Neural control of Motivational Behaviour: control of drinking & eating Flashcards
What are circumventricular organs, what do they include and what do they do?
- In a few brain areas the blood-brain barrier is ‘leaky’. In these regions the capillaries are fenestrated and hormones in the blood can move out into the extracellular space of the brain.
- These areas are called circumventricular organs because they surround the ventricular system; they include the area postrema in the brainstem, posterior pituitary, median eminence, subfornical organ (SFO), subcommissural organ, and pineal gland .
What is one mechanism of control of drinking linked directly to? How does the SFO allow for this?
- One mechanism of control of drinking is linked directly to the osmolarity of the blood. The higher the osmolarity, the stronger the urge to drink. Blood osmolarity is sensed by the subfornical organ (SFO) in the wall of the third ventricle near the interventricular formamen between the thalamus and hypothalamus.
- The SFO has fenestrated capillaries (ie capillaries with gaps between the endothelial cells); this allows it to detect various peptides in the blood. Changes in the osmolarity of the blood are detected by ”osmoreceptor cells” in the SFO which send axons to cells in the hypothalamus.
What is activated by the stimulation of the osmoreceptors in the SFO? What does this project to and what does this cause us to feel?
- Stimulation of the osmoreceptors in the subfornical organ by hypertonic blood activates cells in the medial preoptic nucleus of the hypothalamus.
- This nucleus projects to the limbic system and regulates the sense of thirst. When the medial preoptic nucleus is activated we feel subjectively thirsty and will seek out water. The greater the activity of the nucleus, the thirstier we feel.
Where else does the SFO activate cells? Where do the axons of these cells project to? How does this make us thirsty?
- The subfornical organ also activates cells in the paraventricular nucleus (around the third ventricle) and the supraoptic nucleus (above the optic chiasm). These cells have axons that project to the posterior pituitary and release ADH (antidiuretic hormone) and thus reduce urine flow.
- This reduces loss of water in urine and helps to prevent blood osmolarity rising even further. Angiotensin II is detected in the SFO and high levels of this peptide in the blood also triggers thirst
What does high blood osmolarity trigger?
Thirst and ADH release
What are the three effects of ADH that contribute to decreased loss of water in urine?
- ADH has three effects by which it contributes to decreased loss of water in urine. These are:
o ADH causes additional water channels (Aquaporins) to move into the membrane of the collecting duct epithelial cells. The aquaporins allow water to pass out of the collecting duct and into the renal medulla. This reduces the volume and increases the concentration of urine
o ADH also increases the permeability of the collecting duct to urea, allowing increased reabsorption of urea into the medullary interstitium, which helps to increase the reabsorption of water
o ADH stimulates sodium reabsorption in the thick ascending loop of Henle by increasing the activity of the Na+ K+ 2Cl- cotransporter. This increases the osmolarity of the medullary extracellular (interstitial) fluid, and allows even more water to be reabsorbed from the collecting ducts.
A key idea in understanding feeding behaviour is that it is initiated by two factors. What are these two factors?
- A key idea in understanding feeding behaviour is that it is initiated by two factors.
o One is the immediate availability of food (i.e. is it there in front of you?). This is an EXTERNAL CUE.
o The second is the sense of hunger from inside your body. This is an INTERNAL CUE. (Cessation of eating is triggered by a separate, SATIETY system).
A combination of what types of cues usually cause us to eat? Give examples.
- We normally eat due to a combination of internal and external cues. For example, we may not feel hungry but if appetizing food is presented we will eat it.
- On the other hand if we feel hungry enough we will eat what would normally be unappetising (e.g. raw meat)
What type of tissue provides the major storage of energy in mammals? What model was proposed if body weight and fat are maintained at a constant level for long periods of time? How might weight also be regulated by intestinal absorption?
- Adipose tissue provides the major storage of energy in mammals.
- On the basis of the observation that body weight and fat are maintained at a constant level over long periods in spite of daily fluctuations in food intake, Kennedy in 1953* proposed an “adipostatic model” in which factors released by fat target the hypothalamus to control food intake and maintain weight.
