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Answers to Test Your Knowledge questions for Chapter 17 Feeding and drinking Question 17.1 The term alliesthesia (Chapter 16, 'Motivation') refers to the change in hedonic reaction to a given stimulus as a function of changing internal state. In a state of dehydration, water has a high affective rating, whereas in overhydration it is much lower or even negative. Body fluid level is regulated since there are control actions instigated when it departs from normal. In functional terms, there is a biological imperative associated with near constancy of this parameter. Drinking and urination are controls that serve regulation of body fluids and, to achieve this, their magnitude can vary very widely. Question 17.2 All regulation is not lost since the expansion of body fluids triggers control by an elevated urine production rate, which serves the interests of body fluid regulation. This negative feedback control restrains the rise in body fluid level (In practice, as you might expect, body fluids do swell to some extent, this being the trigger to increased urination. The behaviour illustrates that, under certain special conditions, the control of drinking arising from the monitoring of body fluid level can be overriden). Question 17.3 All cells, whether neural or non-neural, need to exploit a fuel in order derive energy, a process termed metabolism. The activities performed by each cell, e.g. pumping ions across the membrane (Chapter 4, 'Neurons') and synthesizing proteins (Chapters 6, 'Development' and 11, 'Learning and memory'), require fuel. Whereas non-neural cells can exploit a range of different substrates for their energy needs, neurons are much more restricted. The principal fuel that neurons exploit is glucose. Whereas non-neural cells require insulin to transport glucose across their membranes, neurons do not. Question 17.4 So long as insulin level is low, non-neural cells are able to take up only small amounts of glucose from the blood. Therefore, neurons have privileged access to whatever glucose is available. If an insulin injection is made, non-neural cells are able to take up more glucose. Depending upon the dose of insulin and the initial level of blood glucose, this could deprive neurons of glucose. Question 17.5 Let us first return to Chapter 16, 'Motivation' and reconsider the argument on temperature regulation presented there. Temperature-sensitive neurons at the core and periphery play a role in temperature regulation. If core temperature deviates from optimum, autonomic and behavioural control is effected. It is not difficult to appreciate the functional significance of monitoring central temperature. However, threats to temperature homeostasis usually arise not from within, but from outside, the body, e.g. sudden cold winds. They do not immediately affect core temperature (and the neurons there) since the core is somewhat shielded. However, if action is not taken, core temperature will subsequently be affected and so peripherally instigated action is crucial. The role of peripheral temperature-sensitive neurons in behavioural and autonomic control, represents feedforward. By reacting immediately to peripheral temperature, the animal has a chance of pre-empting central shifts of temperature. A similar logic applies to feeding. It appears that neurons at the core, i.e. within the brain, are sensitive to local events concerning glucose and its metabolism. However, events are the liver are somewhat nearer being in contact with the fluctuations in nutrient availability, e.g. a lack or abundance of nutrients arriving from the gut or a conversion of intrinsic sources into metabolizable fuel. It appears that the control of feeding is influenced by both such central and peripheral factors. Question 17.6 Therapy would obviously consist of trying to increase the level of satiety. One could try to devise agonists to the neurotransmitters and hormones involved in mediating satiety. One could try to devise chemical agents that artificially boost their secretion. A consideration would be where they normally act. For example, if a natural agent acted in the brain to induce satiety any synthetic agent designed to mimic it would need to be able to cross the blood-brain barrier (Chapter 5, 'The brain'). However, a further consideration is that ant neurochemicals involved in satiety acting at one location might have roles in other aspects of behaviour acting at other sites. It might be that a sub-group of receptor (Chapter 5, 'The brain') is implicated in satiety and so artificial substances targeting this might be devised. One could try to alter, say, the person's rate of eating and thereby increase the satiety arising from any food ingested. You might well arrive at other possibilities, such as cognitive interventions designed to get the patient to attend more carefully to satiety signals. Question 17.7 This notion of plasticity was introduced in Chapter 2, 'Integrating explanations'. Plasticity refers to the idea that behaviour and the associated properties of the nervous system are not fixed over time, but change as a function of age and experience. Learning is an instance of such plasticity. Taste-aversion learning represents an example of where the reaction shown towards a food changes as a result of the experience after ingesting it. It is assumed to be mediated by changes in the connections between neurons that mediate taste reactivity (Chapter 11, 'Learning and memory'). Question 17.8 One example that illustrates this is the role of insulin at the brain and the periphery. The section noted