Physiology - Neurons (1)

Neuron leak channels

Pores for K+, constutively active.

**High permeability for K+ = resting potential negative.**

Depolarisation

Na+ permeability increase, equilibrium shifts to Na+

Hyperpolarisation

K+ permeability increase, equilibrium shifts to K+

Neuron variations

* **Purkinje cells** - coordination of movement in cerebellum, lots of dendrites
* **Pyramidal cells** - cognition & vision guided movement

Graded potentials

For integrate information, **not for long distance**.

Dendrite signal receptors lead to **change in ion channel activity & membrane potential.**

Allows **responding** with **polarisation** **changes**.

Polarisation change depends on:

* in/out ion concentrations
* equilibrium potentials
* ion channels selectivity

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**The stronger the stimmuli, the stronger the effect on the membrane potential of dendrite.**

Spatial summation

sum of EPSPs that come at the same time to axon hillock

Temporal summation

sum of postsynaptic potentials from the same synapse

Action potential phases

1. **Resting** - channels closed, __resting state__ of the membrane.
2. **Depolarisation** - axon membrane potential reaches __treshold potential__, Na+ gate opens, ion depolarise the membrane.
3. **Repolarisation** - Na gate closes, K+ channels open. K+ ions leave & repolarise.
4. **Repolarisation continues**- membrane potential decrease, K+ equilibrium bring __hyperpolarisation__.

Refractory periods

* **Absolute** - no action potentials due to inactive Na+ channels
* **Relative** - after hyperpolarisation; lower membrane potential require depolarising power to reach treshold.

Due to those periods action potentials travel **only away from the soma & towards the synapse.**

Graded potentials - properties

* Vary in magnitude & duration
* Decay with distance
* Occur in dendrites & cell body
* Caused by opening & closing of various ion channels

Action potentials - properties

* Always the same size, shape, duration
* Occur in axons of neurons & muscle cells
* Caused by opening & closing of voltage-gated ion channels

Dendrite

receive information from other neurons

Cell body

Contains nucleus + organelles

Axon hillock

Information gets collected and integrated, generating action potentials

Axon

Conducts action potentials away from cell body

Axon terminals

Synapse with target cell

Glial cells

Surround neurons, provide support and insulation between them.

* **Astrocytes** - homeostasis
* **Microglial** **cells** - macrophage-like
* **Oligodendrocytes** (PNS-**Schwann** **cells**) - wrap axons for insulation

Nodes of Ranvier

Non-insulated parts of axon, the only place with voltage gated Na+/K+ channels so action potential will jump on nodes.

Saltatory conductions

In nodes of ranvier;

Action potential generated in node, fastly jumps on nodes.

Electrical synapse

Fast, allow for **synchronisation of neuronal activity**

Chemical synapse

Excitatory or inhibitory, only **link cells**.

*Acetylcholine*

EPSP

* Acetylocholine opens cation channel, **K+ leaves the cell, Na+ enter**
* Postsynaptic membrane **depolarise**
* EPSP created
* Easier to trigger a**ction potential** by crossing the treshold

IPSP

* Metabotropic acetylocholine receptor activates G-protein, opening K+ channel
* K+ leaves, postsynaptic membrane **hyperpolarise**
* IPSP created
* More difficult to trigger action potential by crossing the treshold

Neurotransmitter receptors

**Ionotropic receptors** - ion channels open by binding to neurotransmitter. Simple crossing.

**Metabotropic receptors** - coupled with intracellular signal proteins that __open ion channels__.

__Depending on which ion channel it opens__ it will hyper/depolarise postsynaptic membrane.

Excitatory neurotransmitters

**lead to EPSP = graded action potential**

Glutamate, Serotonin

Inhibitory neurotransmitters

**lead to IPSP = no potential**

GABA, Glycine

Excitatory & Inhibitory

**Depends on type of receptors it activates on the neuron.**

Acetylcholine, adrenaline, dopamine, endorphins

GABA

* Synthesized from **glutamate**
* A receptors: chloride channels (**ionotropic receptors)**. Binding opens the channel, Cl goes in, **hyperpolarisation of the membrane = IPSP.**
* Low GABA = axciety, irritiation

Glutamate

* Subtypes: AMPA, Kainate, NMDA - different agonists
* Activation leads to **cation influx = depolarisation = EPSP**

Acetylcholine receptors

* **nAChR** are cation channels, __activated by nicotine & inhibited by alkaloid arrow poisons.__

In __skeletal muscle__ & __ANS__.
* **mAChR** coupled to G-proteins that activate K+ channels; inhibited by __atropin__.

In __PNS__ & __iris__ (control pupil size. Inhibited = big)

Noradrenaline & adrenaline

* adrenaline **hormone**; noradrenaline **neurotransmitter**;
* both acts on the same receptors - metabotropic, multiple function.
* Adrenaline triggers stress response.

Tetrodotoxin TTX

Accumulated in the body of animal, block Na+ channels = **no depolarisation**.

Does not work on venomous animals **due to insensitivity of their channels.**