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How is Information Transmitted through the Nervous System?

1589 words (6 pages) Essay in Biology

18/05/20 Biology Reference this

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How is Information Transmitted Through the Nervous System?

●        Sensory neurons

○        Stimulated by heat, light, sound and pressure e.g the major pressure sensor being the Pascinian corpuscle

○        Action potential — Depolarisation – threshold – peak – repolarisation – hyperpolarisation – refractory period – resting potential

○        Sodium-potassium pumps

○        Sodium channels open/ Potassium closed → potassium closed/ sodium open

○        Saltatory conduction in myelinated neurons – nodes of Ranvier

○        PNS → CNS, long dendrites + short axons

○        POTENTIAL DIFFERENCE ACROSS THE MEMBRANE DUE TO MOVEMENT OF IONS THROUGHOUT THE DENDRON + AXON

●        Relay neurons

○        Synapses

○        Short dendrites + short axons

●        Motor neurons

○        Long axons, short dendrites

○        Stimulate effector muscles

Resting membrane potential:

Higher conc Na+ outside than inside

Higher conc of K+ inside than outside

= steep conc gradients for movement of Na+ and K+ ions into and out of the cell

→ movement of these ions is facilitated by the active ion pumps Na+-K+-ATPase which create transmembrane gradients by moving 3Na+ out and 2k+ in for every Atp molecule hydrolysed – causing the inside of cells to be electrically negative relative to the outside; both intra- and extracellular fluids are electrically neutral

Activation, by specific signals, of voltage-gated Na+ ion channels begins the depolarisation of plasma membrane potential difference which results in the formation of an action potential in neurons – during repolarization these na voltage-gated ion channels close and k ones open to change the permeability of the plasma membrane

Under resting conditions there a group of K+ ion channels that are constantly active and allow K+ ions to ‘leak’ out of cells – neurons contain more K+ and Cl- leak ion channels than Na+ leak channels meaning that the membrane has a much higher permeability for k and cl – as k leaks out the inside becomes more negatively charged relative to the outside – bc opposites attract (and the conc gradient that is established) k is attracted back toward the cell – the na+k+ATPase actively works to move k back into the cell and na back out to maintain the conc gradients and keep the outside pos charged compared to inside

 → there can be deficiencies in these leak ion channels leading to a number of pathological defects including hyperinsulinemic hypoglycemia which can be caused by a mutation in the channel, affecting the resting potential of cells  epilepsy and Parkinson’s disease have also been linked to this defect [1]

→ the conc of cl- inside and outside of the neuron is regulated by a cotransporter found in many second-order sensory neurons in early development called NKCC1 – this Na+-K+-2Cl– cotransporter moves cl- back into neurons in the brain to maintain a high conc (this means that the reversal potential for cl- is increased because higher conc.s will open more gated ion channels to allow cl- to diffuse back out of the cell) during early brain development, this alters the effect over time of GABA from being excitatory/depolarising initially to being inhibitory/hyperpolarising as it is found to be in the adult brain – GABA depolarisation in the immature sensory neurons causes presynaptic inhibition which helps to filter and diffuse the effects of second-order sensory neurons → in contrast KCC2 a K+-Cl– cotransporter has a low expression at birth – it carries out the opposite process as NKCC1; it moves cl- out of nerve cells – so during postnatal development there is a large decrease in the concentration of cl- found within the above mentioned neurons… this changes the driving force for cl- from being inwards to outwards and thus changes the effects of GABA and glycine from excitatory to inhibitory as they are commonly found to be in the mature brain [2]

Potential difference can only range from -96 to +64 because there are not any chemical gradients that can produce larger potential differences

Changing the resting membrane potential:

Graded potentials can be created at neurons – these are localised disturbances that cause a slight change membrane potential – if na+ ion channels open the resultant effect will be depolarisation of the plasma membrane due to rapid influx of na+ ions, the opposite is true for k+ ions and these cause hyperpolarisation of the cell membrane and have an inhibitory effect on APs.

 → summation of graded potentials can cause greater depolarisation as there will be greater influx of na+ ions into the cell causing the inside to become more positive – this may cause an action potential if enough stimulatory graded potentials are initiated

 

ACTION POTENTIALS – only occur if the membrane potential reaches and exceeds threshold value – a weak stimulus will only produce a small graded potential which will not result in an increase in the charge across the membrane large enough to produce an AP

The all-or-nothing principle = every ap has the same magnitude regardless of the strength or frequency of the stimulus which produced it; if threshold value is not reached (due to a small depolarising graded potential) then the plasma membrane will simply return to resting potential (due to action of the na+k+ATPase)

  1. DEPOLARISATION – DGPs cause increase in positive charge which opens many voltage-gated na+ ion channels in the localised area – this allows a rapid influx of na+ ions into the cell which creates a positive feedback system where the increasing amount of na+ inside the cell causes more and more na+ ion channels to open – this results in rapid depolarisation of the plasma membrane and the membrane potential exceeding threshold – causing an ap to occur → k+ ion channels are mostly closed during depolarisation but a few do tend to open slowly; releasing some positive charge back out of the cell but the change is so insignificant that an ap can still occur
  2. REPOLARISATION – after the membrane potential reaches its peak magnitude (all-or-nothing) the PD will start to decrease again – here the na+ ion channels close and voltage gated k+ ion channels open fully to allow k+ to diffuse out of the cell and make the inside of the cell become less positive – the na+ voltage-gated ion channels return to their resting state as the membrane repolarises
  3. HYPERPOLARISATION – as mentioned in depolarisation the k+ ion channels are slow to open, they are also slow to close and this causes a period known as hyperpolarisation where the membrane potential exceeds and becomes more negative than its usual resting potential – the sodium-potassium pumps then work slowly to reestablish resting potential by moving na+ ions back out of the cell and k+ back in

●        Propagation of the AP: graded potentials only depolarise the membrane in localised areas so the ap is actually moved along the axon via diffusion of na+ ions in a process known as saltatory conduction – although this only occurs in myelinated neurons…

○        in unmyelinated neurons the next ap is produced directly next to the previous one – local currents move charged ions down the length of the axon due to the fact that pos charged na ions are attracted to negatively charged areas further down the axon, this movement depolarises the membrane further down and opens more voltage-gated na+ ion channels, thus casing an ap to occur adjacent to the last one as the PD across the membrane exceeds threshold

○        The process of propagating aps is almost the same in myelinated however na+ ions can only cross the plasma membrane at nodes of Ranvier – tiny gaps found between lengths of the Schwann cells that make up the myelin; they are around 1 μm in length and allow the na ions to diffuse into the nerve cell – causes local currents which flow to the next node and open na voltage gated channels there (high conc of na channels at noRs) – myelination increases rate of transmission bc aps ‘jump’ from one node to the next rather than having to travel through every part of the neuron

○        The refractory period (hyperpolarisation) prevents aps from travelling in the opposite direction as the ions either side of the membrane are in the wrong places – na needs to be moved back out of the neuron and k back in to create the high conc differences across the membrane which ultimately drives ap generation

 

Bibliography

[1]. Wright, S. (2004). Generation of resting membrane potential. Advances in Physiology Education, 28(4), pp.139-142.

[2]. Delpire, E. (2000). Cation-Chloride Cotransporters in Neuronal Communication. Physiology, 15(6), pp.309-312.

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