyle, social factors, etc infancy and child hood + adulthood and old age = larks adolescense = night owls/'eveningness' differences between people = social jet lag morning people = happier

Answer 3

- Richter suspecting biological clock --> electrical lesions in various areas of rat brains - lesion in hypothalamus = loss of rhythm suprachiasmatic nucleus = the clock - SCN - lesion disrupted circadian rhythms of wheel running, drinking, hormonal secretion - 'master clock' - neurones in SCN = ore active during light period than in dark period - single cell removed to culture tissue - continue to function in rhythmic patter - transplantation of an SCN into a donor organism = recipient follows donors rhythm How does light reach SCN: - through the retinohypothalamic tract - by special ganglion cells PRGCs - PRGCs have their own photopigment - melanopsin responds directly to light --> do not rely on rods/cones what makes the clock tick? - per genes and per protein - builds up in cells overnight and is broken down during the day - tim gene and tim protein - tim meets per = period gene shut down transcription-translation-inhibition- feeback loop - transcription from DNA to mRNA to translation into proteins - form dimers - dimers enter the nucleus - dimers inhibit transcription then decay - daily rhythm SCN effects on the pituitary and the pineal gland - - SCN regulates waking and sleeping by controlling activity levels in other areas through its effects on the pituitary and the pineal gland - The SCN drives a number of slave oscillators, each responsible for the timing of a different type of behaviour i.e. drinking, sleeping, body temperature,activity etc breeding is controlled by the SCN in winder via the pineal gland: - winter = increased melatonin = shrinks the gonads - spring = less melatonin - enlarged gonads - testosterone - mating - time of day effects human cognitive performance - drug toxicity 20-80% depending on time of day - illness risk depends too - heart attack/stroke us higher in morning

Answer 4

definition: anxiety = apprehensive uneasiness or nervousness over an impending or anticipated ill (Merriam-Webster) - normal part of life - does not have one broad identifiable trigger - similar response to stress e.g. faster heart-rate/breathing - anxiety disorder = more intense fear/anxiety inappropriate for the circumstance - ^ likely due to cumulative effects of stress --> contributes to depressive and substance abuse disorders - women more likely to experience than men Panic disorder: - episodic attacks of acute (seconds-hours) anxiety/terror - symptoms: hyperventilation (low CO2), irregular heartbeat, dizziness, faintness, fear of losing control and dying - Culturally: Asian, African and Latin American countries have lower rates than the USA Agoraphobia: - intense fear/anxiety about leaving home/being in open/public areas, lines/crowds, etc - cope through avoidance due to disproportionate fear e.g. staying home for years due to fear of a panic attack GAD: - excessive, uncontrollable worrying and anxiety from a wide range of situations and difficulties controlling these symptoms - e.g., sense of impending danger, sweating, trembling, difficulty concentration - ^women Social anxiety disorder: - persistent excessive fear of being exposed to the scrutiny of others e.g., public speaking/group conversations --> sweating/blushing - equal in men and women - culturally for GAD and SAD --> more prevalent in Europeans than Asian, latino, African Descent brain changes linked to anxiety disorders: - functional imagine (PET & fMRI) show changes in the prefrontal cortex, anterior cingulate cortex and amygdala - Pfleiderer et al 2007: increased amygdala activity during panic attacks - Phan et al 2005: increased amygdala activity in response to presentations of faces with anger, disgust and fear in SAD - activation correlates with symptoms - Monk et all 2008: adolescents with GAD exhibit increased amygdala and decreased ventrolateral prefrontal cortex activation - also see lack of suppression of amygdala via the vmPFC - which plays a role in the surpression of fear - Treatments: - Benzodiazepines (BDZ) reduces anxiety and anxiety-like behaviours in animals: experiment with rats: - enclosed arm - less anxiety inducing - less likely to fall (walls either side) - open arm (no walls) anxiogenic - BDZ rats spend less time on the open arm - they walk across quicker - less anxious - it binds to the inhibitory GABA A receptor as an agonist - increasing CI- influx which causes hyperpolarisation Paulus 2005: - BDZ reduces amygdala activity when looking at emotional faces - Flumazenil (antagonist) dishibits action at GABA A receptors and produces panic in panic disorder patients --> can treat BDZ overdose - if the treatment reduces the symptoms and opposite treatment causes - correlational evidence that these areas are responsible - abuse is likely because it causes a relaxing effect /withdrawal and patients typically feel less calm when stop taking withdrawal and sedation --> better compounds with fewer side effects are needed Treatment by increasing neurosteroid synthesis: - neurosteroids are neuroactive steroids --> synthesises in periphery and CNS - increase activity of GABA receptor - during anxiety attacks - neurosteroid synthesis = suppressed = suppression of GABA A receptor function Nothdufter et al 2011: XBD173 enhanced neurosteroid synthesis and reduces panic - without the withdrawal and sedation symptoms compounds that affect the serotonin and glutamate systems can also be used to treat anxiety: - Asnis 2001: Fluvoxamine, an SSRI, reduces panic attacks - Ressler 2004: similar findings with D-cycloserine (DCS) - an indirect agonist of NMDA receptor - also facilitates extinction of conditioned fear in animals - walker 2002 - the reduction of symptoms allows patients to attend behavioural therapy and extinguish fear responses

