The plasticity on the level of the neuronal exchanges indicates all the phenomena which result from the changes in the time of the properties of data processing of a neural network. The synapses are one of the levels of the neuronal Plasticité.
Synaptic transmission: 3 different codings, two possible sites of plasticity
On the level of a synapse, a potential of action (Pa) in the presynaptic element causes the release of Neurotransmetteur S in the synaptic slit. The latter interact with their receivers corresponding to the level of the postsynaptic membrane. That they are métabotropes or receiving ionotropes, the activated receivers generate a current postsynaptic (CPS) by the opening of ionic Canaux, and consecutively a potential postsynaptic (PS). Usually it is said that the signal is coded- in the presynaptic element in term of frequency of Pa ,
- in the synaptic slit in term of concentration of neuro-transmitter and
- in the element postsynaptic in term of amplitude of CPS .
Presynaptic plasticity
The same Pa involves the release moreover (or less) of neuro-transmitters, then for the same frequency of Pa, there will be a stronger (weak) concentration of neuro-transmitter, and thus mechanically, a stronger (weak) amplitude of CPS.
Postsynaptic plasticity
The same concentration of neuro-transmitter returns in contact with a stronger density of receiver in the postsynaptic membrane, or many receivers of another nature, then the same quantity of neuro-transmitter will cause a CPS of stronger amplitude, or a CPS presenting of other properties.These two levels of synaptic plasticity underlie in fact several mechanisms which can be classified according to the speed to which the rules of coding are changed, and according to the perenniality of the change.
The principle of Flagstone
A Neuro-transmitter by neuron.
If a neuron is able at the same time to have an inhibiting efference and another exciter, it is thanks to a variation of the receivers postsynaptic of the concealment. who receive his signal (ex channels Cl and Na+ sensitive to the same NT). A neuron cannot be the source of more than one NT. It was discovered that certain neurons are able to secrete peptides in parallel of a NT. But this one remains always the same one, without enfreindre thus the principle of Flagstone.
Possible causes of a modification of the synaptic transmission
- Quantité of released blisters varied (Pr)
- Quantité of receivers postsynaptic varied (BDNF p.ex.)
- Sensibilité of the receivers postsynaptic varied (antagonistic agonist/competitive or not of the NT, or the allosteric conformation of the receiver is modified)
- Recapture NT varied (inhibition or increase): this one is normally carried out by the astrocytes.
N.B. : A extracell of 30mM is sufficient to be toxic with respect to the neighbouring cells; Certain an armature a astrocytose (+ concealment swelling), and a higher concentration, straightforwardly a cellular death (neuronal and astrogliale).
Processes of interactions synaptic and plasticities
Since the discoveries of the Sixties of E.Kandel (Nobel Prize of medicine in 2000), research in neuroelectrophysiology update regularly of new types of synaptic plasticity. Those are declined in multiple forms, whose cardinal ones are Habituation, Sensitization (or desensitizing), Potentiation and the Depression. Each one of these phenomena includes/understands alternatives classified in sub-types. At present, it is obvious that one cannot claim oneself exhaustive in the enumeration of the various types and noted sub-types of plasticity, since one yet entirely did not include/understand which including logic governs their appearance. It may be that the alternatives of plasticity are quasi unlimited and that the frequency of their respective appearance is in direct connection with the type of neurons which they modify like according to their cellular environment. Here are thus some types, drawn from the specialized scientific literature.
Habituation
The post-synaptic answer attenuates with the wire of the stimuli csts coming from the afférences: the simplest form of training: to be unaware of an unimportant and inoffensive stimulus: to be bored!Shorts Term Habituation: 1 ' of stimulation => 2:00 of activity. One notes a reduction in the activation of the presynaptic Ca++ channels.
Long Term Habituation: can last up to 3 weeks. But stimulation should not be hyperä but progessive. In the same order of idea that the STH, one cstmment notices morphological and structural consequences on the discharging level of the synaptic pre termination of the neurons: less blisters, less synapses, losses of contacts and activity.
