Lighting Res. Technol.

2012; 44: 238–252

Alerting effects of daytime light exposure –

a proposed link between light exposure and
brain mechanisms
E Rautkylä MSc, M Puolakka DSc and L Halonen DSc
Lighting Unit, Aalto University, PL 13340, 00076 Aalto, Finland

Received 23 January 2011; Revised 26 February 2011; Accepted 4 April 2011

The effects of light on alertness have been shown several times and the proposed
cause has been suppressed melatonin levels. The relation of melatonin and
alertness applies at night but not by day when there is hardly any melatonin. Still,
light can be used to improve daytime alertness, but how? This paper describes the
brain mechanisms involved in light-induced daytime alertness and proposes a
novel model of two parallel mechanisms. In addition to the well-established
circadian pathway, it is suggested that light can use the amygdala in the limbic
system to send signals to the cerebral cortex. The participation of the amygdala in
light-induced alertness means that light is provoking and modulating emotions
that induce alerting responses. The model is assembled from known relations but
has not yet been verified as a functional system. The paper proposes methods to
test the model.

1. Introduction previous work has focused on the neurologic

Melatonin is a sleep-inducing hormone pro-
duced in the brain by the pineal gland. There
is evidence that exposure to short wavelength
light in late evening induces melatonin sup-
pression resulting in greater alertness in the
middle of the night when melatonin secretion
is peaking.1 This is explained by the fact that
the secretion of melatonin is controlled by the
suprachiasmatic nucleus (SCN), the brain’s
pacemaker responsible for generating circa-
dian rhythms in mammals. The SCN on the
other hand, takes input from the retina via a
photic pathway called the retinohypothalamic
tract (RHT).
However, the fact that the link between
melatonin and alertness applies only at night
but not by day when there is hardly any
melatonin, is often ignored. In fact, much
Address for correspondence: E Rautkylä, Lighting Unit, Aalto
University, PL 13340, 00076 Aalto, Finland
E-mail: emmi.rautkyla@iki.fi
basis for the alerting effects of light exposure
at night, but little is understood regarding
the mechanisms responsible for the alerting
effects of light during daytime. Yet, results
show that light can be used to improve
daytime alertness.2,3 The question is, how?
Over the past decades, research on the
relation of light exposure to daytime alertness
has concentrated on effects instead of
causes.4,5 Only a few studies have attempted
to examine the mechanisms underlying light-
induced daytime alertness.3 This explains why
there is a lot of inconsistent data on the role
of light in alertness during wakefulness.
It also explains why it has not been possible
to find a consensus on the parameters of light,
such as the illuminance, spectrum, duration
and timing of light exposure, that induce the
greatest changes in alertness. The authors
claim that these problems could be overcome
if the brain mechanisms and projections
behind the alerting effects of light were

ß The Chartered Institution of Building Services Engineers 2011 10.1177/1477153511409294

