Didactic organisation

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Didactic organisation is the ability of neurons within a network to impart their pattern of synaptic connectivity and/or response properties to other neurons. The term didactic is used because this kind of influence is unidirectional; each individual instance of didactic organisation between two connected neurons does not involve a bidirectional transfer of connectivity or response property information between them.

Neuron electrically excitable cell

A neuron, also known as a neurone and nerve cell, is an electrically excitable cell that communicates with other cells via specialized connections called synapses. All multicellular organisms except sponges and Trichoplax have neurons. A neuron is the main component of nervous tissue.

Synapse The junction between a nerve fiber of one neuron and another neuron, muscle fiber or glial cell. As the nerve fiber approaches the synapse it enlarges into a specialized structure, the presynaptic nerve ending, which contains mitochondria and synapti

In the nervous system, a synapse is a structure that permits a neuron to pass an electrical or chemical signal to another neuron or to the target effector cell.

Contents

Experimental and theoretical evidence

Evidence for didactic organisation in vivo was first discovered through research into synaptic reorganisation in primary visual cortex that compared the results of neuronal recording experiments and computational models. [1] However, the tendency of spike-timing-dependent plasticity to separate neurons into ‘teachers’ and ‘students’ had previously been predicted in theory based on computational modelling results alone. [2]

Studies that are in vivo are those in which the effects of various biological entities are tested on whole, living organisms or cells, usually animals, including humans, and plants, as opposed to a tissue extract or dead organism. This is not to be confused with experiments done in vitro, i.e., in a laboratory environment using test tubes, Petri dishes, etc. Examples of investigations in vivo include: the pathogenesis of disease by comparing the effects of bacterial infection with the effects of purified bacterial toxins; the development of non-antibiotics, antiviral drugs, and new drugs generally; and new surgical procedures. Consequently, animal testing and clinical trials are major elements of in vivo research. In vivo testing is often employed over in vitro because it is better suited for observing the overall effects of an experiment on a living subject. In drug discovery, for example, verification of efficacy in vivo is crucial, because in vitro assays can sometimes yield misleading results with drug candidate molecules that are irrelevant in vivo.

Spike-timing-dependent plasticity (STDP) is a biological process that adjusts the strength of connections between neurons in the brain. The process adjusts the connection strengths based on the relative timing of a particular neuron's output and input action potentials. The STDP process partially explains the activity-dependent development of nervous systems, especially with regard to long-term potentiation and long-term depression.

Spike-timing-dependent plasticity

Didactic organisation is primarily a consequence of spike-timing-dependent plasticity, because when the neurons within an interconnected network undergo action potentials (or ‘spikes’) at approximately the same time (within the order of tens of milliseconds) the efferent synaptic connections of neurons that spike early will have their efficacy increased (long-term potentiation), while neurons that spike late will have the efficacy of their efferent synaptic connections decreased (long-term depression). [1] [2]

Long-term potentiation

In neuroscience, long-term potentiation (LTP) is a persistent strengthening of synapses based on recent patterns of activity. These are patterns of synaptic activity that produce a long-lasting increase in signal transmission between two neurons. The opposite of LTP is long-term depression, which produces a long-lasting decrease in synaptic strength.

In neurophysiology, long-term depression (LTD) is an activity-dependent reduction in the efficacy of neuronal synapses lasting hours or longer following a long patterned stimulus. LTD occurs in many areas of the CNS with varying mechanisms depending upon brain region and developmental progress.

Causal activity

While spike-timing-dependent plasticity is an essential ingredient for didactic organisation, other features of neuronal activity appear to be required for didactic organisation to occur in vivo. One of these features is that activity propagated through a network needs to have a 'causal' character. [1] For example, chain of reciprocally connected neurons with this ‘causal activity’ characteristic would be capable of propagating a wave of spikes along its length, rather than the wave disintegrating into a cascade of spikes ‘bouncing’ back and forth between neurons in the chain.

Activity propagation

A third important feature for didactic organisation in vivo concerns the spatial scale of spike propagation within a network. While it is expected that didactic organisation will always be present among neurons that exhibit spike timing-dependent plasticity and causal activity (see above), the spatial scale over which didactic organisation can occur between neurons within a network should be limited by the spatial scale of spike propagation. Evidence suggests that the scale of spike propagation can be actively controlled by adjusting the balance of excitation and inhibition within a network (a balance that can be modulated by synaptic scaling, for example), thus providing a means by which a network can actively control when and to what extent didactic organisation can occur. [1] For this reason, and the very specific connectivity patterns that can be achieved via didactic organisation, it has been speculated that didactic organisation may play an important role in brain development.

Excitatory postsynaptic potential process that leads to a temporary increase in postsynaptic potential due to the flow of positively charged ions into the postsynaptic cell; the flow of ions that causes an EPSP is an excitatory postsynaptic current (EPSC)

In neuroscience, an excitatory postsynaptic potential (EPSP) is a postsynaptic potential that makes the postsynaptic neuron more likely to fire an action potential. This temporary depolarization of postsynaptic membrane potential, caused by the flow of positively charged ions into the postsynaptic cell, is a result of opening ligand-gated ion channels. These are the opposite of inhibitory postsynaptic potentials (IPSPs), which usually result from the flow of negative ions into the cell or positive ions out of the cell. EPSPs can also result from a decrease in outgoing positive charges, while IPSPs are sometimes caused by an increase in positive charge outflow. The flow of ions that causes an EPSP is an excitatory postsynaptic current (EPSC).

An inhibitory postsynaptic potential (IPSP) is a kind of synaptic potential that makes a postsynaptic neuron less likely to generate an action potential. The opposite of an inhibitory postsynaptic potential is an excitatory postsynaptic potential (EPSP), which is a synaptic potential that makes a postsynaptic neuron more likely to generate an action potential. IPSPs can take place at all chemical synapses, which use the secretion of neurotransmitters to create cell to cell signalling. Inhibitory presynaptic neurons release neurotransmitters that then bind to the postsynaptic receptors; this induces a change in the permeability of the postsynaptic neuronal membrane to particular ions. An electric current that changes the postsynaptic membrane potential to create a more negative postsynaptic potential is generated, i.e. the postsynaptic membrane potential becomes more negative than the resting membrane potential, and this is called hyperpolarisation. To generate an action potential, the postsynaptic membrane must depolarize—the membrane potential must become more positive than the resting membrane potential. Therefore, hyperpolarisation of the postsynaptic membrane makes it less likely for depolarisation to sufficiently occur to generate an action potential in the postsynaptic neurone.

In neuroscience, synaptic plasticity is the ability of synapses to strengthen or weaken over time, in response to increases or decreases in their activity.

See also

Notes

  1. 1 2 3 4 Young et al., 2007
  2. 1 2 Song and Abbott, 2001

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