Trace Amines and Neurological Disorders. Potential Mechanisms and Risk Factors

400 Pages·2016·16.7 MB·English

by  Tahira Farooqui

TRACE AMINES AND
NEUROLOGICAL DISORDERS
http://booksite.elsevier.com/9780128036037/
TRACE AMINES AND NEUROLOGICAL DISORDERS
Tahira Farooqui and Akhlaq A. Farooqui
TRACE
AMINES AND
NEUROLOGICAL
DISORDERS
POTENTIAL MECHANISMS
AND RISK FACTORS
Edited by
Tahira Farooqui
Department of Entomology, The Ohio State University,
Columbus, OH, United States
Akhlaq A. Farooqui
Department of Molecular and Cellular Biochemistry, The Ohio State University,
Columbus, OH, United States
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THE FUTURE BELONGS TO THOSE WHO BELIEVE IN THE BEAUTY OF THEIR DREAMS.
―Eleanor Roosevelt
v
Dedication
We dedicate this book to “all the teachers” who have made a profound difference in our lives
by teaching with passion, making us able to differentiate between right and wrong, and
molding our lives in the right direction.
vi
List of Contributors
A. Accorroni Scuola Superiore St. Anna, Pisa, Italy
A. Ahmad Department of Zoology, Maulana Azad National Urdu University, Hyderabad, India
S.H. Al Rokayan Research Chair for Biomedical Applications of Nanomaterials,
King Saud University, Riyadh, Saudi Arabia
A.S. Alhomida Department of Biochemistry, King Saud University, Riyadh, Saudi Arabia
G. Andersen German Research Center for Food Chemistry, Leibniz Institute, Freising, Germany
A. Baumann Forschungszentrum Juelich, Institute of Complex Systems – Cellular Biophysics
(ICS-4), Juelich, Germany
M.D. Berry Department of Biochemistry, Memorial University of Newfoundland, St. John’s,
NL, Canada
H. Biebermann Institute of Experimental Pediatric Endocrinology, Charité University Medicine,
Berlin, Germany
W. Blenau Institute of Zoology, University of Cologne, Cologne, Germany
L. Carvelli Department of Biomedical Sciences School of Medicine & Health Sciences, University of
North Dakota, Grand Forks, ND, United States
S. Espinoza Department of Neuroscience and Brain Technologies, Italian Institute of Technology,
Genova, Italy
A.A. Farooqui Department of Molecular and Cellular Biochemistry, The Ohio State University,
Columbus, OH, United States
T. Farooqui Department of Entomology, The Ohio State University, Columbus, OH, United States
E.A. Gozal Department of Physiology, Emory University School of Medicine, Atlanta, GA,
United States
X. Guo Beijing Institutes of Life Sciences, Chinese Academy of Sciences, Beijing, China;
State Key Laboratory of Integrated Management of Pest Insects and Rodents, Institute of Zoology,
Chinese Academy of Sciences, Beijing, China
S. Hart Department of Biochemistry, Memorial University of Newfoundland, St. John’s, NL,
Canada
Y. Hashiguchi Department of Biology, Osaka Medical College, Takatsuki City, Osaka, Japan
S. Hochman Department of Physiology, Emory University School of Medicine, Atlanta, GA,
United States
K. Ikemoto Department of Psychiatry, Iwaki Kyoritsu General Hospital, Iwaki, Japan
L. Kang Beijing Institutes of Life Sciences, Chinese Academy of Sciences, Beijing, China;
State Key Laboratory of Integrated Management of Pest Insects and Rodents, Institute of Zoology,
Chinese Academy of Sciences, Beijing, China
xv
xvi
List of Contributors
N. Khajavi Institute of Experimental Pediatric Endocrinology, Charité University Medicine, Berlin,
Germany
H.A. Khan Department of Biochemistry, King Saud University, Riyadh, Saudi Arabia
G. Kleinau Institute of Experimental Pediatric Endocrinology, Charité University Medicine, Berlin,
Germany
J. Köhrle Institute of Experimental Endocrinology, Charité University Medicine, Berlin, Germany
D. Krautwurst German Research Center for Food Chemistry, Leibniz Institute, Freising, Germany
A. Laurino Department of Neuroscience, NEUROFARBA, Section of Pharmacology, University of
Florence, Florence, Italy
A. Ledonne Department of Experimental Neurosciences, Santa Lucia Foundation, Rome, Italy
D. Leo Department of Neuroscience and Brain Technologies, Italian Institute of Technology,
Genova, Italy