that, by its action in the hypothalamus, insulin inhibits food intake and thereby indirectly limits fat storage. However, its effect in peripheral tissue is to lower blood glucose and convert such fuels as glucose into fat. The latter factor might well indirectly stimulate feeding by denying the brain access to glucose. Thus, only by considering both brain and periphery might we be able to understand the effect of insulin. The section also noted that, following lesions to the VMH, there are changes both at the brain and the periphery. It appears that disruption of the motivational process underlying satiety is only one amongst several factors involved in increased feeding. Such lesions also increase the secretion of insulin by the pancreas and thereby act indirectly on behaviour. Large amounts of glucose are converted into fat and the subsequent low availability of this fuel to the CNS triggers feeding. Question 17.9 This question is a difficult one since it raises all of the philosophical and linguistic issues that were introduced in Chapter 1. It is unlikely that any absolute and water-tight demarcation between these terms can be defined or is even desirable scientifically. However, here is a start at what might be a useful provisional categorization. We might use 'physiological' in the sense of an identifiable event within the body such as a fall in insulin level or a rise in the secretion rate of CCK. This would be particularly the case if the events were outside the nervous system. We might speak of the 'physiological basis' of a feeding disorder in terms of the contribution that an abnormality in such identifiable physiology makes to it. However, any such physiological change must communicate with psychological processes having a base in the CNS, if it is to influence behaviour. We might use the term 'psychological' to refer to causes of feeding defined in terms of information processing within the CNS. This would include cognition that involves goals, such as the rejection of food in the interests of obtaining a slim body image or feeding to seek comfort. We might also want to include classical conditioning under this heading, such as eating triggered by cues that in the past had been associated with eating. These might be such as to provoke abnormalities in metabolism and weight. However, in using the term 'psychological' in this sense, we would not, of course, be denying that information processing requires a physical basis in terms of neurons. Question 17.10 Arginine vasopressin is a hormone that controls the rate of production of urine (Chapter 3, 'Coordinated action'). When its secretion rate is high, little urine is formed and when it is low large amounts are produced. If a disturbance suppresses the production of the hormone, large amounts of urine are produced, homeostasis is disturbed and a large amount of compensatory drinking is triggered. Such an effect of hormone loss on behaviour is an indirect one, not mediated by an action of the hormone directly on motivational processes. The effect is somewhat comparable to feeding triggered by disturbances to the physiology outside the CNS associated with, say, abnormal insulin secretion. Question 17.11 Some feeding and drinking behaviour makes obvious sense in terms of homeostasis and its contribution to biological function. (a) Drinking in association with feeding and thereby pre-empting dehydration is an example of feedforward control, which makes sense in terms of biological function. This prevents water being pulled into the gut, which would dehydrate the body fluids. Similarly, the reduction of feeding that occurs at a time of dehydration is an example of something that makes sense in terms of function. Food would draw water into the gut and make dehydration worse. (b) schedule-induced polydipsia is an example of behaviour that does not make sense in terms of homeostasis. Large amounts of water are heated to body temperature and then excreted as urine. However, the expression 'make sense' invites some discussion. You might object that, if we look closely enough and we knew enough, at some level everything should make some sense in terms of biological function. Thus, the animal exhibiting schedule-induced polydipsia is placed under abnormal conditions unlikely to be encountered in its evolution (Chapter 2, 'Integrating explanations'). It might be displaying the output of behavioural processes that, under normal circumstances, would produce behaviour that makes adaptive sense. Question 17.12 The section notes that preferences can emerge in utero. Taste-aversion learning appears to be possible under these conditions. Later, the suckling infant is able to form associations between (a) taste and other sensory properties and (b) the consequences of ingestion. Preferences and aversions appear to depend in part upon such early associations. In the development of the control of nutrient state over suckling in mammals and pecking at food objects in birds, the animal monitors the consequences of behaviour. Suckling is open to some operant control. Question 17.13 Chapter 6, 'Development', made the point that some aspects of development make sense only in terms of their later role in behaviour. For example, the development of sex organs makes functional sense in terms of their role in reproduction when adult. Other aspects of development make sense in terms of surviving to reach adulthood. The development of suckling is to be understood in terms of survival in early age. However, in addition, associations formed during the suckling phase can be carried over and used during adult ingestive behaviour.