Sensitization
Classically, a first abrupt and unexpected sensory summation (Unconditional Stimulus: US) induced of the reactions plus sharp vis-a-vis various neutral stimuli sensory (" state of hypervigilance, alerte"). There was sensitization.Indeed, the way of this US (a sensitive/noxious neuron) activates on its way a neuron with serotonin (5-HT), a facilitating neuromodulator. That Ci forms a first axono-synaptic synapse, with the presynaptic button (according to the paradigm including 1 pre cell and 1 postsynaptic cell at Aplysia californica).
Indeed, in presynaptic position, another neuron is which leads a neutral input (Conditional Stimulus) towards a sensory intégratif center (or a motoneurone/interneurone p.ex. if it is about a loop reflex) which, represents the neuron to him postsynaptic. With the relaxation of the 5-HT on the level of the first synapse (i.e between the axon of modulating neuron 5-HT and the button of the synapse of the presynaptic neuron glutamatergic), an important potentiation takes place on the level of the “principal” synapse (pre-postsynaptique). There is thus, without counting the neuron of US, 3 cellular actors on the level of this synapse: 2 presynaptic, and 1 postsynaptique.
The 5-HT will act on receivers 5-HT on the presynaptic neuron, and will induce a I¢ which leads to a reduction in the activity of the K+ channels. Thus, the " synapse becomes more in reply and the depolarization persists". => " greater NT (lime) release onto postsynaptic ¢" , without there being of postsynaptic component activated in this phenomenon, i.e in fact that the neuron of the sensory intégratif center is not activated.
There also exists:
Shorts Term Sensitivity.
Long Term Sensitivity.
N.B.: Until now, one did not discover activation of CREB in the phenomenon of sensitivity. Moreover, sensitivity can be started thanks to other Nm that of the paradigm of serotonin!
Potentiation
Potential Post-Synaptic Exitateur (PPSE) or Excitatory Post Synaptic Potential (EPSP): phenomenon neuroexcitator infraliminal of a Pa, médié by receivers AMPA (entered of Na+ >> Ca++) and NMDA (entered of Ca++ >> Na+) with glutamate. N.B.: Ach can also induce IPSP/EPSP, but also the other Nm (5-HT, and DA) which have them a more variable action
Long Term Potentiations (LTPs): thanks to detecting receivers the “of coincidence” NMDA (Ca2+ channels >> Na+) and with the receivers “igniters” AMPA (in general: because GABAAr are, before being inhibiting during the adult life, responsible for the consolidation of the first exiting synapses in the embryonic development of the brain, i.e start the prestimulation of receivers NMDA). N.B.: CaMKinase II, target of Ca++Calmoduline, exist in form 4 S-units of CaMK, therefore is a very large complex. Since the half-life is of 10'' for CaMKII*P, which is very long, it remains active still a long time after the end of the spike Calcique and is supposed to transform the frequency into intensity, or the initial impulse in dynamic inertia within the cell. : “rectifying protein of current”. Moreover some isoformes of CaMKII migrate of the cytosol to the core and seems to play a part in the activation of Tx of dependant early constrained CRE. Several types of currents, of which:
Homosynaptic (activity dependant) Associative Hebbian Plasticity (conditioning): Bliss and Lømo, hippocampus 1973; . “Associative” means that the discharges of the n.présyn are synchronized with that of the n.postsyn., and homosynaptic, that there are two cellular actors of comparable nature (neurons glutamatergic p.ex.) on the level of the synapse: “coincide pre and postsynaptic firing”. e.g. of localizations: hippocampus, cerebellum, PF cx and the amygdala.
Early-LTP (E-LTP) is inductible with individual a 100Hz tetanus stimul. who activates kinases (CaMKII p.ex.): do not last more than a few hours (between 1 and 3:00).
Late-LTP (L-LTP) persistent (approximately 24:00 lasts) requires a very strong tetanic stimulus on the other hand even several to be induced, with i¢ and recruitment of several kinases, like e.a. PKA and MAPK which activates the transcription of CREB most of the time (but of another TF seem certain times being activated in the place of CREB, cf Kandel and Gass P. and Al 1998). The L-LTP is well correlated with Length-Term Memory (Kandel). A traditional example: Hebbian LTP in Schaffer Collateral pathway is well correlated with the memory dependant on the hippocampus.
