Answers to Test Your Knowledge Questions For

Answers to Test Your Knowledge questions for

Chapter 2 Integrating explanations

Question 2.1

In order to be around to reproduce and to care for offspring, clearly an animal must look after the integrity of its body. Excessive departures from the normal values of body temperature can be lethal. Even if not pushed to lethal limits, departures can disrupt optimal physiological functioning and thereby impair efficiency.

Question 2.2

Chapter 1 briefly introduced the notion of detectors of tissue damage and, together with this, you will need to use your imagination and long-term memory. As will be discussed in detail at various points throughout the book, the behaviour shown in response to tissue damage is basically of two kinds: (1) local reflexes (e.g. the 'automatic' removal of your hand from a hot object) and (2) whole-body pain-related behaviour. Unless you have been very cautious and lucky throughout life, you will surely have experienced both of these.

In terms of causation, the reflex of withdrawal of a limb from an offending object is triggered by detectors of tissue damage. These detectors also play a crucial role in whole-body pain related behaviour, though in a less stereotyped one-to-one way. Let us focus for the moment on whole-body pain-related behaviour. Pain causes us to do such things as retire to bed (e.g. in response to the pain of an intestinal discomfort or the headache of influenza) or walk differently (e.g. in response to a sore toe). The immediate consequence of such behaviour can be a reduction in pain, which presumably encourages the behaviour. The function of whole-body pain-related behaviour is to facilitate recovery, whether of a local part of the body that has been damaged or the whole body as in an infection. The function of the withdrawal reflexes is to protect the body from tissue damage.

The answer to this question sets up the discussion for the following sections of Chapter 2.

Question 2.3

In terms of the homeostasis of body fluids, schedule-induced polydipsia does not make sense in that body fluids are not regulated by such behaviour. The animal does not start in a state of water deficit that needs the correction of ingesting large amounts, since the rats had water ad libitum prior to the experiment. Only very much smaller amounts are needed to maintain fluid level accompanying ingestion of food. Rather, fluid volume is increased to above the homeostatic norm by this behaviour.

If you want to speculate a bit further, you might note that neither does it make sense in terms of the homeostatic aspect of energy balance. The rat has been food deprived prior to the experiment. The large amounts of water ingested are heated to body temperature and then lost from the body as urine with an associated energy cost.

Question 2.4

You might reasonably extrapolate that, under these conditions, the activity level of neuron 4 would be something like that shown in part (b) of the Figure. The frequency of action potentials would be less than that shown in part (c), which indicates the result of activity in the excitatory neurons 1 and 3 without there being any activity in the inhibitory neuron 2. Activity of 2 is bound to lower it to below the level of part (c).

Question 2.5

A neurotransmitter conveys information the short distance from a presynaptic neuron to another, immediately adjacent, postsynaptic cell. This postsynaptic cell can be another neuron or a muscle cell. For example, in Figure 2.4b, neurotransmitter conveys information the very short distance from neuron 1 to 2, 2 to 3 and from 3 to 4. It also conveys information from neuron 4 to the muscle. This process is shown in greater detail in Figure 2.6. In Figure 2.8, neurotransmitter released from neurons 1 and 3 would be responsible for excitatory effects on neuron 4, whereas that released from neuron 2 has an inhibitory effect on neuron 4.

Question 2.6

As a similarity, both replication and reproduction are processes by which new cells are produced, in the case of reproduction, a single fertilized cell, the zygote. The differences are as follows. Replication is a process intrinsic to a given animal, whereas reproduction involves two animals (at least in the cases of sexual reproduction, which concern us). In replication, the genetic material is a copy of that of the precursor cell. In reproduction, the genetic material is a novel combination of chromosomes taken from the mother and father and is therefore not an exact copy of the genes of either. Replication is responsible for the generation of millions of cells whereas (depending on the species) reproduction might produce only one.

Question 2.7

The reason is that the phenotype depends upon all the events experienced, at various levels, along the way. Thus, the genes exist within the fluid environment of the cell and the cell is surrounded by fluids. Cells contribute to a whole animal and the whole animal exists and behaves within an external environment having physical and social dimensions. Along with the genes, at each of these levels events contribute to the outcome of the phenotype. Clearly, for no animal are all of these events predictable on the basis simply of age.

Question 2.8

As the inhibitory link arising from neuron 1 gets strengthened, then so any given level of activity in neuron 1 will cause increased levels of inhibition to be exerted on neuron 2. For a given level of excitation of neuron 2 from elsewhere, the frequency of action potentials seen in neuron 2 will get less.

Question 2.9

The answer here is bound to be somewhat speculative since we do not know the exact neural basis of such conditioning. However, based upon Figures 2.12 and 2.13, we are in a position to make some intelligent 'first guess' speculation as to the kind of changes that might be involved. Consider Figure 2.13 and compare parts (b) and (d). We might speculate that, as we move from part (b) to part (d), there is increased strength of connection between the neuron marked 'bell' and that marked 'salivation'. This could take the form of increased receptors at the salivation neuron just beneath the synapse from the bell neuron, rather as shown comparing the top synapse in Figure 2.12 (b) and (a).

This really is very much a first guess and the discussion of Chapter 11, 'Learning and memory', will introduce complications to any such model. Figure 2.13 could capture just a feature of what happens when conditioning occurs, other features also being present.

