This article argues that mirror neurons
originate in sensorimotor associative learning
and therefore a new approach is needed to
investigate their functions. Mirror neurons were
discovered about 20 years ago in the monkey
brain, and there is now evidence that they are
also present in the human brain. The intriguing
feature of many mirror neurons is that they fire
not only when the animal is performing an
action, such as grasping an object using a power
grip, but also when the animal passively
observes a similar action performed by another
agent. It is widely believed that mirror neurons
are a genetic adaptation for action
understanding; that they were designed by
evolution to fulfill a specific socio-cognitive
function. In contrast, we argue that mirror
neurons are forged by domain-general processes
of associative learning in the course of
individual development, and, although they may
have psychological functions, they do not
necessarily have a specific evolutionary purpose
or adaptive function. The evidence supporting
this view shows that (1) mirror neurons do not
consistently encode action "goals"; (2) the
contingency- and context-sensitive nature of
associative learning explains the full range of
mirror neuron properties; (3) human infants
receive enough sensorimotor experience to
support associative learning of mirror neurons
("wealth of the stimulus"); and (4) mirror
neurons can be changed in radical ways by
sensorimotor training. The associative account
implies that reliable information about the
function of mirror neurons can be obtained only
by research based on developmental history,
system-level theory, and careful
experimentation.
Commentary Cook et al.: Mirror
neurons: From origin to function
Contagious behavior: An alternative
approach to mirror-like phenomena
Robert R. Provine
Abstract
Contagious behaviors such as yawning and
itching/scratching have mirror-like properties
and clearly defined stimulus and motor
parameters; they are also relatively easy to
study and should be part of the debate about
mirror neurons and the neurological mechanisms
of social behavior. The broadly tuned,
multimodal stimuli of contagious behavior
challenge present accounts of mirror mechanisms
that focus on specific, mirrored acts.
The range of mirror-like processes under
investigation should be broadened to include
contagious behavior, a class of social behavior
that is largely neglected by mirror neuron (MN)
researchers. The study of contagious behavior
offers the highly desirable properties of
identifiable stimuli and motor responses. In
contrast, mirror neurons (MNs) seem lost in
thought, like disembodied computers not hooked
up to printers &endash; full of potential, but
short on demonstrated function. Once the
relation between the brain's inputs and outputs
are defined, we will be well on the way to
understanding the mechanism of mirror-like
behavior. The study of contagious behavior also
offers an economic incentive; it can be a
low-budget affair that requires only behavioral
observation, not the pricey technology of
neurophysiology labs or fMRI machines.
Upon first hearing about MNs, students often
ask about their involvement in contagious
yawning, laughter, and the like. They are
surprised to learn that what seems obvious to
amateurs is often ignored by professionals,
including the authors of the target article. My
present comments focus on yawning and
itching/scratching, representative contagious
behaviors. These and other contagious acts
&endash; laughing, coughing, nausea/vomiting,
and vocal crying &endash; are reviewed and
contrasted in my recent book, Curious Behavior:
Yawning, Laughing, Hiccupping, and Beyond
(Provine 2012).
Yawns are propagated, being passed from one
person to another, in a behavioral chain
reaction. This mindless connectedness involves
social behavior of the most primal sort. When
you yawn contagiously, you do not consciously
decide to imitate the observed yawn &endash; it
happens automatically. The rippling of yawns
through a group is heritable, neurologically
programmed social behavior that synchronizes the
physiological and behavioral state of the group.
Details about themechanism of this contagion,
its evolution, and its development are still
being worked out. However, it is clear that the
motor act of yawning is phylogenetically
ancient, characteristic of most vertebrates, and
develops early in prenatal life. Contagious
yawning, in contrast, is phylogenetically more
modern, confined in various degrees to great
apes and, perhaps, dogs and other highly social
mammals, and develops several years after birth
(see reviews in Provine 2005; 2012; Walusinski
2010). One of the most striking features of
adult human yawning is its extreme
contagiousness. Almost anything associated with
yawning can be a vector for the contagious
response, including viewing yawning faces,
hearing yawn-related sighs, thinking about
yawning, or even reading about yawning, as you
are now doing. Given the broad, multimodal
spectrum of yawn stimuli, the involvement of a
single, narrowly tuned detector or MN sensitive
to a specific aspect of a yawning person seems
unlikely. Instead, contagion is probably
mediated by a variety of detectors of
yawnrelated stimuli, each capable of producing a
yawn. In the pre- MN research era, I proposed
that an ethological releasing stimulus was
responsible for triggering the stereotyped motor
act of contagious yawning (Provine 1986; 1996).
Although the stereotypy of yawning is
unchallenged, the detector activated by the
releasing stimulus is much more broadly tuned
than I had anticipated.
Itch and associated scratching, like
yawning, are highly infectious, and the stimulus
vector for their contagion is broadly tuned and
multimodal (Provine 2012). Although eczema,
contact dermatitis, and other skin irritation
can trigger itch, so can such abstract stimuli
as hearing a lecture about itch, viewing
itch-causing parasites, or seeing someone else
scratching, especially among individuals with
pre-existing dermatological conditions (Holle et
al. 2012). The itch/scratch complex provides
intriguing research opportunities because it has
more potential response variability than
stereotyped behaviors such as yawning. For
example, Ward et al. (2013) investigated how the
behavior of a model influences the specific site
of itchiness and scratching of an observer. When
participants in their study viewed a movie
depicting scratching, they were more likely to
scratch themselves, but the hand that they used
to scratch (left or right) and the site of
scratching did not necessarily match the model.
Although the model scratched only the arms and
chest, the majority of participants viewing the
video directed their scratching upward toward
their face and hair. The authors concluded,
"contagious itchiness may be more driven by
vicarious perception of the feeling state
(itchiness/unpleasantness) than contagion of the
motor act or bodily target" (Ward et al. 2013,
p. 2).
Many questions about contagious behavior and
MNs remain. Building on the above results for
contagious yawning and itching/scratching,
should we conclude that the sufficiency of a
variety of multimodal stimulus triggers is
evidence against the behavioral involvement of
MNs, instances of broadly tuned or multiple MNs,
or examples of a different class of mirror-like
acts that do not involve MNs? Do environmental
contingencies influence the tuning of stimulus
triggers or MNs, possibly contributing to the
acquisition of multimodality? And what about
other contagious behaviors? To what extent does
the contagiousness of nausea/vomiting, coughing
(but not sneezing), vocal crying, laughing, and
yawning involve shared feeling states or
another, more specific trigger (Provine 2012)?
The answers to these questions may come from
developmental, comparative, and perceptual
studies that are now underway. Whatever the
outcome, such research will broaden our
understanding of the neurological basis of
sociality.