An interesting example: Pairing CS & US in the amygdala (Ledoux): A weak CS coupled spatio-temporellement with US extremely (noxious), sees its potential exitability to increase considerably thereafter, even by taking place in the absence of US: this, in logic to allow to a CS to be prédictible, with stronger reason to adapt to survival.
N.B. : Modulatory Inputs inducing LTP: Nm such that DA (D1/D5 agonists) increases the rates of camp and induces the glutamatergic L-LTP of the neurons in Schaffer coll Pathw. ! (cf Kandel and Bach). so we edge infer that heterosynaptic plasticity and effective sensitization are both one classical present hebbian LTP in the hippocampus.
Heterosynaptic (modulatory input-dependant) Plasticity : Nonassociative process independent of the activity of the synapse. 3 synaptic speakers (idem sensitization but) all glutamatergic: 1 n.présyn., 1 N. axono-synaptic modulator présyn. and 1 n.postsyn. A synapse can thus be reinforced or weakened without the need for a pre activity nor postsynaptic, but only for the modulating neuron being next to the presynaptic button of the synapse (Kandel). The reinforcing effect of the modulating neuron will be increased if its activity coincides with that of the presynaptic neuron. This kind of plasticity activates the form of the sensor intra¢ CREB which induces long-term changes as regards gene transcription responsible for the engramme (put in memory of the events), much more frequently than Hebbienne plasticity (according to Kandel). Indeed heterosynaptic plasticity is necessary but also sufficient to activate the transcription. This can lead to the growth/retraction of a cone axonal p.ex.
N.B. : Modulatory Inputs inducing LTP (continuation): let us center ¢ of Locus Coeruleus (NA), Raphé Dorsal (5-HT), and VTA (DA) skirt Schaffer coll, Mossy Fibers, Perforating Paths and the cortico-amygdala pathway and are able to modify the LTP on their level (Kandel). “The increased release off glutamate might lead to its spillover to presynaptic glutamate receptors one the terminals off the NA and DA centers, causing the release off thesis Nm independently off activity in the modulatory center themselves” (Kandel butt Whitton P.S. paper: 1997 in Neurosci.Biobehav. Rev.). Further Kandel postulates that maybe long Hebbian homosynaptic term plasticity boat persist per, and modulatory transmitters edge produce persists exchanges by themselves, becoming necessary and sufficient also for Hebbian plasticity!
Associative LTP Heterosynaptic plasticity (LTPHA): Humeau & Lüthi, Nature 2003; Associative (i.e condition: synchronization of the 2 presynaptic inputs) but independent of the postsynaptic activity (including depolarization, postsynaptic NMDA receptors activation gold increase in post synaptic). The expression of the LTP is translated in fact like an increase persistent in the presynaptic probability of relaxation vésiculaire. In this case, there does not exist modulating neuron; one is in the presence of 3 neurons glutamatergic. The coupling between a heterosynaptic facilitation (n.1pré - n.2pré) and a homosynaptic activity (n.2pré - n.post) is responsible for an increase for the i¢ and synaptic reinforcement. This type of changes is more important than the sum of those which are produced individually by processes homo and heterosynaptic. This combination can be regarded as a new category of plasticity (Kandel).
Metaplasticity : Abraham & Baer, Tr Neurosci. 1996: Change in the capacity to induce a subsequent synaptic plasticity. The quality of change (LTP or LTD p.ex.) is not determined, it is only the reactivity/receptivity with the presynaptic stimuli which is increased/varies.
