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Lecture 11: EmotionsWhat are emotions? ● Consistent & discrete responses to an event of significance ● Help direct an appropriate course of action and associated with particular physiological states ● Help organise other aspects of cognition e. attention ● The study of emotions & the...

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Lecture 11: Emotions What are emotions? ● Consistent & discrete responses to an event of significance ● Help direct an appropriate course of action and associated with particular physiological states ● Help organise other aspects of cognition e.g. attention ● The study of emotions & their impact on cognition is called affective neuroscience ● Stimulus -> perception -> emotion -> physiological response (James-Lange) ● In every emotion, there is a cause i.e. a sense impression, and an effect i.e. changes in bodily & mental function ● Cannon & Bard argue that perception leads to an emotion, but also response control ● Schachter-Singer argues physiological response comes before emotion ● The most common model comes from Ledoux & Phelps - sensory processing & long term memory interact to form working memory (substrate of our awareness), emotional processing informs working memory and emotional responses ● Also argue emotions are an independent process in the brain but contribute to WM & emotional responses Limbic system & emotions: ● Limbic system hypothesis - an emotional system mediates functions required for survival of individual & species ● Brain areas included in this - hypothalamus, anterior thalamus, cingulate gyrus, hippocampus ● Amygdala, septal nuclei, orbitofrontal cortex & parts of the basal ganglia also play a role ● The Papez circuit has expanded to include the amygdala, as well as part of the frontal cortex (a neural circuit for the control of emotional expression) ● The limbic system concept has limited utility as by its definition the whole brain would need to be included in emotion but many of these areas are involved in other processes ● The amygdala is a key conduit and conductor of emotional responses, which allows quick responses to relevant external stimuli as well as integrating finer details from the cortex Understanding emotions through emotional faces: ● Duchenne believed that you can see the soul through the face ● In 1882 he showed how specific muscles were recruited to give rise to specific expressions through electrical responses ● There are universal emotional states of faces e.g. anger, fear, disgust, surprise, happiness & sadness (Ekman et al 1969) ● By 10 years old children are as good as adults at discriminating displays of emotional ● Computers can also categorise emotional faces

Dedicated circuits for emotional processes: ● Some people with cortical lesions can’t smile on request but can smile in response to relevant stimuli eg. a joke ● There are two streams for facial emotion - a volitional motor system (includes motor cortex & basal ganglia) and an automatic system (includes hypothalamus, amygdala & frontal cortex) An emotional role for the amygdala: ● Kluver & Bucy (1937) - removed the temporal lobes of monkeys & discovered behavioural changes e.g. hypersexuality & lack of fear ● The emotional component of these changes is due to the destruction of the amygdala (Weiskrants 1956) ● Conditioned fear - rats, US + NS = CS, CR, amygdala key in conditioned fear ● The amygdala consists of at least 13 subnuclei, the most important being the central nucleus, basal nucleus & lateral nucleus ● Lateral nucleus - gets the input from the hippocampal formation, the thalamus & the cerebral cortex ● Basal nucleus - integration between lateral & central nucleus ● Central nucleus - projects to the hypothalamus, organises emotional responses ● Auditory thalamus projects to amygdala and auditory cortex (same with somatosensory thalamus & cortex), which are linked to the pairing of stimuli ● Therefore, the sensory input can be routed via the thalamus or the sensory cortex to the amygdala, the cortex is not required but can contribute to the responses the amygdala makes ● Dual-route hypothesis - the cortex provides a slow, fined grained route for fear, while the thalamus provides a quick and dirty route which helps fast reactions ● Thalamus allows a quick response but the cortex is more refined and slower (low road vs high road) ● Low road (thalamus) may prime the amygdala to receive the inputs from the sensory cortex ● The two roads converge to elicit a greater emotional response ● There is evidence for this hypothesis in rats & humans ● Fearful faces attract more attention than neutral faces, better at perceiving them quickly ● Awareness and cortical processing isn’t necessary for emotional stimuli ● Criticism of dual-route hypothesis - faster processing doesn’t necessarily mean subcortical involvement, there is no obvious subcortical visual route to the amygdala in primates, the amygdala may not be always needed to detect emotional states