Answer 5

- aggression is common across many species ---> survival, mates, protecting offspring - behaviours relate to threat (warning), defensive (attack) and submission (defeat) Brain circuits and aggression: - Gregg and Siegal 2001: - Electrically stimulating the periaqueductal gray (PAG) in cats --> elicits aggressive attack and predation - excitatory and inhiborty connections between the hypothalamus & amygdala and the PAG can affect - medial hypothalamus --> Dorsal PAG --> defensive rage - lateral hypothalamus --> ventral PAG --> predetory attack - amygdala nuclei control these pathways Aggression and serotonin: - animal studies - Audero 2013: increasing serotonin transmission reduces aggression - Mosienko 2012: reducing serotonin synthesis increases aggression - Vergnes 1988: reducing serotonin transmission via destruction of serotonergic axons increases aggression - Howell 2007: low levels of serotonin metabolite (5HIAA) in cerebrospinal fluid in rhesus monkeys ins linked with aggression - picking fights with bigger monkeys - higher risk taking - this suggests serotonin inhibits aggression and controls risky behaviours Human studies: - mixed evidence that serotonergic neurons play an inhibitory role in aggression - Duke 2013 - Low serotonin metabolite in cerebral spinal fluid = linked with antisocial behaviour and aggression - SSRI have shown to reduce aggressive behaviour in some cases Aggression as a reward: - a reward: objects, actions, experiences that attain positive motivational property THEY INCREASE THE PROBABILITY OF THE ACTIONS THAT LEAD TO THEM street addiction - former gang member - sight of yellow police tape - 'my heart is beating, my hands are sweating, i am not scared - i am excited - i want back in the game' - Elbert 2010: some individuals exhibit appetitive aggression, motivated by intrinsic reward - Cronbach 2013: this is an adaption to violent environments --> makes individuals more functional in violent settings (e.g. war-afflicted communities) --> elevated social status - Animal models allow us to study this behaviour under controlled conditions: - conditioned place preference (CPP) - instrumental conditioning Conditioned Place preference (CPP): Golden 2016 - REWARDS: drug, food, social rewards - mice/rats - two chambers with a door between the two BEFORE CONDITIONING: - all chambers are neutral stimuli CONDITIONING: - one chamber is paired with a rewards - the other is not AFTER CONDITIONING: - several reward-chamber pairings --> reward paired side acquires motivational significance - acts as the conditioned stimulus - if the substance is 'rewarding' --> animals spend more time in the chamber it has been paired with --> preference CPP with aggression: BG info: male rats are very territorial after sexual experience and will attack an unfamiliar intruder DURING CONDITIONING: - resident attacks intruder in the 'paired side' - no intruder in the 'unpaired side; AFTER CONDITIONING: - resident mouse spends more time in the paired side in the absence of the intruder MEANING: - mouse finds the attacking as rewarding and associates the chamber with it Operant/instrumental conditioning: - animals press lever for food reward in operant 'Skinner' chamber - the reward sustains the lever press response (reward self-administration) - reward-seeking - animals press lever even in absence of reward EXPERIMENT: Golden 2019 - animals press lever and intruder chamber opens - letting an intruder in (aggression self-administration) - trained animals will press lever even in absence (aggression seeking) Does aggression self-administration and seeking activate the reward system in the brain? - nucleus accumbens (NAc) - key role in reward and motivated actions e.g. food and drug-seeking - activated by rewarding experiences e/g/ drugs of abuse, food, water and sex - measured by: activity-sensitive protein - 'Fos'

Answer 6

what is pain? - an unpleasant sensory and emotional experience associated with actual or potential tissue damage or described in terms of such damage - promotes avoidance of situations that may decrease biological fitness - promotes resting behaviour that enhances recovery following injury or modifies behaviour so that further injury or death become less likely

Answer 7

detecting pain: - activate sensory receptors and nociceptors nociceptors: - sensory neurones specific to pain - free nerve endings - synapse in spinal cord to ascending neurons to brain polymodal nociceptor: - free nerve endings - contain receptors sensitive to noxious stimuli - respond to multiple stimuli such as intense pressure, heats, acids, capsaicin and ATP release high threshold mechanoreceptors: intense pressure stretching, striking, pinching vanilloid receptor, TRP channels (temperature-gated channels): heat, acids, capsaicin (chilli) purinergic receptors: ATP release --> channels opne neuron depolarizes - fires action potentials

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