Topic 4: EPSPs, IPSPs & Intracellular Signaling

What is an EPSP and how does it affect action-potential firing?

An EPSP is local depolarization caused by positive ion influx, such as Na⁺ through AMPA or nicotinic receptors. It moves the membrane toward threshold (~−55 mV), increasing the chance of an action potential.

What is an IPSP and what ion movements can produce it?

An IPSP inhibits firing. It can result from Cl⁻ influx through GABA-A receptors or K⁺ efflux through GABA-B signaling, making the neuron less likely to reach threshold.

How do EPSPs/IPSPs differ from action potentials?

EPSPs and IPSPs are graded—their size varies with synaptic input. Action potentials are all-or-none—once threshold is reached, a full action potential occurs.

What is the difference between spatial and temporal summation?

Spatial summation: signals from different locations arrive at the same time. Temporal summation: signals from the same synapse arrive rapidly one after another.

How are postsynaptic potentials integrated, and why does synapse location matter?

EPSPs/IPSPs spread passively toward the axon hillock and decay over distance/time. They are summed at the integration zone. Synapses closer to the axon hillock, such as axosomatic synapses, generally have greater influence.

What causes paired-pulse facilitation (PPF)?

A second presynaptic action potential arrives soon after the first → residual presynaptic Ca²⁺ → more neurotransmitter released → larger second EPSP.

What are dendritic spines and why are they important?

Small head-and-neck protrusions on dendrites where many excitatory synapses form. Their shape can change during synaptic strengthening/plasticity.

What is a kinase and what can phosphorylation do in neurons?

A kinase transfers a phosphate from ATP to a target protein. Phosphorylation can change protein activity/shape, regulate ion channels, and trigger signaling that affects gene transcription.

How do NMDA receptors and CaMKII strengthen a synapse during LTP?

NMDA activation → Ca²⁺ enters the postsynaptic neuron → activates CaMKII → AMPA receptors are phosphorylated and more AMPA receptors are added → stronger synaptic response. LTP = long-term potentiation, a long-lasting strengthening of a synapse.

How are PKC, tyrosine kinases, and CREB involved in long-term synaptic plasticity?

PKC and tyrosine kinase signaling can contribute to pathways affecting CREB. CREB is a transcription factor that alters gene expression, supporting longer-term cellular/structural changes.