FoundationalConceptsNeuroscience

terminal that respond to released neurotransmitter. For example, at
a glutamatergic synapse, glutamate neurotransmitter may interact
with glutamate receptors located on the presynaptic axon terminal to
open Na‘ or Ca** ion channels and thus prolong depolarization in the
axon terminal, thereby strengthening the synapse.
Or, there may be retrograde signals from a postsynaptic cell that
influence neurotransmitter release in the axon terminal. Endo-
cannabinoids released from a postsynaptic dendrite may interact
with presynaptic cannabinoid G-protein-coupled receptors to prolong
depolarization or influence gene expression. For example, influencing
the transcription and translation of genes that code for presynap-
tic reuptake transporters can have a long-term effect on synaptic
strength. More reuptake transporter proteins means neurotransmit-
ter is removed from the synaptic cleft more rapidly after release—a
smaller signal and thus a weaker synapse. Fewer reuptake transporter
proteins means neurotransmitter remains in the synaptic cleft for a
longer time after release—more signal and thus a stronger synapse.
A postsynaptic mechanism for changing the strength of a synapse
is to influence gene transcription so that greater or lesser numbers of
neurotransmitter receptors are produced and inserted into the post-
synaptic membrane. More neurotransmitter receptors means a larger
impact from incoming neurotransmitter—a stronger synapse. Other
things being equal, fewer postsynaptic neurotransmitter receptors
mean a weaker synapse.
Likewise, G-protein-coupled receptor effects on transcription of
nerve growth factors may influence the branching of axons and den-
drites, the sprouting of dendritic spines, and the formation of new
synapses.
The formation of new neurons from precursor cells provides
another potential avenue of neuroplasticity. In contrast to what had