 Mechanisms of light-induced daytime alertness
to be more thoroughly investigated and
discussed.
Animal studies done in the 1970s have
shown that there is a direct visual input from
the retina to the limbic system, also known
as the centre of emotions. This suggests that
light cues may affect emotional behaviour.6
Furthermore, it has been shown that the
limbic and preoptic systems project to brain
areas that play key roles in the arousal
system, such as the lateral hypothalamus
(LHA), orexin neurons and the locus coeru-
leus (LC).7,8 These neural connections from
retina via the limbic system to the arousal
system exist but they have never been
discussed from a light-induced alertness
point of view.
This paper combines known relations on
the theoretical level and proposes a tentative
and hypothetical model of two parallel mech-
anisms that allow light to affect alertness in
daytime. It suggests that in addition to the
circadian pathway, the alerting effects of light
can be based on light cues that travel to the
amygdala and further to the arousal system.
This novel model has not been verified as a
functional system, but the paper does suggest
some experiments that could be used to
confirm the proposed mechanism.
This paper first describes the neurotrans-
mitters and receptors that make up the two
branches of the ascending reticular activating
system. After that the projections from the
retina to the brain areas promoting arousal
and sleep will be discussed on the basis of
these projections a model of two parallel
pathways for the light stimulus to induce
alertness is proposed. In the central role is the
amygdala that provides a limbic pathway
alternative to the SCN and the circadian
pathway. The amygdala is known to perform
a primary role in the processing and memory
of emotional reactions. Hence, if the amyg-
dala is involved in light-induced alertness, it
means that alertness can result from an
emotional stimulus caused or modulated by
239
the light. Therefore, the relationship of light,
emotion and alertness is discussed more
thoroughly. Finally, practical suggestions on
how to test the hypothetical model are given.
2. The ascending reticular activating
system
Alertness is based on stimuli travelling from
the brainstem through the thalamus, hypo-
thalamus and basal forebrain to the cerebral
cortex.9,10 This activation system, also known
as the ‘ascending reticular activating system’,
is located in the reticular formation in the core
of the brainstem near the junction of the pons
and the midbrain (Figure 1). There are many
neurons in the reticular formation, the mid-
brain and the hypothalamus that play an
essential role in that the regulation of alert-
ness. The most important of them are the
noradrenergic, histaminergic, dopaminer-
gic, serotonergic and cholinergic neurons
located in the locus coeruleus (LC), tubero-
mammillary nucleus (TMN), ventral tegmental
area (VTA), dorsal raphe nucleus (DR) and
laterodorsal and pedunculopontine tegmental
area (LDT/PPT), respectively.11 These nuclei
have many afferents and efferents and they are
also connected to each other. Their involvement
in alertness is described briefly in Table 1.
As shown in Figure 1, the activation
system contains two branches12 along which
the reticular neurons sends projections to the
cerebral cortex. The first branch, the dorsal
one, innervates the thalamus by projections
originating in the two cholinergic structures –
the LDT/PPT nuclei. The second branch, the
ventral one, projects into the lateral hypo-
thalamic area (LHA), basal forebrain and the
cerebral cortex from the monoaminergic LC,
DR, VTA and TMN pathways. These pro-
jections promote arousal. For a more detailed
review of the activation system and its
branches see reference 9.
Lighting Res. Technol. 2012; 44: 238–252
240 E Rautkylä et al.

Celebral cortex

Midbrain

SCN

Thalamus
Hypothalamus
Amygdala
Pons

Brainstem
Reticular formation

Figure 1 A schematic drawing showing the most important components of the ascending reticular activating system
and their projections. The cerebral cortex receives messages via the thalamus but also directly from a number of
nuclei in the brainstem.Note: LC, locus coeruleus; VTA, ventral tegmental area; TMN, tuberomammillary nucleus; DR,
dorsal raphe; LDT, laterodorsal tegmental nucleus; PPT, pedunculopontine tegmental nucleus; BF, basal forebrain;
SCN, suprachiasmatic nucleus; LHA, lateral hypothalamus (Redrawn and modified from Saper et al. with permission)

3. Connections from the retina to brain
regions promoting alertness
Figure 2 shows the most essential connections
from the retina to the brain regions that are
involved in promoting alertness.
The SCN, located in the hypothalamus, is
the brain’s master clock13 that coordinates the
circadian rhythms based on light input from
the outside world during daytime and by
melatonin secretion during night time.14
Photic information is transmitted to the SCN
directly along the RHT from the melanopsin-
containing intrinsically photosensitive retinal
ganglion cells (ipRGCs) located in retina.15
Although the ipRGCs are sufficient for photo-
entrainment, recent findings have shown that
the classical rod and cone photoreceptors also
Lighting Res. Technol. 2012; 44: 238–252
contribute in the photic entrainment of circa-
dian rhythms.16
In humans, the SCN also seems to rece-
ive indirect input from the retinorecipient
intergeniculate leaflet (IGL) via the geniculo-
hypothalamic tract (GHT).17,18 There is,
however, contradictory literature on whether
the retinal afferents to the IGL are from the
melanopsin expressing ipRGCs19 or from the
classical photoreceptors.20 The SCN projects
to many brain structures involved in arousal
regulation.21
Orexin is a neuropeptide produced in the
hypothalamus.22 It has been suggested that
neurons containing orexin increase arousal by
innervating with the nuclei that take part in
activation between the autonomic nervous
system and the cerebral cortex.23,24 Among
 Table 1 A summary of the nuclei of the ascending reticular activating system and their involvement in alertness

