Positive emotion and anhedonia Flashcards
The basic emotions
Happiness, Anger, Disgust, Sadness, Surprise, Fear
Conserved facial expressions, non-reducible, non-overlapping
Why are emotions useful?
Drive bodily responses (or are driven by them..? Schacter and Singer, 1972, adrenaline and stooges), important for survival
Drive cognitive responses - affect decision-making, attention, memories
Drive behavioural responses - important in flexibility, communication, motivate (reward-seeking and avoidance behaviour)
Patient SM
1994 - Urbachs-Wiethe disease, calcification of amygdala
impaired at recognising negative emotion - failed Doris Day test (shown her screaming, ‘what is she doing?’)
Showed no fear to various stimuli, inc movies and handling snakes and spiders
BUT experienced fear herself, and panic attacks worse than controls, when exposed to feelings of suffocation from CO2 inhalation.
Impaired at judging trustworthiness, impaired at recognising negative social cues
Understands the concept of personal space, but doesn’t require it (will comfortably stand nose-to-nose with full eye contact)
Parsing positive emotion - what subtype and how’s it measured
Learning - cognitive (verbal explanation, expected reward) and associative (pavlovian or operant conditioning)
Affect - conscious ‘liking’, measured by survey, and subconscious hedonic response measured by facial expressions etc
Motivation - conscious ‘wanting’, stated desires, and subconscious drive, implicit incentive salience, measured by autoshaping, pavlovian-to-instrumental transfer (general is CeN-dependent, specific is BLN-dependent, Fernando et al 2013)
Dopamine is involved in motivation (animal studies)
Salamone et al 2007 - Rats with DA depletion or antagonists in nucleus accumbens will do less lever pressing for sucrose solution,
Correa et al 2002 - DA depleted rats won’t go over an obstacle for sucrose (will take the regular food and no obstacle instead).
Dopamine is not involved in affect (animal studies)
Cannon and Palmiter, 2003 - Dopamine depleted mice (can’t produce any DA without daily injections of L-DOPA) still prefer sucrose over regular water when neither are obstructed. Juvenile DD mice who’d never been exposed to food+DA still preferred sucrose water, so DA isn’t required to learn the preference. BUT less licking overall in DD mice.
Kaczmarek and Kiefer, 2000 - DA agonists AND antagonists both reduce consumption of reward, but not reward itself - HOWEVER this study used ethanol as a reward, which is thought to act more as a reinforcer - i.e. rats initially find ethanol aversive, but systemic administration has been shown to cause DA release in NAc and rats grow to find the taste itself pleasurable. Another study (Samson et al 1993) using the same dose of DA agonist found it increased consumption
Dopamine pathways
Nigrostriatal - substantia nigra to dorsal striatum, important in motor coordination and habit forming
Mesocortical - terminates in insula, anterior cingulate, medial PFC and OFC, important in attention, working memory, inhibitory control
Mesolimbic - VTA to anterior striatum inc NAc, hippocampus, amygdala, important in reward motivation, associative learning, reinforcement. Tonic (under GABA inhibitory control) or phasic release of DA onto medium spiny neurons. Tonic stimulates low affinity D2-like receptors (Gi), makes neurons less sensitive to glutamate, ‘down-state’. Phasic stimulates high affinity D1-like receptors (Gs), makes neurons more sensitive to glutamate, ‘up-state’.
Opioids are involved in affect - hotspots and coldspots
Hotspots - opioid agonists increase ingestive but not aversive responses - shell of NAc, posterior ventral pallidum (destruction changes ingestive responses to sucrose to aversive!! Cromwell and Berridge, 1993), insula (interoceptive mapping and ‘feeling states’), amygdala, OFC, medial PFC, parabrachial nucleus of pons
(OFC especially important in stimulus evaluation, reward association, motivation and self-recognition. BUT not found to be active after opioid treatment, Petrovic et al 2002)
Coldspots - opioid agonists reduce ingestive responses - posterior NAc, anterior ventral pallidum
Opioids are involved in affect - neuroimaging
medial OFC - reward valence, value, doesn’t track rewards
middle OFC - subjective experience of pleasure
lateral OFC - punishment by removal of reward
– from meta-analysis of fMRIs, so correlational rather than causal evidence, but BOLD signal does change when stimulus is kept constant but subjective value altered (e.g. an mince pie before vs after Christmas lunch) –
Evidence against hotspot involvement
Thousands of lobotomy patients from the 50s show intact affective responses, despite total or partial separation of PFC from rest of brain
Hydranencephalic children, who have little or no cortex at all, can still show predictable affective responses ranging from smiling to giggling to laughing, as well as negative responses like crying and fussing. These can be elicited by carers using predicable stimuli.
What is anhedonia? Who gets it?
The inability to find pleasure in activities previously found enjoyable.
37% of Major Depressive Disorder patients have it (normally a transient state)
Also common in schizophrenia (normally a pervasive state), Parkinson’s disease, drug addiction (where ‘wanting’ the drug increases pathologically, but ‘liking’ does not), eating disorders, Alzheimer’s
Doesn’t respond well to SSRIs
In schizophrenia, it’s not a diagnostic criterion in DSM-5, but could be part of ‘flat affect’ or ‘avolition’. In depression, it’s one of the two core symptoms required for diagnosis.
Blanchard et al 2001 - schizophrenic self-reports of anhedonia remained elevated, whereas recovered depressed patients’ decreased after 1 year follow-up.
Three phases of pleasure, their corresponding anhedonia types
Laid out by Berridge and Robinson in the 90s
Appetitive - driven by dopamine, approach behaviour, seeking out the reward, this is where reinforcers come in. Motivational anhedonia.
Consummatory - driven by opioids, actually experiencing the reward. Consummatory anhedonia
Satiety - driven by dopamine, learning phase. Decisional anhedonia.
Motivational anhedonia - is there DA depletion in depression?
DA agonists can improve or worsen symptoms in depression
Low DA predicts depression in Parkinson’s
Animal models of depression show reduced DA in NAc and DA agonists are anti-depressants
MDD patients have reduced uptake of L-DOPA and reduced levels of homovanillic acid in spinal fluid
Pearson-Fuhrhop et al 2014 - No single polymorphism comes up significant for MDD on a GWAS, but if you produce a combined score including SNPs in COMT, DAT, DRD1, 2 and 3 it is predictive
Motivational anhedonia - is dopamine depletion associated with anhedonia, and the mesolimbic pathway?
Depleting DA with alpha-methyltyrosine in MDD patients in full remission will give them anhedonia, anxiety and depressive symptoms. PET scans - Increased activity seen in OFC (correlated with depressive symptoms) and NAc (correlated with anhedonia), and ventral striatum.
Motivational anhedonia - Is reward motivation reduced in depressed and schizophrenic patients?
Treadway et al 2013 - Schizophrenic and depressed patients are less likely to work for rewards. This correlated with anhedonia.
BUT humans work for secondary rewards, and these may be processed differently
