THE CONTRIBUTIONS OF PRESYNAPTIC ALPHA-2 (α2) RECEPTORS AND PROSTAGLANDIN E-SERIES TO THE CONTROL OF SYMPATHETIC NERVOUS ACTIVITY.

      ABSTRACT

The Sympathetic nervous systems (SNS) is an efferent division of the

Autonomic nervous system (ANS) with neurons which anatomically originates in

the central nervous system (CNS). It has a short preganglionic neuron which

comes from the thoracic and lumbar regions (T1 to L2) (also termed,

thoracolumbar outflow) of the spinal cord. The axons of the postganglionic

neuron extend from these ganglia to the tissues that they innervate and

regulate. In most cases, the preganglionic nerve endings of the sympathetic

nervous system are highly branched, enabling one preganglionic neuron to

interact with many postganglionic neurons. This arrangement thus enables this

division to activate numerous effector organs at the same time (Whalen, 2015). The activities of the SNS are initiated at the

effector organs by the binding and stimulatory actions of specific

neurotransmitter chemicals which are released by exocytosis at the presynaptic

terminals of neurons. The transmitter released by all preganglionic sympathetic

neuron except those supplying the sweat gland is Noradrenaline (NA). The

preganglionic sympathetic neuron supplying the sweat gland is Acetylcholine (Ach). The activities

(effects) initiated by the SNS are predominantly under the control of α2-adrenargic receptors and prostaglandin

E-series.

TABLE OF CONTENT

1.0       INTRODUCTION:…………

1.1             Sympathetic Nervous System (SNS)…………………….

1.2             SNS Activities………………………………………………………

1.3             Transmitters Of SNS…………………………………………… 

2.0       PRESYNAPTIC RECEPTORS……………………… 

3.0       CONTRIBUTIONS OF PRESYNAPTIC α2-ADRENERGIC

RECEPTORS TO THE CONTROL OF SYMPATHETIC NERVOUS ACTIVITY……………….

3.1             α2–Adrenergic

Receptor…………………………………………

3.2             Signal

Transduction Pathway Of α2-Adrenernoceptor Regulation Of SNS…

3.3             Neurotransmitter

(Noradrenaline) Release…………

3.4             Involvement

Of The Membrane Na+-K+-ATPase In The Modulation Of Norepinephrine

Release Through Presynaptic Inhibitory α2-Adrenergic Receptors…………………………………………………………

3.5             Influence

Of Neuronal Uptake Of Noradrenaline On Negative Feedback Mechanism Mediated By

Presynaptic α 2- Adrenoceptor…………………………

3.6             Presence

Of Presynaptic Inhibitory α2 –Adrenoceptors In The Brain…………

3.7             Physiological

Significance Of Negative Feedback Mechanism Mediated By   Presynaptic α 2 –Adrenoceptors………………………………………………………………

3.8             Mechanism

Of Action Of α 2-Adrenergic Receptors In The Release Of Na…

3.9              Molecular

Evidences Of The Role Of α 2—Adrenergic Receptors In The

Release  Of Na……………………………………………………………………………………

 

4.0       CONTRIBUTIONS OF PROSTAGLANDIN TO THE CONTROL OF

SYMPATHETIC NERVOUS ACTIVITY………………………………………

4.1             An

Overview Of Prostaglandins…………………………………………………………….

4.2             Prostaglandin Receptors…………………………………………………………………

4.3             Prostaglandin E Synthase………………………………………………………………………

4.4             Prostaglandins

E2 Receptors………………………………………………

4.5             Some Sympathemometic Effects Of

Prostaglandins E2 Series…………………

4.6             Presynaptic Inhibition Of

Noradrenergic Neurotransmission By Prostaglandins E Series…………………

4.7             Actions Of Pg E-Series On Adrenergically Innervated

Tissues…………………

                       Diminished Vasoconstrictor

Spleen:-………………………………………………………

                     Chronotropic And Inotropic

Responses To Sympathetic Nerve:-………………

                     Vascular Beds:-………………………………………………………………………………………

                       PGE Inhibit Twitch Response To Nerve

Stimulation:………………………………..

                       Enhancement Of Synaptic Transmission………………………………………………….

                     Hippocampus………………………………………………………………………………………… 

5.0      SUMMARY/CONCLUSION……………………………………………………….

                         

                                REFERENCES……………………………………………………….