5 – Metaboloic rank order
Not only does the inferior colliculus have the greatest
blood flow and glucose utilization in the mammalian
brain, investigations by Hovda et al. (1992),
Calingasan et al (1994), and Gonzalez-Lima (1997)
have shown that this auditory nucleus also has the
largest amounts of enzymes for aerobic metabolism
[1-3]; and Rahner-Welsch et al (1995) and Zeller et al
(1997) found the highest concentrations of glucose-
transport proteins in the inferior colliculus 4, 5].
Sokoloff (1981) commented on measurements in his
laboratory of regional glucose uptake, “The inferior
colliculus is clearly the most metabolically active
structure in the brain” [6].
Why should the inferior colliculus be the most
metabolically active structure in the brain? What are
its functions that merit greater blood flow, glucose
transport, and enzymes for aerobic metabolism? The
auditory system appears to be the most highly active
component of the brain, and much orchestration of
excitatory and inhibitory functions within this important
sensory system appears to take place in the inferior
colliculus. To understand the workings of this
metabolically most active site in the brain should be a
priority for neuroscience research.
As will be discussed in the following pages, protective
biofeedback mechanisms act to protect the inferior
colliculus during periods of hypoxia and in other
adverse circumstances. In these situations the
inferior colliculi are spared at the expense of less
active regions of the brain. A need to protect function
within the inferior colliculus would appear to be
important; the inferior colliculi must play an important
role not just for the auditory system but for the brain
as a whole.
Impairment of function within the inferior colliculus
deserves investigation as a possible cause of
attentional deficits in children with autism. In addition
to its auditory functions, the inferior colliculus may be
essential for general awareness and perhaps in
humans even for elementary cognizance of social
norms. This may sound simplistic, but it should be as
worthy of discussion as theorizing about the location
of autism genes on chromosomes.
The possibility that autism might be the result of
dysfunction within the higher auditory system, its
connections to the temporal and frontal language
areas, and its developmental and ongoing influence
on the cross-modal association tracts of the cortex
merits consideration. Music, we know, exercises the
memory system of the human brain; acoustic
stimulation ascends the auditory pathway to the
temporal lobes and beyond. Neurotransmission
beginning in the auditory system would appear to be
uniquely significant to higher cognitive function.
Language disorder should be recognized as the most
disabling aspect of autism. If for no other reason
research on auditory dysfunction deserves to be
made a priority. Before presuming that frontal-lobe
executive functions are impaired in autism because of
hypothetical genes on diverse chromosomes, it is
time to look at how maturation of the frontal lobes
derives from earlier maturing brainstem sensory
systems.
There are good reasons to look at other subcortical
nuclei like the amygdala and growth within the limbic
system. But the auditory pathway is the most active,
phylogenetically newest, and earliest maturing system
of the brain. Clear evidence exists that the auditory
system is easily damaged by a number of
environmental factors. For these reasons it deserves
attention.
- Hovda DA et al (1992)
Maturation of cerebral
oxidative metabolism in the
cat: a cytochrome oxidase
histochemistry study.
- Calingasan NY et al (1994)
Distribution of the alpha-
ketoglutarate dehydrogenase
complex in rat brain.
- Gonzalez-Lima F et al. (1997)
Quantitative cytochemistry of
cytochrome oxidase and
cellular morphometry of the
human inferior colliculus in
control and Alzheimer's
patients.
- Rahner-Welsch S et al (1995)
Regional congruence and
divergence of glucose
transporters (GLUT1) and
capillaries in rat brains.
- Zeller K et al (1997)
Distribution of Glut1 glucose
transporters in different brain
structures compared to
glucose utilization and
capillary density of adult rat
brains.
- Sokoloff L (1981) Localization
of functional activity in the
central nervous system by
measurement of glucose
utilization with radioactive
deoxyglucose.
- Hovda DA, Chugani HT, Villablanca JR, Badie B, Sutton RL (1992) Maturation of
cerebral oxidative metabolism in the cat: a cytochrome oxidase histochemistry study.
Journal of Cerebral Blood Flow and Metabolism 12:1039-1048
- Calingasan NY, Baker H, Sheu KF, Gibson GE (1994) Distribution of the alpha-
ketoglutarate dehydrogenase complex in rat brain. Journal Of Comparative Neurology
346:461-479.
- Gonzalez-Lima F, Valla J, Matos-Collazo S (1997) Quantitative cytochemistry of
cytochrome oxidase and cellular morphometry of the human inferior colliculus in
control and Alzheimer's patients. Brain Research 752:117-126.
- Rahner-Welsch S, Vogel J, Kuschinsky, W (1995) Regional congruence and
divergence of glucose transporters (GLUT1) and capillaries in rat brains. Journal of
Cerebral Blood Flow and Metabolism 15:681-686.
- Zeller K, Rahner-Welsch S, Kuschinsky W (1997) Distribution of Glut1 glucose
transporters in different brain structures compared to glucose utilization and capillary
density of adult rat brains. Journal of Cerebral Blood Flow and Metabolism 17:204-209.
- Sokoloff L (1981) Localization of functional activity in the central nervous system by
measurement of glucose utilization with radioactive deoxyglucose. Journal of
Cerebral Blood Flow and Metabolism 1:7-36.