Brain area Abbreviation Location Neurotransmitter Role in alertness References

Locus coeruleus LC Brainstem Noradrenaline Enables the body to perform well Aston-Jones et al.,70
in stressful situations by secreting Samuels and Szabadi80
noradrenaline to the cortex and Aston-Jones81
Dorsal raphe nucleus DR Brainstem Serotonin Creates a calming or an arousing Jacobs and Azmitia82
effect depending on where in the
brain serotonin is secreted
Laterodorsal tegmental LDT Brainstem Acetylcholine Modulates sustained attention Jacobs and Azmitia82
area and mediates alerting responses
together with the PPT
Pedunculopontine PPT Brainstem Acetylcholine Modulates sustained attention Jacobs and Azmitia82
tegmental area and mediates alerting responses
together with the LDT
Ventral tegmental area VTA Midbrain Dopamine Increases vigilance as well as Oades and Halliday83
secretion of many other hormones
by secreting dopamine
Ventrolateral preoptic VLPO Hypothalamus Galanin Blocks the arousal system Saper et al.12 and
nucleus and GABA by efferents containing Gaus et al.38
gamma-aminobutyric acid (GABA)
and galanin
Tuberomammillary TMN Hypothalamus Histamine Supports maintenance of cortical Parmentier et al.84
nucleus activation and wakefulness
by secreting histamine

Lighting Res. Technol. 2012; 44: 238–252

242 E Rautkylä et al.

LC: Noradrenaline, OX1R

DR: Serotonin, OX1R & OX2R

VTA: Dopamine, OX1R & OX2R

LDT/PPT: Acetylcholine, OX1R & OX2R Exitatory

Inhibitory
TMN: Histamine, OX2R

LHA: Orexin neurons

IGL: Neuropeptide Y

VLPO: GABA and galanin T IGL

GH

Thalamus

Hypothalamus
RHT SCN
ipRGCs
MPON Midbrain
DMH
VTA
Rods &
cones LHA
vSPZ
Retina
DR
VLPO
TMN
LDT/PPT

Limbic system
Amygdala LC
Brainstem

Figure 2 ipRGCs project to the SCN directly via the RHT15 and indirectly via the IGL and the GHT.17,18 Also rods and
cones are likely to take part in these projections.16,19,20 In addition, the IGL receives input from the LC,67 DR68 and
TMN69 (these projections are not present in this figure). The SCN projects indirectly to the LC using the ventral
subparaventricular zone (vSPZ), the dorsomedial nucleus of the hypothalamus and the LHA as relays.70,21 The SCN
also projects to the VTA using the medial preoptic nucleus as a major intermediary.71 The LHA contains orexin
peptides72,73 that innervate the orexin-1 receptors (OX1R) and/or orexin-2 receptors OX2R74 in the LC26, DR27, TMN28
and LDT.29 The DR and LC also send inhibitory feedback to the LHA.30 The LC and DR have reciprocal connections.31
The VTA excites the LC.75 The PPT and the LDT are both excited and inhibited by the LC and PPT and LDT76 project
back to the LC.77 The TMN inhibits noradrenaline release in the LC.32 In contrast to other hypothalamic nuclei, the LC
does not project reciprocally to the TMN.78 In addition to the SCN and the vSPZ,36 the ipRGCs also project directly to
the amygdala.36 The amygdala sends limbic inputs including the CRF neurons to the orexin neurons in the LHA33,34 as
well as to the LC.35,79 The VLPO promotes sleep by inhibiting the LHA, TMN, LC and DR12. Note that the majority of the
connections have been found while testing rodents or monkeys

others, Saper et al.11 and de Lecea et al.22
state that the LHA is involved in the ascend-
ing arousal system and that loss of the orexin
neurons in the LHA results in narcolepsy.
Conversely, Harris and Aston-Jones25 have
recently proposed that orexin neurons located
in perifornical and dorsomedial hypothalamic
areas increase arousal, whereas those located
in the LHA would primarily be involved in
reward processing.
Lighting Res. Technol. 2012; 44: 238–252
The LHA innervates the orexin receptors of
the LC26,24 as well as other nuclei in the
ascending activation system.27–29 Serotonin
and noradrenaline neurons in the DR and LC
also send inhibitory feedback to the orexin
neurons in the LHA.30 As shown in Figure 2,
cholinergic and monoaminergic nuclei also
project to each other.31,32 The amygdala is a
subcortical structure of the limbic system, the
centre of emotions. The neurons of the
 Mechanisms of light-induced daytime alertness 243

