TABLE OF CONTENTS

Title Page    –         –         –         –         –         –         –         –         –         i

Certification –         –         –         –         –         –         –         –         –         ii

Dedication   –         –         –         –         –         –         –         –         –         iii

Acknowledgement –         –         –         –         –         –         –         –         iv

Table of Content    –         –         –         –         –         –         –         –         v

CHAPTER ONE 

1.0 INTRODUCTION – –         –         –         –         –         –         1

CHAPTER TWO

2.0     Dopamine    –         –         –         –         –         –         –         –         4

2.1     History of Dopamine       –         –         –         –         –         –         6

2.2     Comparative Biology and Evolution    –         –         –         –         8

2.3     Functions of Dopamine   –         –         –         –         –         –         10

2.3.1  Cellular Effects      –         –         –         –         –         –         –         11

2.3.2  Neuromuscular Junction  –         –         –         –         –         –         12

2.3.3  Autonomic Nervous System      –         –         –         –         –         12

2.3.4  Direct Vascular Effect      –         –         –         –         –         –         13

2.3.5  Memory       –         –         –         –         –         –         –         –         14

2.4     Diseases and Disorders of Dopamine  –         –         –         –         15

CHAPTER THREE

3.0     Pharmacological Activities of Dopamine

3.1     Biosynthesis of Dopamine         –         –         –         –         –         18

3.2     Mode of Action of Dopamine    –         –         –         –         –         21

3.3     Degradation of Dopamine          –         –         –         –         –         21

CHAPTER FOUR

4.0     Summary and Conclusion

4.1     Summary     –         –         –         –         –         –         –         –         24

4.2     Conclusion  –         –         –         –         –         –         –         –         24

References

CHAPTER ONE

1.0     INTRODUCTION

Initially, studies on neural cell communication focused exclusively on electrophysiological aspects but, in the beginning of twentieth century, scientists such as John N. Langley and Thomas R. Elliot introduced the concept of chemical release upon nerve stimulation (Starke 2014). These ideas were confirmed later by the work of Otto Loewi, Henry Dale, Ulf von Euler, and others, who demonstrated that acetylcholine and adrenaline acted as chemical transmitters in the parasympathetic and sympathetic nervous systems. Subsequently, the physiological roles of another chemical transmitter, dopamine, were described by Carlsson et al. (1957). Chemical transmitters such as acetylcholine and dopamine belong to a class of molecules termed neurotransmitters that are the primary mode of cell-to-cell communication in the nervous system and associated with many diseases.

Typically, neurotransmitters are synthesized endogenously and act as signaling molecules. Neurotransmitters are stored in vesicles in presynaptic terminals and released into the synaptic cleft in response to an action potential or after a graded potential threshold is met (Steinhardt et al. 1994). Once released, they can elicit a physiological response in postsynaptic or nearby cells. In general, neuro transmission occurs quickly and the compound is rapidly (i) metabolized by enzymes, (ii) taken back up by presynaptic neuron, or (iii) bound to postsynaptic neurons or target cells’ receptors (Garris et al. 1994).

Many compounds are released by cells, but bona fide neurotransmitters must meet a distinct set of criteria (Sourkes, 2009): (i) the compound should be synthesized in presynaptic neurons; (ii) when the presynaptic neuron is activated, the release of this compound should lead to an effect on postsynaptic neuron(s) or target cell(s); (iii) when administered exogenously, similar outcomes to endogenous stimulation would occur; and (iv) a mechanism of neurotransmitter removal, from synaptic cleft after signaling, should be in place.

Neurotransmitters can be subdivided according to their molecular identity: small organic molecules, peptides, monoamines, nucleotides, and amino acids (Kandel et al. 2013). A functional classification may also be utilized, since these molecules can act as excitatory or inhibitory transmitters and can also bind to fast response ionotropic receptors or slower response metabotropic receptors (Kandel et al., 2013).