Posts Tagged ‘ signal transduction ’



When an axon ends, the action potential which it carries can no longer be transmitted by the same medium. Axons end in a structure known as a synapse, the synapse allows the action potential to be propagated by means of chemicals (as opposed to electrically charged ions). An axon which terminates on an individual muscle fibre is known as a neuromuscular junction.

The terminating end of the axon has a bulbous structure, known as the presynaptic bulb. Within this bulb there can be one of many types of chemicals known as neurotransmitters. These neurotransmitters are the chemicals which transmit the action potential across the synapse (the space between the presynaptic bulb and the post synaptic structure is known as the synaptic cleft).

The most commonly found chemical used as a neurotransmitter is acetylcholine; however others include adrenaline, serotonin and dopamine. These neurotransmitters are housed in the presynaptic bulb contained in vesicles.

The process of transmission is as follows:

  • An action potential propagated to the presynaptic bulb (caused by an earlier stimulus)
  • The action potential depolarises the plasma membrane, this opens voltage gated channels in the membrane that allow the influx of Ca2+
  • The influx of Ca2+ results in some of the neurotransmitter containing vesicles to fuse with the presynaptic bulb membrane, resulting in the expulsion of the neurotransmitter into the synaptic cleft
  • The neurotransmitter diffuses across the synaptic cleft and binds to neurotransmitter specific receptors on the postsynaptic bulb
  • These receptors are ligand-gated ion channels and once the ligand (neurotransmitter) binds to the receptor, it opens allowing Na+ and K+ to diffuse through the channel
  • The influx of Na+ and efflux of K+ ions generates an action potential in the postsynaptic bulb which is propagated further
  • The neurotransmitter is released from the receptor causing it to close
  • The neurotransmitter is recycled, initially being broken down by an enzyme in the synaptic cleft (e.g. acetycholinesterase breaks down acetylcholine into acetate and choline)
  • Some of the neurotransmitter is taken up again by the presynaptic bulb (e.g. choline is pumped back into the presynaptic bulb by a choline carrier)
  • Enzymes convert the molecule back into a neurotransmitter (e.g. choline converted into acetylcholine) and the neurotransmitter is repackaged in an empty vesicle

It is possible for the neurotransmitter to be inhibitory as well i.e. prevent the generation of an action potential, e.g. glutamate is the primary excitatory neurotransmitter of the brain whereas GABA is the brain’s primary inhibitory neurotransmitter.

Types of Post Synaptic Receptors

As mentioned in the typical transmission above, neurotransmitters bind to a post synaptic receptor to result in either the inhibition or generation of an action potential. However, there are other types of post synaptic receptors which do not bind the neurotransmitter directly. The main 3 types are given below:

  • Ligand-Gated Ion Channels: (Fast – 0.1ms delay) also known as ionotropic receptors, these are the type of postsynaptic receptors spoken about earlier. They require the binding of a specific neurotransmitter, the binding of this neurotransmitter results in a conformational change causing the channel to open and allow the passage of ions. They are associated primarily with excitatory neurotransmitters such as acetylcholine and glutamate.
  • Metabotropic Receptors: (Slow – 10ms delay) unlike ionotropic receptors, these receptors are not directly associated with an ion channel. Instead they indirectly link with ion channels by means of signal transduction mechanisms, often G-proteins. Neurotransmitters will bind to the metabotropic receptor, resulting in the activation of these secondary messenger signal transduction mechanisms. The result is the opening of an ion channel and from this point, the process continues as in an ionotropic receptor.
  • Electrical Synapses: (Very Fast – <0.1ms delay) unlike either the ionotropic or metabotropic receptors, there is no association with an ion channel. Instead gap junction like channels pass directly through the presynaptic bulb and synaptic cleft heading directly into the postsynaptic bulb. This means the action potential can head straight through into the next axon without having to stop. This type of system is extremely fast and very uncommon. It is found in only a few specialised systems within the body.


The process of action potential propagation across synapses can vary. Most post synaptic terminals have a threshold which must be met in order for the action potential to be propagated. Therefore if a weak action potential arrives and is sub-threshold, the action potential ends there. It is not transmitted any further. There is an exception to this – summation.

A post synaptic structure such as a motor neurone may synapse with more than one presynaptic sensory neurone. If this is the case, then it is possible for summation to occur. Summation is when two sensory neurones fire simultaneous sub-threshold action potentials. Normally, as they are sub-threshold, they would not be propagated any further, but as there are two, the effect stacks in the process known as summation.

The above form of summation is known as spatial summation – the action potential of two neurones combine to allow threshold to be reached.

There is another form of summation however, temporal summation. Temporal summation is possible from just one sensory neurone. It works when a neurone is able to generate two action potentials in short succession. By the time the second action potential reaches the synapse, neurotransmitters from the previous action potential have not yet unbound from the postsynaptic receptors. This means the effects from both action potentials stack and threshold is reached.

Special Senses – Taste


The tongue is the organ of taste. Perception of taste is also known as gustation and in a similar manner to smell it depends on chemoreceptors to detect specific chemicals from the environment. Specialised epithelial cells (Taste cells) detect these chemicals (tastants). In aquatic animals there is no distinction between olfaction and gustation. Insects use sensory hairs on their feet to taste. Taste probably evolved as a means for animals to detect whether what they were about to consume should be ingested or rejected.

In mammals, taste cells are clustered into taste buds which are scattered around the tongue and mouth. These taste buds are located very slightly beneath the surface of the tongue, a taste pore allows tastants to access the taste bud.