Impact of emotions on other processing: ● Emotional networks are highly interconnected with the amygdala being at the center ● Emotions influence all actions of brain processing ● The prefrontal cortex contributes to emotion-informed decisions eg would you kill one person to save many ● Emotion changes memory - increased arousal increases memory formation but not accuracy ● Two distinct mechanisms support memory enhancement for emotional information:● Enhancement for valence items - supported by PFC-hippocampal network ● Enhancement for arousing items - mediated by the amygdalar-hippocampal network Lecture 12: Social bonding Affiliation: ● Encompasses social bonding between individuals, sexual partner relationships & parent-infant relationships ● Social support promotes adaptation & stress coping ● Social isolation is common in psychiatric disorders ● The ability to recognise conspecific (animal of same species) is imperative in determining the proper response & forming social memory ● To study affiliation 3 tasks are explored - approach to the parent/infant/partner, recognising individual amongst others, and looking at how animals invest their time in other animals they are bonded to ● Approach to parent, infant or partner - driven by smell, pheromones secreted which trigger a social response in the same species, vomeronasal organ detects pheromones & relays info to the accessory olfactory bulb (AOB) ● Humans don’t have a vomeronasal organ, it regresses during foetal development ● Social memory is commonly examined in rats by two paradigms:● Social recognition - a subject animal is exposed to a stimulus animal and later re-exposed to it or a novel stimulus animal, the animal usually spends more time investigating the novel stimulus animal, the time length tells you how much the subject recognises the original animal ● Social discrimination - on the re-exposure, the animals are presented simultaneously, forcing the subject to choose between the two ● Humans are semi monogamous, we show bonding with different animals ● Oxytocin and vasopressin play a role ● Montane voles are non-monogamous & prairie voles are monogamous ● Nucleus accumbens is important in repeating behaviour ● Prairie voles injected with oxytocin want to mate more

Oxytocin & vasopressin: ● Neuropeptides (protein molecules) that act slowly & regulate social bonding ● Both made in the hypothalamus ● Transported to the posterior pituitary gland where they’re released into the bloodstream from axon terminals ● Use cells in the hypothalamic areas to transmit information to molecules ● Infusion of oxytocin increases performance in facial recognition tests in humans ● Responsiveness of the amygdala to emotional faces is reduced after infusion of oxytocin (Domes et al) ● The amygdala is about reacting and needs to be suppressed to engage in prosocial behaviours Parenting behaviour: ● Seen in vertebrates and invertebrates including insects, reptiles, mammals ● The most common form of parenting is female uniparental ● Many species show biparental & some male uniparental, 90% of birds are biparental ● Appears to be highly conserved & antagonistic circuits controlling affiliative & aggressive behaviour towards offspring ● Adult animals may display parental care or aggression according to their physiological & environmental state ● Male mice stop committing infanticide and become parental towards pups after mating with a female, there are similar patterns in wild female mice but in lab females, they don’t show aggressive behaviour towards pups ● What causes the aggression to shift? - there is a time-dependent synaptic change triggered by mating & chemical cues released by females during pregnancy ● The default attack of the male mice is driven by factory information from the vomeral nasal organ which is shut down during parental care ● Estrogen, progesterone & prolactin are implicated in the regulation of female maternal behaviour ● Testosterone levels decrease during fatherhood in humans ● Two main circuits in social bonding & parental control - parental care & pup avoidance/aggression, which are mutually exclusive (one suppresses the other) ● Involve subcortical nuclei and prefrontal cortex ● These drive changes in the hypothalamus ● In male & most female virgin rats, the aversive circuit is dominant & suppresses parental care ● The facilitative circuit is activated & the avoidance circuit is silenced in postpartum females ● Oxytocin is involved in the initiation of maternal behaviour ● The ventral tegmental area of the dopaminergic system is involved in initiating & maintaining behaviour in rats ● Noradrenergic & serotonergic circuits are also involved ● Neurons in the MPOA that express galanin proteins are important, the presence of them leads to parenting behaviour in rats (Wu et al) ● A sexually dimorphic hypothalamic circuit controls maternal care & oxytocin secretion

Lecture 13: Sex & gender Sex: ● ● ● ● ● ● ● ● ● ● ● ●

For gene mixing, universal in most living things Sexual strategies can be complex The different requirements of the male vs female gamete-carriers has led to the evolution of sexual dimorphism Sexual dimorphism - the condition where the two sexes of the same species exhibit different characteristics beyond the differences in their sexual organs Dimorphism is also present in behaviour In humans there are 3 types of sexual dimorphism:Sex - refers to the assignment to male/female that was made at birth based on genital morphology Gender - refers to the psychological sense of being male or female Sexual orientation - refers to the gender of the people an individual is sexually to Male morphology + female identity = M-F transsexual OR transgender female Cis woman is female morphology + female identity Gender, sexual orientation & physical sex are nowadays on a spectrum