Z. Ma Beijing Institutes of Life Sciences, Chinese Academy of Sciences, Beijing, China; State Key
Laboratory of Integrated Management of Pest Insects and Rodents, Institute of Zoology,
Chinese Academy of Sciences, Beijing, China
N.B. Mercuri Department of Experimental Neurosciences, Santa Lucia Foundation, Rome,
Italy; Department of System Medicine, University of Rome “Tor Vergata”, Rome, Italy
A.D. Mosnaim Department of Cellular and Molecular Pharmacology, Neuroimmunopharmacology
Laboratory, The Chicago Medical School at Rosalind Franklin University of Medicine and Science,
Chicago, IL, United States
C.-U. Pae Department of Psychiatry, The Catholic University of Korea College of Medicine, Seoul,
Republic of Korea; Department of Psychiatry and Behavioral Sciences, Duke University Medical
Center, Durham, NC, United States; Department of Psychiatry, Bucheon St. Mary’s Hospital,
Wonmi-Gu, Bucheon, Kyeonggi-Do, Republic of Korea
A. Pryor Department of Biochemistry, Memorial University of Newfoundland, St. John’s, NL,
Canada
L. Raimondi Pharmacology Unit, Department of Neuroscience, Drug Sciences and Child Health,
University of Florence, Florence, Italy
T. Roeder Department of Zoology, Molecular Physiology, Kiel University, Kiel, Germany
S.I. Sherwani Department of Internal Medicine, Division of Pulmonary Medicine, Dorothy
M. Davis Heart and Lung Research Institute, The Ohio State University College of Medicine,
Columbus, OH, United States
Q. Ullah Department of Chemistry, Maulana Azad National Urdu University, Hyderabad, India
L.J. Wallace Division of Pharmacology, College of Pharmacy, The Ohio State University, Columbus,
OH, United States
S.-M. Wang Department of Psychiatry, The Catholic University of Korea College of Medicine,
Seoul, Republic of Korea; International Health Care Center, Seoul St. Mary’s Hospital,
The Catholic University of Korea College of Medicine, Seoul, Republic of Korea;
Department of Psychiatry, Seoul St. Mary’s Hospital, Seocho-Gu, Seoul, Republic of Korea
M.E. Wolf International Neuropsychiatry Consultants, Highland Park, IL, United States
R. Zucchi Department of Pathology, University of Pisa, Pisa, Italy
Foreword
It is a true honor for me to write this Foreword for Tahira Farooqui and Akhlaq
Farooqui’s book Trace Amines and Neurological Disorders: Potential Mechanisms and Risk
Factors, which comes at an opportune moment. Just as long journeys invite the avid trave-
ler to reflect on the wonders and awe-inspiring places discovered along the way, travels
through the history of science often lend themselves to contemplation and jubilation. More
than a hundred years after Polish biochemist, Marceli Nencki, first isolated phenylethyl-
amine from decomposing gelatine, and following many decades of a tenacious quest for
the neurobiological substrate of the mysterious neurophysiological actions of trace amines,
a group of naturally occurring and endogenous compounds chemically related to pheny-
lethylamine, research into this most intriguing aminergic system has been burgeoning with
ever-increasing momentum. Long regarded as “false transmitters” and believed to exert no
more than indirect sympathomimetic actions, this collection of endogenous amines is today
regarded as protean neurotransmitters, featuring both transmitter and neuromodulatory
actions. Both the topographical distribution of trace amines in the brain and their signal-
ing transduction pathways are currently undergoing extensive mapping and delineation. As
new breakthroughs occur in this fast-moving field, new avenues are opened for understand-
ing normal brain function and unraveling the pathogenesis of neurological disease. Today,
for us, travelers through the history of neurological science, it is a fitting moment to reflect
and rejoice on what we have achieved. This remarkable book is in many ways a celebra-
tion of the work of hundreds of physiologists, biochemists, neurologists, and neuroscientists
who have delved into the significance of the trace amines, carving out a new understanding
of the brain and its functions.
