Download 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 wholebody 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'.