Biological basis for di/multi-morphisms: ● Hormones are chemicals produced by glands in the body which communicate with cells and regulate expression of genes ● The hormones of most relevance are oestrogen & testosterone ● Testosterone is an androgen, oestrogen is an oestradiol ● Both genders make oestrogen & testosterone there is just a difference in how much ● Effects of sex hormones are at two levels:● Organisational - control sexual differentiation ● Activation - acute effects, control behaviour ● The difference in gender is from a gene carried on the Y chromosome, either XX (female) or XY (male) ● SRY gene has organisational effects on sexual development ● Genital ridge embryo is undifferentiated at first, SRY causes undifferentiated to develop into a testis which leads to testosterone development ● In the absence of SRY gene, gonads form into an ovary ● In men, wolffian ducts develop & mullerian ducts regress (leads to male genitalia) ● Puberty is governed by gonadal hormones ● Under androgens influence, testosterone is developed ● Absence of testosterone & presence of oestrogen is developed which causes breast development

Organisational & activational control of sexual behaviour: ● Sex related behaviours fall into two categories - reproductive behaviours & sexassociated non-reproductive behaviours ● Studies of rats & mice quantify male-typical and female-typical behaviours ● A 1959 study showed that prenatal or neonatal testosterone organises later behaviour ● This implies that the brain is masculinised by androgens during foetal development (and the other way round) ● Masculinisation achieved via estradiol which is a metabolite testosterone ● The sexually dimorphic nucleus of the preoptic area (SDN-POA) in the hypothalamus is much larger in males (Gorski et al 1978) ● Removing testosterone in males early in life reduced SDN-POA volume ● Volume of SDN-POA has been found to be larger in rams who prefer female partners (Roselli 2020) ● In humans, early exposure to gonadal steroids has organisational effects, as well as postnatal socialisation & self-socialization ● In monkeys & human males have a preference for male toys Organisational effects of testosterone in humans: ● 3 conditions have helped elucidate the mechanisms of sexual differentiation congenital adrenal hyperplasia (CAH), congenital androgen insensitivity (CAIS) & 5alpha reductase deficiency (5-ARD) ● CAH - condition that arises from a faulty gene that affects pituitary hormones, gene defect means adrenal cortex doesn’t produce cortisol, so there is not a feedback loop to stop the pituitary from producing ACTH, so a foetus is exposed to high levels of androgens, if it’s a girl it has masculinisation of genitalia, also have male play patterns, diluted female identity & more likely to be lesbian ● CAIS - a chromosomally male XY foetus lacks testosterone receptors & becomes phenotypically female, they are infertile, no menstruation, short vagina, but appear & identifyas entirely female, usually heterosexual ● 5-ARD - an enzyme that converts testosterone to dihydrotestosterone (DHT), which is required for normal masculinisation of external genitalia, condition means this doesn’t occur and males are born with ambiguous genitalia, testosterone surge at puberty usually makes it more obvious they are male, sometimes switch from female identity to male identity ● 2D:4D ratio - ratio of 2nd finger to 4th finger, in women they tend to be same length, in men the 2nd is shorter, a marker of prenatal testosterone exposure, trans men have a similar ratio to females but trans women have a greater ratio than men and more similar to women, suggesting their masculinisation of the brain was lower than cis men ● INAH3 in humans is a sexually dimorphic nucleus in the brain, meaning its size is bigger in males ● Humans also have sexually dimorphic grey matter, which correlates with foetal testosterone

