TThe plasticity of neural synapses – that is, the dynamic relationship between two neurons in the brain while one sends signals to another – ultimately underlies cognition, learning, and memory. The increase in synaptic strength after a burst of stimulation, also called post-tetanic potentiation (PTP), is driven by an increase in the amount of neurotransmitters ready to be released from the presynaptic site. Called moss fiber synapses in the hippocampus. A new study finds that this potentiation can be regulated by the postsynaptic cell by sending the neurotransmitter glutamate back to the presynaptic side – a form of retrograde signaling that neuroscientists did not expect to exist in this synapse.
BACK TALK: Communication across synapses is generally viewed as one way: neurotransmitters leave the presynaptic terminal (left cell in each panel) and bind to receptors on the postsynaptic cell (right cell of each panel). Under typical in vitro conditions, when neuroscientists examine so-called moss fiber synapses of the hippocampus, calcium availability is low (top row), and a high-frequency stimulation surge leads to excitation of the postsynaptic cell and an increase in the easily releasable pool of the neurotransmitter glutamate in the presynaptic terminal , a phenomenon known as post-tetanic potentiation. In a new study, researchers found that this post-tetanic potentiation can be blocked by reverse synaptic signaling. When calcium availability is high (bottom row), excitation of the postsynaptic cell leads to retrograde glutamatergic signaling – in which glutamate from the postsynaptic cell binds to receptors at the presynaptic end – which prevents this potentiation.