Limbic

Monoaminergic
Orexin and cholinergic
Light Retina
neurons neurons

Circadian
Brainstem

Projections to the
celebral cortex

Figure 3 Two parallel pathways from the retina to the activation system. The light stimulus can travel via the RHT in
the circadian system or use the limbic system to create an emotional response to the light cue. Both pathways project
to orexin neurons in the LHA and promote cortical arousal through the neurons of the activation system. The retinal
photoreceptors involved in both pathways are ipRGCs. In addition, it is possible that rods and cones take part in the
photoreception of the pathways

amygdala containing corticotrophin-releasing
factor (CRF)33 stimulate the orexin neurons in
the LHA34 and activate the LC35 contributing
to maintenance of arousal. The amygdala gets
significant projections from the ipRGCs36 but
projections from rods and cones are also
possible.37
During sleep, neurons of the ventrolateral
preoptic nucleus (VLPO) block the arousal
system by efferents containing gamma-
aminobutyric acid (GABA) and galanin.38
The interaction between the VLPO branches
is mutually inhibiting, and it has been said to
work like an ‘on-off’ switch.12
4. Circadian and limbic pathways in
light-induced alertness
On the basis of the neurologic connections
reviewed in the previous section, the authors
propose a model of two separate major paths
from retina to the activation system and then
on to the cerebral cortex. The model is pre-
sented in Figure 3. The first path is formed by
the RHT in the non-image-forming visual
system. When this path is used, the light
stimulus enters the ipRGCs in the retina and
travels via the RHT or GHT giving input to the
SCN and further to the circadian system. The
involvement of rods and cones in the circadian
pattern is also possible.16 This path is from now
on referred to as the circadian pathway.
The second path starts from the retina, but
instead of continuing directly or indirectly to
the SCN, it continues to the amygdala, a
limbic structure involved in many brain
functions, including emotion. The fact that
light of shorter wavelength has been found to
elicit a stronger effect on emotional responses
than longer wavelengths37 indicates that the
photoreceptors involved in this pathway are
ipRGCs and not rods and cones. It also
means that the visual system in question is
non-image-forming. However, the involve-
ment of the classical photoreceptors cannot
be ruled out.37 It is possible that part of the
emotional response is related to the image-
forming visual system and that light stimu-
lates the classical photoreceptors in the same
way as other visual stimuli.39 This path is
from now referred to as the limbic pathway.
As shown in Figure 2, the amygdala and
the SCN both use orexin neurons in the LHA
to deliver messages to the LC, the core of the
activation system. Therefore, the authors
suggest that the different paths are parallel
to each other and that they unite in orexin
Lighting Res. Technol. 2012; 44: 238–252
244 E Rautkylä et al.
neurons continuing on the same path to the
activation system (Figure 3). Light’s ability to
affect alertness via melatonin suppression is
well established40–43 and it has been used to
explain the changes in alertness during night-
time light exposure. Therefore, the circadian
pathway can be considered a known pathway
for light-induced alertness. The limbic path-
way, on the other hand, has never before been
considered as the mechanism behind the
alerting effects of light although the theory
is in accordance with the findings of
Vandewalle et al.20 who report that light can
modulate emotional processing by the amyg-
dala. The theory is also consistent with
Figueiro et al.44,45 who recently conducted a
series of studies with long-wavelength, red
light and short-wavelength, blue light and
reported that more than one mechanism, not
just the melatonin pathway, must be involved
in light-induced alertness.
There is also recent evidence that these two
proposed pathways work at the same time
and influence one another. In mice, distur-
bances of limbic system have been found to
affect the circadian system46 and vice versa.47
It should be noted that some neural connec-
tions presented in Figure 2 have been
characterised in only a few mammalian spe-
cies, primarily nocturnal rodents and not
diurnal mammals.48 Therefore, in future stud-
ies, it should be ensured that the circadian
and limbic pathways as described in Section 4
are present in humans. If they are, they could
explain why it is so hard to reach consensus
on the parameters of light, in terms to
the timing and duration of exposure, light
spectrum, colour temperature and light
level that produce the greatest responses in
alertness.1,2,5,20,49,85–87
5. Relationship of light, emotions, and
alertness
If the limbic system, and more precisely the
amygdala, is involved in light-induced
Lighting Res. Technol. 2012; 44: 238–252
alertness, it means that alertness can result
from an emotional stimulus caused or mod-
ulated by the light. Hence, the alerting
response depends strongly on what kind of
emotions the light induces. The hypothetical
model opens two questions. First, how can it
be verified and second, what is the relation-
ship of light, alertness and emotion. This
section will discuss what is currently known
about the relationship of light, alertness and
emotion. In Section 6 suggestions on how to
test the model will be presented.
