Dendritic excitability and synaptic plasticity

2. Question: How dendritic properties control synaptic plasticity rules.
Answer: Dendrites serve to connect neurons and conduct information from synapses to the soma, but they serve little or no
specific role in triggering synaptic plasticity.

3.  In neuroscience, synaptic plasticity is the ability of synapses to strengthen or weaken over time, in response to increases
or decreases in their activity.
 Plasticity changes with alteration of the number of neurotransmitter receptors located on a synapse, including changes in
the quantity of neurotransmitters released into a synapse and changes in how effectively cells respond to those
neurotransmitters.
 Synaptic plasticity in both excitatory and inhibitory synapses has been found to be dependent upon postsynaptic calcium
release.
 Synapses are plastic, but also the dendritic tree itself
 Dendritic electrical properties can change in an activity-dependent manner with a time course of milliseconds up to
hours and perhaps even days, which means there exist dendritic as well as synaptic learning rules.
Synaptic plasticity

4. Hebbian Plasticity
 It is widely believed that learning and memory as well as the development of
neural circuitry depend critically on long-term changes in the strength of synaptic
connections.
 This view is often attributed to the Canadian neuropsychologist Donald Olding
Hebb and both the neuroanatomist Santiago Ramo´ n y Cajal and the psychologist
William James came to similar conclusions_
“When an axon of cell A is near enough to excite B and repeatedly or persistently
takes part in firing it, some growth process or metabolic change takes place in
one or both cells such that A’s efficiency, as one of the cells firing B, is increased.”
 Hebb argued that a memory trace of the event that triggered the synchronous firing
of cells A and B could be stored in this way.

5. Drawback of Hebbian Plasticity:
 First of all, a temporal and causal order is implied: cell A evokes the firing of cell B, so the presynaptic cell A is active
before the postsynaptic cell B
 Second, cell A needs to act in cooperation with other presynaptic cells to induce synaptic strengthening
 Third, the weakening of the connection is never mentioned, nor implied
 Fourth, strengthening is synapse-specific, which means that only active inputs are affected by this learning rule
 Fifth, Hebbian plasticity is in and of itself unstable: correlated firing leads to synaptic strengthening, which in turn
generates more correlated firing
 Finally, the Hebbian postulate treats all synapses as if they are equal and disregards any impact that the dendritic
location of a synapse may have on the induction of synaptic plasticity, as Hebb explicitly treats both dendritic and
somatic synapses as somatic.

6.  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.
 LTP is widely considered one of the major cellular mechanisms that underlies learning and memory.
 LTP is frequency-dependent, a property that probably is connected to the need for NMDA receptor-
mediatedCa2+influx
long-term potentiation (LTP)

7. The early phase of LTP
The Late phase of LTP
 LTP also exhibits at least two phases, denoted early and late LTP. The early phase
of LTP lasts only 1–3 h and does not require protein synthesis
 whereas the late phase lasts for at least a day and requires both translation and
transcription
 Different areas of the brain exhibit different forms of LTP. The specific type of
LTP exhibited between neurons depends on a number of factors
1. Age/ Maturity, The molecular mechanisms of LTP in the immature
hippocampus differ from adult hippocampus
2. Depends on different receptor (NMDA receptor, AMPA, glutamate
receptor (mGluR), etc)
3. Depends also anatomic location in which LTP is observed. eg, Schaffer
collateral pathway, or mossy fiber pathway

8. Long-Term Depression
 When the presynaptic axon of cell A repeatedly and persistently fails to excite the postsynaptic cell
B while cell B is firing under the influence of other presynaptic axons, metabolic change takes place
in one or both cells such that A’s efficiency, as one of the cells firing B, is decreased.
 Long-term depression (LTD), in neurophysiology, is an activity-dependent reduction in the efficacy
of neuronal synapses lasting hours or longer following a long patterned stimulus.
 LTD has also been found to occur in different types of neurons that release various
neurotransmitters, however, the most common neurotransmitter involved in LTD is L-glutamate. L-
glutamate acts on the NMDARs, AMPARs, kainate receptors and mGluRs during LTD.