Ex 1: The STP (shorts term potentiation) is easily induced with “shorts burst” (30Hz, 150ms) in area CA1. In oneself, such a burst induces only one transitory STP which decreases quickly to turn over to the baseline. However, it would seem that there exists indeed of “length-lasting effects off this seemingly in activity”, and those are apparent during the later tests of stimulation of the same cell (with an aim of inducing a plasticity). These effects include/understand and a LTP, and a LTD, by not very clear mechanisms sub¢ (1996). Ex 2: The induction of the LTP on the level of Schaffer coll by a fort tetanus was inhibited when a weaker tetanus (5Hz) was managed beforehand on the same input (Schaffer Collateral). The effect was input specific and lasted less than 30'. Moreover, in the course of of experiences, the first stimulation rather seems to increase the threshold of stimulation necessary to induce the LTP, rather than to block it completely. In other cases, with same “the priming” stimulation (5Hz), one witnesses a facilitation of the LTP at the time of the successive fort tetanus. It is thus a plasticity of synaptic plasticity. According to the author and its experiments, the MP would be NMDAr dependant (“the priming stimulation”), therefore i¢ dependant, but would imply also metabotropic receivers mGlu with glutamate; and p.ex a LTP could transform into LTD!
Phenomena/observations attached to the LTP
Deaf, transfers and whispering silent synapses
(Voronin L. and Cherubini E. 2004): ) deaf A: postsynaptically silent: unable to detect glutamate release and C not conduct At rest because off the lack off AMPA R. B) transfers: presynaptically silent synapses gift' T conduct because the Pr is closed to zero C) whispering: the released is insufficient to produce has detectable quantal response, Q. N.B.: Often, the amount off glutamate in the cleft would Be sufficient to activate high affinity NMDARs drank not AMPARs, so yew there is only NMDARs, nothing could happen! See also Malenka.
Occlusion
Also called saturation. It is about the maximum limit or Ceiling of the Potentiation (Potentiation) which depend on factors limiting such as the number of receivers postsynaptic or the quantity of releasable presynaptic blisters, etc the occlusion of the LTP occurs typically when the NT (lime) saturated all the receivers postsynaptic (effective maximum glutamatergic per unit of time reached). 2 implied cells:Ex1: Increase in the number of blisters released by electric stimulation présyn more intense p.ex: multiplication 3x (arbitrary) of the potentiation until reaching the saturation of the receivers postsyn. : use of the margin existing between the no. of receivers and the number of NT.
Ex2: The BDNF will induce an increase in the number of receivers postsynaptic; what induces also a higher potentiation 3x, therefore a less important occlusion 3x, if the no. of released NT is sufficient to occupy all the receivers (old and new).
Ex3: Synergistic effect if combination of the 2 phenomena Ex1 and Ex2 at the same time: multiplication of the factors facilitating between them: 9x!! => occlusion reached 9x less easily. 1 implied cell: Ex4: a stimulus can occlude of them another on the level of the same cell: The st1 prevents the expression of the st2 by preceding it in time: competition in the use of the cellular machinery to the profit of the st1: this occurs when the 2 phenomena take place on the same cell, e.g.: stimulation E and BDNF: the first stimulus entered in action will prevent the second stimulus from making some in the same way, by overexploitation of the cell: example: does a type of plasticity occlude another of them on the same cell? i.e to answer the question: do the 2 types of plasticity have actors common to the level of the cell?
Facilitation
It is about the short-term increase in the number of exocytées blisters following a Pa. As it is thought that each blister contains the same quantity of neuro-transmitter, the concentration of neuro-transmitter in the synaptic slit depends mainly on the number of blisters released their contents. However the exocytose is caused by the abrupt increase in the intracellular calcium concentration which follows a Pa. In certain type of synapse, the increase in the calcic concentration is summoned when Pa follow one another a certain rate/rhythm. Blow, for Pa final, the rate of exocytose is more important than for the first. To postsynaptic measures of the currents, one typically observes greater amplitudes plus the presynaptic neuron discharges from Pa lengthily.
Depression
Short-term depression and potentiation
Long-term depression and potentiation
Glutamatergic depression on synaptic stimulation low frequency, independent of GABAergique inhibition and dependant on NMDAr.
IPSP: inhibitory postsynaptic potential
Phenomenon neurodepressor médié by receivers GABA (A): slow and durable inhibition médiée by the GABA which opens the channels Cl; GABA + Glycine induce a fast inhibition but évanescente.
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