In every journey, the traveler finds historic landmarks, places where history was made
and paradigms shifted. If I had to choose one moment in time when a fundamental change
of ideas took place, invigorating a renewed interest in the long-known and elusive trace
amines, then the turn of the 21st century would be that moment. Albeit another trace amine,
octopamine, had previously met the status of bona fide neurotransmitter with the identifica-
tion of octopamine receptors in Aplysia neurons, the historic landmark of this decades-long
quest was the serendipitous discovery of the trace aminergic receptor system in vertebrates,
owing to the work of Beth Borowsky and her collaborators. In the search for additional
subtypes of the serotonin receptor class, a large family of G-protein-coupled receptors was
cloned from human and rodent tissue. Such a family of receptors exhibited a high degree of
within-species homology but low similarity across orthologs, thereby suggesting that these
receptors had been rapidly evolving in the vertebrate brain. Of the newly cloned mamma-
lian receptors, some were shown to be bound and directly activated by trace amines, ini-
tiating components of intracellular signal transduction cascades. To account for the orphan
receptors that were insensitive to trace amines, Lothar Lindemann and collaborators
xvii
xviii
Foreword
proposed a uniform nomenclature, which has been widely adopted since, with this assort-
ment of receptors being currently referred to as the trace amine-associated receptor (TAAR)
family. In addition to the canonical olfactory receptors, evidence showed that many of these
receptors played a fundamental role as vertebrate chemosensory receptors. Indeed, the pres-
ence of TAARs in the olfactory epithelium of unique subsets of sensory neurons seemed to
allow the identification of many odorants, including a number of volatile amines carrying
key social information and, possibly, pheromones, thus guiding aversion to, and attraction
towards, salient external stimuli. Fittingly, an important part to this book is devoted to the
exploration of the prominent role of TAARs in olfactory behavior and olfactory learning.
Most notably, in the course of these ground-breaking investigations it became apparent
that one such receptors for trace amines, TAAR1, was exceptionally unique, for only TAAR1
displayed affinity for all of the trace amines and only the TAAR1 gene was found to be
phylogenetically conserved in the brain of all mammalian species studied thus far, includ-
ing human. Such remarkable discoveries shed new light on this field and brought TAAR1
under the spotlight in the realm of neurology and neuroscience. Although traces amines
have long been known to regulate, and be themselves susceptible to regulation by, associ-
ated neurotransmitters, evidence of direct interactions between aminergic systems and
receptors for trace amines had been lacking. Mapping studies indicated that Taar1 expres-
sion was enriched throughout the limbic and ascending aminergic pathways, encompassing
the ventral tegmental area/substantia nigra and dorsal raphe nucleus, regions that contain
the dopamine- and serotonin-producing neurons, respectively, and was therefore strategi-
cally positioned to regulate the activity of these transmitter systems in the terminal regions
of the basal ganglia and limbic brain. Moreover, transgenic mice models revealed that Taar1
deletion led to elevated discharge rate of dopamine and serotonin neurons, suggesting that
TAAR1 activation acted as a brake for aminergic neurotransmission. Soon thereafter, the
advent of the first selective agonists and antagonists at TAAR1 contributed to reinforce the
notion that TAAR1 might be exquisitely sensitive to fluctuations in aminergic transmitter
signaling. Having focused on the dopamine transporter for a considerable time, I was then
actively searching for novel pharmacotherapeutic targets for addiction-spectrum disorders
and I first learnt about these new compounds through my colleagues at Hoffmann-La Roche
Ltd. Indeed, such a discovery was also a turning point in my personal career. Using these
newly developed pharmacological tools, the experiments of my colleagues lent further cre-
dence to the thesis that TAAR1 activation could indeed modulate aminergic transmission
in complex fashion, in fact, producing contrasting effects on dopamine and serotonin neu-
ronal discharge depending on the level of agonist activity at TAAR1. My own experiments
showed that TAAR1 activation could reduce a range of drug-related behaviors, including
psychomotor stimulant self-administration and relapse to drug-seeking. The overall conclu-
sion of a large body of freshly accrued neurophysiological data was that TAAR1 seemed to
be constitutively active and/or tonically activated by endogenous ligands, such that partial
agonism would result in antagonistic-like effects. If this held true then it would appear that
the use of a partial agonist could be more advantageous in situations where neurochemi-
cal imbalances lead to deficient or excessive TAAR1 stimulation, providing a means to “sta-
bilize” TAAR1 activity. Furthermore, through induction of pacemaker activation, partial
TAAR1 agonism could potentially promote “normalization” of dopamine and serotonin
neuron discharge. What is more, in addition to altering the major aminergic pathways, trace