الفهرس 
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Abstract
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Certain transmitters are utilized in different
areas of the brain. It was thought that only one neurotransmitter
is released at each nerve ending, but
this was challenged by the discovery that some neuropeptides
share the same nerve ending as the conventional
neurotransmitter e.g. dopamine and cholecystokinin.
The study of neurotransmitters is done by testing
neurones along their pathways on brains of lower
mammals. The fluorescent microscopy was used for the
study of noradrenergic neurones by the glyoxylic acid
method •. Two noradrenergic systems have been discovered;
one arises from cell bodies in the pons and medulla
and projects in the ventral bundle to the hypothalamus.
The other projects in the dorsal bundle. The
former i’8 concerned with homoestasis, and the latter
ts concerned with learni’ng and attention. Serot”-e%’tlJic
cell bodies are arranged in eight clusters in the
midbrain raphe. They are concerned with a tonic inhibttory
control on.ACTH secretion, and with thermal regulation,
sleep cycles and interpretation of individual
to cognitive i’nformation. Dopaminerglc neurones are
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found mainly in the basal ganglia and nigrostriatal
system. Its functions are concerned with extrapyramidal
motor control and regulation of hormone release.
Acetylcholine neurones have short axons. It has an
excitatory function concerned with rapid responses,
thinking and knowing aspects. GABA neurones have
inhibitory functions on eNS and they are intermediary
in cell metabolism. Its functions are similar in many
aspects to that of acetylcholine. They playa role in
extrapyramrdal functions and inhibitory components 1n
sensortmotor reflexes.
Endorph~ns, small endogenous proteins which Interact
with the same receptors of morphine and share
many of its actions, are found mainly in basornedial
and basolateral hypothalmus and send axons to the anterior
hypothalmus nuclei, pons and midbrain. They have
generally a depressant function and mediate analgesic
effects.
It was shown that antidepressants facilitate transmission
in aminergic neurone systems, while reserpine
whl’ch deplete their storage vesicles increase.! symptoms
of depression. So, the amine hypothesis arised which
claimed catecholamine deficiency in depression and
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increase in mania. It was shown also that metabolites
of these amines e. g. homovaai.111c acid of dopamine and
MHPGof noradrenaline, are lowered in depression. And,
it was shown that precursors, e.g. tryptophan tile
precursor of seroton!”’, have ant1depre8Saht effect.
This hypothesis have many dr,awbacks, it does not explain
the latent therapeutic effect of antidepressants (MAOr
and tricylic). Also, it does not explain how some antidepressants,
e.g. iprindole, have antidepressant effects
whiLe they have no effect on amine reuptake.
A recent hypothesis .of dysregulation explains the
aetiology of depression by comparing it with type II
diabetesmellttus, where genetic and environmental factors
are involved.
So, noradrenaline levels like insulin may be increased,
decreased or normal depending on phase of illness,
and noradrenergtc receptors like insulin receptors may
regulate mechanism which is impaired in disease.
It was shown that most depressed patients have
increase in cortisol output and that dexamethasone
suppression test is impai’red in most melancholic patients.
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Study of endorphins by using Anta~on1.ts, radioimmunoassay
and radioreceptor assay, has shown excess
endogenous opioid act! vi ty contributing to manic symptoms.
Dopamine hypothesis of schizophrenia 1s based on
the anphetamine assembling to schizophrenic sy~toms.
Amphetamine enhances effects of noradrenaline and dopamine
by releasing them in synaptic cleft and preventing
reuptake. It was also observed that, efficient antipsychotic
drugs can cause parkinsonism and that dopaamine
is deficient in parkinsonism.
Transmethylation hypothesis postulates that many
hallucinogens were methylated substances. It was shown
that methionine produces manifestations of schizophrenia
by enhancing transmethylation.
Recently, many studies on the role of endorphins
in schtzophrellia were done. The results were conflicting.
A ~;J:.gnificant higher plasma B endorphin and B liptoropin
was observed in schizophrenic patients in recent studies.
Studies on biochemical basis of anxiety have shown that
noradrenaline may be concerned with fear anxiety behavior.
Plasma MHPG(NEmetabolite) was observed to increase
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after panic attacks. Imipramine which inhibits presyna-
\
ptic reuptake of noradrenaline may reduce their symotoms.
A decrease of choline acetyltransferase activity
(marker of cholinerqic neurones), was observed in Alzheimerts
disease. Recent studies on CSF immunoreactivity of endorphi~~
show marked decrease in p endorphin like immunoreactivity
levels in Alzheimer’s disease. So, p endorphin
may have a role in the pathophysiology of Alzheimer’s
disease. The role of neurotransmitters in psychiatric
disorders is a qrowinq field for study. It may be that,
in the near future, all the mysteries of this subject
would be discarded.