Brain imaging studies show that emotions
and arousal are connected and that functional
brain differences are associated with stimulus
arousal.50 Activation of the visual cortex is
greater when people are exposed to emotional
as compared to neutral stimuli.50 In skin
conductance measurements, unpleasant stim-
uli have been shown to increase electro-
dermal activity more than pleasant stimuli.
Interestingly, women show a bias towards
more activation for unpleasant than for
pleasant stimuli and men show a tendency in
the opposite direction.51 On the assumption
that the alerting response depends on the
pleasantness of the stimulus, it is important to
consider what makes a light stimulus pleasant
or unpleasant.
The psychology of colour has been widely
studied52 and it is well known that colour
elicits positive or negative feelings and emo-
tions.53,54 For instance, the colour red has
been associated with excitement, yellow with
cheerfulness and blue with comfort and secu-
rity.55 In a study of college students, a blue
colour was found to elicit both negative and
positive feelings;56 positive, because blue was
associated with the ocean and relaxing,
calming effects, and negative, because blue
was also associated with night and depres-
sion. This means that colours can provoke
either type of feeling and that the alerting
response depends on the emotions that it
provokes. However, it also means that cau-
tion should be taken when asserting
 Mechanisms of light-induced daytime alertness
relationships between specific colours and
emotional states because it is subject to large
individual and even cultural differences45 in
response.
Because colour is clearly connected to
emotions, the same can be expected to apply
to the colour of light. In fact, in psychophys-
iological tests colour of light has been shown
to relate to the pleasantness and activating
effects of light.57 In a workplace study con-
ducted in 2008, blue-enriched white light was
found to improve subjective measures of
alertness and positive mood58 compared to
normal white light. In a laboratory study
conducted in 2010,45 both red and blue lights
reduced sleepiness and improved momentary
mood. These results indicate that light can
directly affect mood and alertness and that
the spectral composition of the light plays a
role in these effects.
The parameters of light in the investigations
of the relationship of light, emotions and
alertness are highly interesting to lighting
researchers. So far the studies have concen-
trated on the impact of colour or the combi-
nation of colour and intensity of light on
emotions, and the impact of the duration and
timings of the light exposure on emotions still
remain largely unknown. To be able to develop
a broad understanding of the physiological
mechanisms behind the relationship Plitnick
et al.45 suggest that the light stimulus should be
defined independent as its apparent colour.
It is important to distinguish between the
direct or indirect effects of light on emotions
and hence on alertness, because that allows
using light in different applications. A direct
effect is when light itself is able to induce
emotion, such as a sunny sky that makes a
person happy. An indirect effect is caused by
light or lighting that modulates the response
to another stimulus and therefore indirectly
affects the mood and alertness. This is the
case in theatre lighting.
Recently, Vandewalle et al.37 investigated
the indirect effects of the light spectrum in the
245
presence of vocal stimuli and demonstrated
the acute influence of light on emotional brain
processing. The next step would be to study
whether light has direct effects on emotions
by excluding all other stimuli in laboratory
conditions. Knowledge of the direct effects
could be used in different light treatment
applications to acutely enhance alertness by
light. Indirect effects of ambient light could be
applied to working places and other environ-
ments where there is need to modulate the
mood to retain a good level of alertness.
6. Proposal for how to test the model
As reported by Phan et al.,59 the amygdala
has a specialised role in processing visual
emotional stimuli compared to auditory or
recall stimuli. Passive viewing, hence emo-
tional visual stimuli without any cognitive
task, activates the amygdala. However, it has
been suggested that the visual stimulus has
to be strong to create a conscious emotion.60
If the emotional stimulus is too brief or
too weak the amygdala might not process it
and direct it to conscious thinking.61
Therefore a wide range of irradiance values
should be used to achieve a broad under-
standing on the relationship of light and
emotions.
It seems that both classical and non-
classical photoreceptors contribute to non-
image-forming responses in rodents.40,41 Lall
et al.42 have suggested that low and high
irradiances of light activate different retinal
photoreceptors. At low scotopic light levels
(irradiance of 107 photons/cm2/s at 500 nm43)
rods play a dominant role probably signaling
solely via the visual pathway. At moderate
light levels (irradiance of 1012 photons/cm2/s
at 500 nm43) both rods and cones give input to
non-image-forming vision. There is recent
evidence that under dark-adapted conditions
cones dominate these responses but that light
adaptation limits their influence.42 Although
these photopic irradiances are within the
Lighting Res. Technol. 2012; 44: 238–252
246 E Rautkylä et al.

