Download Answers to Test Your Knowledge questions for

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.