Taste buds are further localised onto raised clusters visible on the tongue, these are known as papillae. Differently shaped papillae are located at different sites on the tongue.

Taste Transduction

Mammals are able to detect the four conventional tastes (sweet, sour, bitter & salty) as well as ‘umami’, which is considered a savoury taste.

The sensory receptor cells (taste cells) which make up the taste buds contain smaller receptors in their plasma membranes. These receptors are specific to one of the above tastes.

When a tastant arrives at one of these receptors, it binds to it, resulting in a secondary messenger cascade. The receptor is coupled with a G-protein and the binding of a tastant activates the G-protein, beginning the secondary messenger process within the sensory receptor cell.

The G-protein eventually activates phospholipase C which in turn generates a secondary messenger known as IP3. IP3’s role in this secondary messenger system is to open IP3 gated calcium channels on the endoplasmic reticulum of the cell.

Opening of these channels causes Ca2+ to leave the endoplasmic reticulum and enter into the cytoplasm of the cell. Ca2+ also acts as a secondary messenger; it causes sodium channels to open allowing an influx of Na+ ions.

The sudden influx of Na+ ions causes the sensory receptor cell (taste cell) to depolarise, this depolarisation results in the local release of neurotransmitters (as taste cells do not have axons). This excites local sensory neurones which generate action potentials in response.

The axons of these neurones bundle together to form part of the facial nerve (VII), the glossopharyngeal nerve (IX) or the vagus nerve (X). Which one depends on the origin of the axon, anterior taste is carried by the facial nerve (VII) and posterior taste is carried by the glossopharyngeal nerve (IX). The throat/ epiglottis are dealt with by the vagus nerve (X).

All three cranial nerves eventually reach the gustatory nucleus of the ‘nucleus of the solitary tract’ in the medulla. From here the information can be sent to one of three places, each of which solicits a different response:

  • The gustatory cortex (via the thalamus) – Here taste is integrated and perceived as a taste.
  • The brainstem – From here reflexes associated with taste may be activated e.g. salivation
  • The Limbic system (especially the hypothalamus) – Emotional responses to taste (e.g. pleasure) can be elicited from here.

Special Senses – Smell


The sensation of smell is also referred to as olfaction. The sensory cells of olfaction are chemoreceptor neurones with a direct connection to the brain. The organ responsible for smell is the olfactory organ (‘nose’), also responsible for olfaction is the vomeronasal organ. Odour molecules, which stimulate the olfactory cells, can be either present in gases or dissolved in vapour droplets. Molecules present in gas are detected by the main olfactory organ, whilst those dissolved in liquid are detected by the vomeronasal organ.

The important structures of the olfactory organ are as follows:

  • An external pair of ‘nares’ (nostrils) which act as the entrance to the organ.
  • An internal pair of ‘nares’ located just before the nasopharynx.
  • A richly vascularised anterior nasal mucosa, involved in heat exchange.
  • Turbinate bones, which refer to any of the spongy bones of the nasal passages. The turbinates divide the nasal airway into air passages, responsible for forcing inhaled air to flow in a steady, regular pattern around the largest possible surface of cilia and climate controlling tissue.
  • The sensory cells of the olfactory organ, the olfactory cells which are ciliated chemoreceptors.

Vomeronasal Organ

Located ventrally to the nose, this small organ is able to detect dissolved odours (e.g. pheromones) this makes it important for signalling related to sexual behaviour. The vomeronasal organ is present in many animals including humans and although functionality in animals has been shown there is still debate over whether such functionality is exhibited in humans.

Similarly to the olfaction organ, the vomeronasal organ contains receptors whose neurons possess axons which travel from the vomeronasal organ to the brain. The difference is that the neurons from the olfactory organ travel to the olfactory bulb of the brain whilst vomeronasal neurones travel to the accessory olfactory bulb.

Transduction Pathway of Signals

The pathway of transduction begins in the epithelial lining of the olfaction organ. Chemoreceptor neurones project from the epithelium into the mucosal layer of the organ. The projections are ciliated which increases the surface area of the receptors.

Lining the plasma membrane of the cilia are smaller receptors, these receptors are responsible for detecting individual odour molecules or odourants. The odour receptors are odorant specific, so different odours bind to different receptors. There are a few thousand, different odour receptors.

The odour receptors are G-protein coupled, so when an odour receptor binds its specific odourant the G-protein is activated and a secondary messenger cascade begins.

In the majority of these secondary messenger systems (a relay system where the activation of a receptor causes many changes in the cell, eventually leading to the desired outcome), the enzyme adenylyl cyclase is eventually activated. This enzyme converts ATP to cAMP. The production of cAMP opens Na+/Ca2+ permeable ion channels in the plasma membrane.

The influx of Na+/Ca2+ ions causes the chemoreceptor to depolarise. This causes the chemoreceptor to generate action potentials which are sent directly to the olfactory bulb of the brain.

The unmyelinated axons of the chemoreceptors bundle together in small groups, they then travel through the olfactory foramina, (Small holes in the cribriform plate [part of the skull which makes up the roof of the nasal cavity]) to the olfactory bulb.

These axons synapse with mitral cells in the olfactory bulb. From here the bundled axons from the mitral cells travel directly to the olfactory (piriform) cortex without first heading to the thalamus.

Here odours are processed; typically one smell is made from many different odourants. The different odourants are detected individually and eventually pieced back together to form the perceived, one smell.