30- Motivation Flashcards
define motivation
a driving force affected by physical needs, wants and likes. controlled by the hypothalamus
describe metabolism in relation to anabolism and catabolism
metabolism is a balance of anabolism and catabolism
anabolism = making larger molecules from smaller molecules
eat food, excess glucose stored as glycogen in the liver, excess fatty acids as triglycerides in adipose tissue
catabolism = breakdown of complex molecules
during fasting when neurons need energy, glycogen and triglycerides broken down to be used as energy
explain the long-term hormonal control of feeding behaviour as proven by the parabiosis experiment
parabiosis experiment:
parabiosis between an ob/ob mouse that lacks ob gene and a normal mouse - connect their circulatory systems
shared blood circulation between mice = ob/ob mouse is exposed to leptin from the normal mouse
leptin reduces feeding behaviour = will see visual weight loss for ob/ob mouse due to leptin effects - acts on receptor in the arcuate nucleus
hormonal control:
leptin = produced from adipose tissue after feeding, acts on receptors in arcuate nucleus, suppresses feeding behaviour and regulates body weight
those with leptin insensitivity or leptin receptor dysfunction = harder to regulate body weight and feeding behaviour
the role of the hypothalamus in feeding behaviour
hypothalamus contain different sub-hypothalamic nuclei that influence feeding behaviour:
paraventricular, lateral hypothalamic, ventromedial and arcuate
paraventricular = magnocellular neurons project to posterior pituitary, release oxytocin and ADH
lateral hypothalamus = hunger and initiation of eating. lesions can cause diminished appetite and anorexia
ventromedial = terminating eating, satiety. lesions cause overeating and obesity
arcuate = leptin receptors respond to leptin, suppress feeding behaviour
the short-term regulation of feeding
satiety-orexigenic signal balance
- satiety signals increase in response to eating, reach a peak and food consumption stops. decrease as stomach empties
- orexigenic signals increase to stimulate feeding, decrease following food consumption
how leptin levels stimulate anorexic/ orexigenic responses
leptin reduces feeding behaviour, regulates body weight
increased leptin = anorexic effect
- detected by arcuate nucleus neuron receptors
- release alpha-MSH and CART
- act on various structures:
1. brainstem and pre-ganglionic sympathetic NS neurons = increase sympathetic activity
2. paraventricular nucleus = increases TRH and CRH secretion, ACTH and TSH secretion, cortisol and thyroxine increase basal metabolic rate, metabolism and body temperature
3. lateral hypothalamic nucleus = inhibits feeding behaviour
decreased leptin = orexigenic effect
- detected by arcuate nucleus neuron receptors
- release AgRP and neuropeptide Y
- act on various structures:
1. brainstem and autonomic NS = inhibits sympathetic activity, increases parasympathetic activity
2. lateral hypothalamic nucleus = stimulates feeding behaviour, releases MCH and orexin = both produced by lateral hypothalamic neurons with widespread projections
3. paraventricular nucleus = inhibits TRH and CRH release, decrease in basal metabolic rate & body temperature
describe the three phases of feeding
cephalic, gastric, intestinal
cephalic:
- initiated by sensory stimuli, anticipating food
- increased salivation, parasympathetic activation, increased digestive juice secretions
- ghrelin released = activates AgRP and NPY neurons in arcuate nucleus
gastric:
- food is consumed, transported to stomach causing gastric distention
- triggers release of digestive juices, mucin secretion, enteric and parasympathetic activation
intestinal:
- food moves from stomach to intestines, signalling gastric distention
- vagus nerve from the stomach to nucleus solitary tract signals satiety
- CCK released in response to fatty acids in intestines, signals satiety via nucleus solitary tract
- insulin from pancreatic beta cells in response to increased plasma glucose = acts on arcuate nucleus
CCK, insulin and vagus nerve activity to nucleus solitary tract, signal satiety
dopaminergic involvement in food
increased dopamine release in nucleus accumbens with food = rewarding
VTA releases dopamine to pre-frontal cortex and nucleus accumbens = stimulates reward pathway
dopamine involvement in addiction for drugs of abuse
higher than natural dopamine surge with drugs of abuse, plays a part in addictive behaviours
affect dopamine surge through different mechanisms -e.g. cocaine blocks DA reuptake transporter, heroin blocks GABA
define drug addiction
a chronic relapsing disorder characterised by:
- compulsive seeking of the drug
- loss of control over drug taking
- negative physical & emotional states when drug is absent
describe stages of the addction cycle
social drug taking = take drug for the first time, hedonic effects
self administration
- pleasurable effects are positive reinforcement for further drug self-adminsitration
- mediated by mesolimbic pathway (VTA to nucleus accumbens) = reward pathway, higher than natural DA surge
tolerance and drug dependence
- need to increase drug dosage for same rewarding effect, develop dependence
withdrawal
- withdrawal symptoms when drug is absent = physical and emotional such as anxiety, tremor, depression
- triggers motivation to relapse and self-medicate withdrawal symptoms
- positive to negative reinforcement for self administration = involves amygdala, hippocampus and nucleus accumbens
relapse
- influenced by withdrawal symptoms, environmental cues, stressors
- addiction cycle repeats, urged by negative reinforcement
describe dopamine receptors in obesity and drug abuse
two groups of receptors: D1-like (D1,D5) and D2-like (D2,3,4) receptors
D2 receptors are present in the brain
obesity:
- downregulation of D2 receptors = suppressed reward system
- self-administer food to stimulate D2 receptors and reward system
- BMI and D2 receptors inversely related
drug abuse:
- D2 receptor decrease in those with drug/alcohol dependence
D2 receptor presence can be used as a biomarker for addiction
describe the relationship between food and serotonin
serotonin rises when anticipating food, peaks whilst eating food and decreases afterwards
low levels of serotonin in those with eating disorders - antidepressants are effective at managing feeding behaviour
neural circuits involved in reinforcement behaviour
mesolimbic dopamine system
- reward pathway from VTA to nucleus accumbens
- releases dopamine and induces reward and pleasure
hippocampus
- memory and learning, forms memories of rewarding experiences
- stronger memories reinforce behaviours
amygdala
- emotional processing and memories, link emotions to stimuli
- reinforces emotions behind a food/drug
pre-frontal cortex
- decision making and impulse control, assessing rewards
striatum
- habit formation, motor functions
nucleus accumbens
- reward pathway, processing and reinforcement