Question 2.10

As a first simplifying dichotomy, we can consider that differences between individuals are due to differences in both genes and environment (That this dichotomy is not so neat or clear-cut as we might have supposed is discussed later, in Chapter 6, 'Development'. For the present purposes, we might simplify and think in terms of such a dichotomy). In such terms, Chapter 2 defines heritability as "the degree to which differences in a characteristic are due to genetic differences". It follows that, if environments are made more equal, then the contribution that differences in environment can make will get smaller. Hence, as a percentage, the differences contributed by genetic differences will increase. That is to say, heritability will increase.

Question 2.11

Suppose that a mutation occurs in some genetic material, i.e. a genotype involves a mutation. The phenotype that develops from this genotype might be termed a 'mutant phenotype'. By comparison, if one imagines a genotype not carrying the mutation, the phenotype that develops would be a non-mutant type of phenotype.

Question 2.12

This might be expected when the beneficiaries of the behaviour have a close genetic similarity with the animal doing the sacrificing, e.g. they are offspring. The chapter considered the example of a bird staying on the nest to incubate eggs, even in the face of hunger. There might be, say, 6-8 eggs being incubated with thereby a strong genetic representation of the mother. You might also have thought of the example of defending young against a predator.

Though it was not discussed there is also the example of animals forming pacts, such that animal A runs a risk in the interests of B on one occasion. In return, B runs a risk for A on a later occasion. For instance, some male baboons form such coalitions and A will distract a mating male so that B can quickly copulate with the female, a favour that is later returned. From the perspective of genetic perpetuation, it is assumed that the advantage in terms of the increased chances of future fertilization outweighs the disadvantage in terms of the risk of injury from a fight.

Question 2.13

Only the combination of alleles gg allows this characteristic to appear. This is exemplified by Figure 2.20, which shows that a white colour appears in the phenotype only given the combination gg.

Question 2.14

This term might be used as a kind of 'analogy' or 'metaphor' in that the mutation is other than a faithful copy of the genetic material. A difference is introduced. It is something like a typist copying a page of text and making a spelling mistake. As will be discussed in more detail in Chapter 6, 'Development', though such terms might help you to understand what is going on, they have inherent dangers if pushed too far or taken literally. In the literal sense, a mistake implies some criterion of what is right and a human observer to note the difference between the way something is and how it should be.

Question 2.15

It can prove much easier to exert control over the physical environment than over the social environment. This was illustrated by the experiment of Hahn and Haber (1982) described in the section 'Strain differences'. The experimenters were able to control for such aspects of the physical environment as temperature, lighting and food, and compare two populations. They could assume that such features of the physical environment were constant for the two populations. In the absence of a social factor, one might then conclude that any differences between populations are due to genetic differences at the level of the animals being studied. However, where social contact is involved, as in suckling, this would not control for differences in the reaction shown by the parents towards the young. Differences in behaviour of the young could reflect differences in behaviour towards the young shown by the parents, rather than genetic differences between the young. What is an environmental difference at the level of the young might reflect genetic differences at the level of the parents.

Question 2.16

This would suggest that differences in genes between individuals would be associated with corresponding differences in the tendency to exhibit depression. Differences in genes would be reflected in differences in nervous systems. Note that, no matter what the tendency, we are not suggesting that depression is necessarily 'written in the genes' in a one-to-one predetermined way. Multiple genes and complex levels of gene-environment interaction could be involved. The environment of the individual might be such as to protect. A genetic contribution need not be in the simple way described in the chapter for phenylketonuria and Huntington's disease.

Question 2.17

Suppose that we were to make the reasonable suggestion that differences in individuals in their tendencies to depression are associated, amongst other things, with genetic differences. There is, of course, not a direct gene -> behaviour or gene-> mental state link. Rather, such genetic differences would need to be mediated in some form and the most likely form would be differences in the structure of the nervous system between different individuals. Thus, genes and the nervous system cannot be compared and given relative weight, since differences in the nervous system might depend upon differences in genes.

Question 2.18

Such an observation would be entirely in keeping with the spirit of the present study, where cognitive events are assumed to be represented by particular patterns of activity in parts of the nervous system. That is, 'cognition' represents a particular level of description of certain events in the nervous system.

It might be easy for you to accept that certain changes in the nervous system initiated at a biological level (e.g. increased levels of a biochemical as a result of taking an antidepressant drug or increased strength of connection between neurons) would have manifestations at a cognitive level. Reciprocally, changes initiated cognitively by therapy that targets cognition would be expected to be associated with changes definable biologically. By 'biological state' would be meant such things as neurotransmitter levels and levels of hormones in the blood.

You might like to consider the effect of cognitive changes on biological events in terms of emergent interactionism proposed by Sperry and described in Chapter 1. In such terms, cognition would be an emergent property of the nervous system but one that affects the neural components on which it depends.

Question 2.19

There could hardly be a single gene that triggers adultery or promiscuity in the way that single genes can be associated with phenylketonuria or Huntington's disease. No matter what the genotype, differences in environmental experience are going to play a major role in these behaviours. Behaviour will be susceptible to its consequences (discussed earlier in the present Chapter and in more detail Chapter 11, 'Learning and memory'). Thus, there is not a one-to-one relationship between gene and behaviour any more than there is for depression (discussed as Question 2.17). Also, the motivation underlying such behaviour will vary very much with individuals.

An evolutionary psychologist would probably note that complex behaviour is a function of many factors acting in interaction. He or she would probably add that differences in genes between individuals could contribute to differences in their tendency to show such behaviour. Thus, one might imagine that differences in a number of genes might determine different brain structures with different tendencies to novelty seeking. This kind of issue is explored in Chapter 16, 'Motivation' and Chapter 19, 'Psychoactive drugs'.