Neurohumoral transmission refers to the transmission of impulse through synapse and neuro-effector junction by the release of humoral (chemical) substances. The term ‘conduction’ stands for the passage of an impulse along an axon or muscle fibre. Almost all autonomic drugs, which are used clinically, exert their pharmacological actions by altering essential steps in the neurohumoral transmission process.
The principal neurotransmitters released from the postganglionic sympathetic and parasympathetic nerve endings respectively are noradrenaline (NA or norepinephrine, NE) and acetylcholine (ACh), whereas the transmitter released in ganglia from the preganglionic nerve ending of both systems is acetylcholine.
Steps in Neurohumoral Transmission
1. Impulse conduction:
The resting transmembrane potential is established by high K+ permeability of axonal membrane and high axoplasmic concentration of this ion coupled unit’s low Na+ permeability and its active extractions. Stimulations or arrival of an electrical impulse causes a sudden increase in Na+ conductance depolarization and overshoot (reverse polarization), K+ ion than move out in the direction of their concentration gradient and repolarization occurs. Ionic distribution in normalized during the refractory period by the activation of Na+, K+ pump.
2. Transmitters release:
The transmitter (excitatory or inhibitory) is stored in pre-junctional nerves ending within ‘Synaptic vessels’. Nerve impulse promotes fusion of vascular and axonal membrane, through Ca++ entry which fluidized membranes.
The release process can be modulated by the transmitter itself by other agents through activation of specific receptors located on the prejunctional membrane e.g. noradrenalin (NA) release is inhabited by NA (α2 receptors), dopamine, adenosine, prostaglandins and enkephalins, while isoprenaline (β2 receptor) increases NA release. Similarly α2 and muscarinic agonists inhibit acetylcholine (ACH) release autonomic neuroeffector site.
3. Transmitter action on postjunctional membrane:
The release transmitter combines with specific receptors on the postjunctional membrane and depending on its nature induces an excitatory postsynaptic potential (EPSP) or an inhibitory postsynaptic potential (IPSP).
EPSP – Increase in permeability to all cation – Na+ or Ca+ influx causes depolarization followed by K+ efflux.
IPSP – Increase in permeability to smaller ions. That means K+ and Cl– moves in resulting in hyper polarization
4. Post-junctional activity:
A suprathreshold EPSP generates a propagated postjunctional action potential which results in nerve impulse (in neuron), contraction (in muscle) or secretion (in gland). An IPSP stabilized the postjunctional membrane and resists depolarizing stimuli.
5. Termination of transmitter action:
Following its combinations with the receptor, the transmitter is either locally degraded (e.g. ACH) or it’s taken back into the prejunctional neuron by active uptake or diffuses away (e.g. NA, GABA).