Test setting Measurements

Scotopic vision
Baseline: darkness (<0.01 lX) Limbic
Stimulus: blue and red, irradiance Amygdala
107 photons/cm2/s at 500 nm
fMRI:
-deactivation and activation of
the amydala, the SCN and the
LC measured in consequent Brainstem
Retina scanning sessions
Light LC
Rod&cone/ipRGC
Self-reports:
-Kiss and POMS measured in
Photopic vision 1-minute intervals
Baseline: darkness (<0.01 lX)
Stimulus: blue and red, irradiance Circadian
1015 photons/cm2/s at 500 nm SCN

1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20
KSS & POMS 1min
Baseline (8 min) Stimulus (4 min) Baseline (8 min)
fMRI consequent scanning sessions (20 min)

Figure 4 The second step in the experimental design on how to test the effects of light on alertness via the amygdala.
It consists of four 20-minute subtests, each subtest containing a 4-minute exposure to the selected light stimulus in
between two 8-minute baseline lighting conditions (darkness). The selected light stimuli are blue and red light from
the scotopic and photopic range. Each subtest is recorded with fMRI, and the activation and the deactivation of the
amygdala, the SCN and the LC as a function of time are compared to the self-rated sleepiness and mood. They are
measured at 1-minute intervals by the KSS and POMS. In the third step, the study protocol is advanced by four more
subtests to investigate the gradient change from photopic to scotopic light level