- Weight may also be regulated by regulating intestinal absorption, by altering intestinal transit time and thus altering absorption of caloric material in the intestine.
Where did early evidence for a role of the hypothalamus in appetite come from? What was demonstrated in this study? What ideas and studies did this lead to?
- Early evidence for a role of the hypothalamus in appetite came from studies of patients with pituitary tumors pressing upwards on the hypothalamus.
- These patients often demonstrated a voracious appetite, morbid obesity and hypogonadism. This was known as the “adiposogenital syndrome”.
- The hypogonadism led to the idea that hypothalamic damage was occurring; thus the voracious appetite could be due to damage to a ‘satiety centre’ in the hypothalamus.
- This led to studies where different parts of the hypothalamus were deliberately damaged in rats
What did the studies on rats with hypothalamus damage show?
- Rat studies showed:
- Lesions in the Lateral hypothalamus produced anorexia (due to damage to orexigenic/feeding centre?)
- Lesions in the Medial hypothalamus lesions produced obesity (due to damage to satiety centre?)
What does damage to the medial hypothalamic nuclei reduce a person’s ability to do? How is their feeding behaviour affected? What about damage to the lateral hypothalamus?
- Damage to the medial hypothalamic nuclei reduces a person’s ability to sense internal cues. Their feeding behaviour is then controlled by external cues alone. So if a rat or human has a ventromedial lesion, they will overeat if given palatable food but starve if given unpalatable food.
- Such individuals can become very ‘finicky’ in their diet, i.e. only eating particular kinds of food, if this food is unavailable they will starve, but if this food is available in quantity they will overeat and become obese.
- Lesions in the lateral hypothalamus can cause anorexia but these are harder to interpret as these lesions may interrupt several neuronal pathways. For example, dopamine pathways will be interrupted which may destroy the pleasure (reward) from eating.
Which nuclei of the hypothalamus are damaged by medial lesions? What is the effect of this? What about the lateral lesions? What did lesions here lead to the idea of?
- The medial lesions involved the arcuate nucleus and periventricular nuclei of the hypothalamus. Animals with lesions here overate and became enormously obese. This led to the concept of an ventromedial ‘satiety centre’ that inhibited feeding when stimulated.
- The lateral hypothalamic lesions damaged the lateral hypothalamic nucleus. This led to the idea that there is a lateral hypothalamic ‘orexigenic’ (hunger) centre.
- N.B. Don’t confuse the periventricular nucleus (next to arcuate & to do with satiety) with the paraventricular nucleus (to do with release of ADH & oxytocin)
What happened when unpalatable food was given to the rats with ventromedial lesions? What did this lead to the idea of?
- If unpalatable food (e.g. food tasting bitter but nutritious) was substituted for normal food, the animals with ventromedial lesions did not overeat but became anorexic! i.e. previously fat rats became anorexic
- This led to the idea that the hypothalamus regulates food intake depending on the balance between ‘internal’ and ‘external’ stimuli.
- Internal stimuli are things like contraction of the stomach (hunger pangs), and the levels of various blood chemicals like glucose, insulin, ghrelin, cholecytokinin and leptin.
- External stimuli are the sight and smell of food. In normal individuals eating is controlled by a balance between these two factors. If the internal stimuli are strong, we feel hunger, and depending on how intense, we will go and seek out food above all other actions.
- If the internal stimuli are very weak, we will not eat even if attractive and tasty food is presented to us. However, normally the internal stimuli are at some intermediate level, and whether or not we will eat food presented to us depends on the balance between the external stimuli (how attractive the food is) and the internal stimuli (how hungry we feel).
Where are internal cues now known to be detected? What ‘centre’ are these part of? What effect does damage to these areas have?
- It is now known that the arcuate nucleus is where internal cues such as levels of blood hormones are detected. There is some uncertainty about where the arcuate nucleus ends and the periventricular nucleus begins. Probably both are part of the classic ‘satiety centre”
- Arcuate lesions destroy the animal’s ability to detect internal signals. So if presented with palatable food it will eat until it can physically eat no more; It has no ability to detect internal satiety signals. On the other hand if presented with unpalatable food it will starve to death, as it has no ability to detect internal hunger signals.