Lecture 14: Reinforcement & the striatum Why do we do the things we do? ● To satisfy a basic drive ● They bring us pleasure ● They will make something pleasurable happen in the future ● We feel compelled to ● To avoid unpleasant consequences ● Most things are done because of a range of combinations of these factors ● There are neurotransmitter systems in the brain involved with happiness, pleasure, motivation & reinforcement What is reinforcement? ● Most goal-directed motivation is learned ● This learning occurs through the selective reinforcement of associations between rewards & otherwise neutral stimuli ● Appetitive reinforcement is positive e.g. receiving food ● Aversive reinforcement is negative e.g. a painful stimuli ● Conditioned fear is the most used example of conditioning ● Olds & Milner - positive reinforcement produced by electrical stimulation of septal area and other regions of rat brain (self stimulation) ● Ventral tegmental area & substantia nigra are key for dopamine ● Ventral striatum (nucleus accumbens in humans) is part of the basal ganglia complex ● Two pathways run through medial forebrain bundle, which are the mesolimbic pathway & mesocortical pathway ● Nucleus accumbens has widespread projections, e.g. into motor cortex, and is a driving centre for activation for movement for actions in terms of providing a reward signal ● Accumbens dopamine rises in response to food & sex Reinforcing drugs & lesion approaches: ● Nicotine causes a rise in nucleus accumbens dopamine ● Nicotine exerts its influence via the ventral tegmental area, ● Cannabis also causes a rise in dopamine ● Cocaine & amphetamines cause a rise in dopamine ● Blockade of dopamine increases cocaine self-administration ● Lesions to the nucleus accumbens reduce cocaine self-administration ● Thus NA is vital for maintaining the drive to self-administer ● Heroin and morphine act via endogenous opioid system whose normal function is to suppress pain until danger has passed ● Injections of opiates cause a rise in NA dopamine ● However, lesions to the NA do not impair opiate self-administration (meaning there must be a separate pathway) ● It’s thought that opiates act in the VTA by reducing GABA inputs to the neurons, hence increasing dopamine release in NA

Does dopamine signal pleasure? ● Some counter arguments - addicts often continue to take drugs even when they don’t feel pleasure, dopamine surges also occur after unexpected or painful events ● Affective neuroscience has identified dissociable subcomponents of reward:● Liking - refers to the subjective feeling of niceness ● Wanting - having the desire to obtain something, an addict may want a cigarette despite not liking smoking ● Liking & wanting processes lead into our subjective feeling of if we have had a reward (Berridge 2018) ● Wanting is dominant across the brain, a kew output is dopamine from the VTA to the NA, also contains circuits out into the amygdala, brainstem nuclei, stratium ● Brainstem nuclei & orbitofrontal area are key for liking ● Orbitofrontal cortex activity may code for stimulus valence (Rolls et al 2003), the activity correlated with the subjective ratings of pleasantness in an experiment with 3 pleasant & 3 unpleasant odors ● Araujo et al 2003 found something similar with water ratings in a thirst experiment ● O’Doherty et al 2001 also found this correlation with monetary rewards in an experiment ● The nucleus accumbens is thought to be doing the learning process i.e. expecting rewards in the brain ● Unexpected juice reward led to dopamine release in monkeys, which drove VTA to fire neurons ● Dopamine neurons respond to expectation of reward, not reward itself (Schultz et al 1997) ● If you don’t give the monkey a reward even if it is expected, there is an absence of firing of neurons (prediction error signal) ● The ventral striatum is likely linked to expected reward also ● The longer people are willing to wait for a monetary reward, the less the activity is in the striatum (Ahmad et al) ● The striatum seems to be linked to immediate reward obtaining ● The prefrontal cortex is key for suppressing the drive to ‘act now’ and to wait for a bit of pay off later on Summary: ● Early studies pointed to the mesolimbic dopamine system as a pathway for reward ● This system involves the ventral tegmental area & its projections via the medial forebrain bundle to the nucleus accumbens ● More recently, it has been recognises that reward has subcomponents wanting, which is dissociable from liking ● The VTA-NA pathway may be more involved with monitoring & prediction ● Other structures collaborate to form the full picture of pleasure e.g. orbitofrontal cortex may encode stimulus valence

Lecture 15: Amnesia What is amnesia? ● The profound loss of memory in the presence of relatively preserved cognitive abilities ● By studying a system when it breaks down we can learn a lot about how that system functions normally Types of amnesia: ● Psychogenic amnesia:● Hard to study & prove people have it ● People have no brain damage but report having amnesia ● Different types, sometimes people have split personality disorder ● Organic amnesia:● Most research is on this ● Transient - patients have memory loss but over time their memory function recovers somewhat ● Persistent - degenerative (eg Alzheimers) or non-degenerative (brain injury -> amnesia but there is no decline) ● Non-degenerative - material specific (profound loss of visual or verbal material) vs global (sudden, temporary episode of memory loss that can't be attributed to a common neurological condition) Brain regions involved: ● Hippocampus:● The most well known region to be involved ● Memory needs new neurons to be grown ● Perihinal cortex & parahippocampal cortex communicate to send signals to entorhinal cortex which communicates with hippocampus ● A lot of structures linked to Papez’s circuit are important for memory e.g. retro...