sensitivity range of cones it seems that their
involvement in non-image-forming vision can
mainly be seen after abrupt changes in
irradiance. Therefore, currently undefined
rod pathways are considered to play the key
role in these circumstances. Melanopsin in the
ipRGCs seems to encode high irradiances
(irradiance of 1015 photons/cm2/s at
500 nm43) and drive responses in most day-
light conditions.
To test the suggested model and see
whether light can evoke emotions that
induce alertness, the following three-step
study protocol is proposed.
In the first step, the subjects are exposed to
different light stimuli as well as darkness and
they are asked to rate their mood on the
Visual Analogue Mood Scale (VAMS)64 in
the absence of any other stimuli or tasks. The
purpose of the first step is to simply
Lighting Res. Technol. 2012; 44: 238–252
investigate how the light stimuli affect the
emotional state. Using the same light stimul in
the second step allows the comparison of the
results.
The second step consists of four subtests
with darkness as a baseline as illustrated in
Figure 4. The first two subtests are done at
scotopic lighting levels with blue and red light
as the stimuli, and the following two at
photopic lighting levels with blue and red
light, respectively. Mesopic lighting levels are
included in the third step.
In the third step, the study protocol is
advanced by four more subtests to investigate
the gradient change from photopic to scoto-
pic light level during the 4-minute light
exposure and vice versa with both blue and
red light. This simulates the change in lighting
conditions at dusk and dawn, respectively,
and is needed to test whether such changes
 Mechanisms of light-induced daytime alertness
intensify the emotional and alerting effects of
light stimuli.
Each subtest in steps 2 and 3 is recorded
using functional Magnetic Resonance Imaging
(fMRI) scanning sessions over the baselines
and the light exposure. Self-ratings of sleepi-
ness and emotion are measured verbally
throughout the recording at 1-minute inter-
vals. Sleepiness is measured with the
Karolinska Sleepiness Scale (KSS)63 and emo-
tion with a shortened version of the Profile of
Mood States (POMS).65 Mood state is used as
an indicator of emotion66 because measuring
emotional reaction is complex.
From the fMRI scans the activation and
the deactivation of the amygdala, the SCN
and the LC are analysed as a function of time.
The activation patterns will reveal whether
there is any order of activation and therefore
a causal relationship between the light-
induced activation of the amygdala or the
LC and the increase in experienced levels of
emotions or alertness; whether the amygdala
and the SCN are activated simultaneously or
in turns depending on the light stimulus; and
whether different light stimuli induce non-
image-forming responses that outlast the
exposure and decline slowly, or classical
image-forming responses that cease very
shortly after the stimulation.3
It is hypothesised that the activation and
the deactivation patterns induced by photopic
and scotopic light stimuli will differ from each
other. Also, it is hypothesised that the acti-
vation and the deactivation depend on the
spectral composition of the stimuli. However,
it is not possible to predict which stimuli will
activate the amygdala, the SCN and the LC
the most, because not enough is yet known
about the projections from the three photo-
receptors to the brain areas in question.
7. Conclusions and perspectives
The direct link from the retina to the limbic
system was identified6 in the 1970s creating
247
the basis for understanding how light cues
may affect alertness. This paper is the first to
suggest that the limbic pathway for light-
induced alertness operates in parallel with the
well established circadian pathway.
According to this novel theory the visual
light stimulus can travel via the RHT in the
circadian system or use the limbic system, the
centre of emotions, to create an emotional
response to the light cue. The paper suggests
that the two pathways unite in orexin neurons
and continue as the same path to the arousal-
promoting nuclei.
The existence of the limbic pathway for
light-induced alertness would mean that the
alerting effects of light can depend on what
kind of emotions the light induces or modu-
lates. For example, a person can become more
alert in daylight compared to darkness
because he is either happy (pleasant direct
stimulus), or because the light exposure is
disruptive (unpleasant direct stimulus), or
because the light has an influence on how he
feels about his view (indirect effect on external
emotional stimulus).
The theory of a second pathway is sub-
stantial, because it extends knowledge of the
mechanisms behind the alerting effects of
light and gives a possible explanation as to
how light affects alertness during daytime
where there is hardly any melatonin. To verify
the theoretical model, it is essential to study
the relationship of light, emotions, circadian
processes and alertness. The fact that people
have very individual reactions to light com-
plicates the design of scientific tests and the
interpretation of the results. Therefore, it is
challenging to find appropriate objective
methods to study emotions and alertness.
Some methods to test the novel model are,
however, suggested.
An open question is whether these two
proposed systems, the circadian and the
limbic, work simultaneous or alternatively.
More research is needed to see how these two
systems influence one another. The involvement
Lighting Res. Technol. 2012; 44: 238–252
248 E Rautkylä et al.
of an emotional factor in the circadian pro-
cesses could explain why people show such
different responses in tests concerning light-
induced alertness.
This paper is expected to be of great
interest to both lighting and brain researchers
because if the model is verified, it can reveal
the missing link between the light exposure
and the enhancement of brain responses
driving daytime alertness. Therefore, it
has the potential to set the basis for future
studies.
Acknowledgements
The authors thank Timo Partonen MD from
the Department of Mental Health and
Substance Abuse Services, National Institute
for Health and Welfare for his valuable
comments on the theory.
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