Key Concepts of Section 22.5

Key Concepts of Section 22.5

Forming and Storing Memories

  • Experience changes the number and strength of connections between neurons in the brain through a process known as synaptic plasticity. Synaptic plasticity provides a biological basis for the formation and storage of memories.

  • Studies of habituation and sensitization of the gill-withdrawal reflex in the marine mollusk Aplysia californica demonstrated that learning produces changes in synaptic connectivity. Habituation involves decreases in the connectivity of the sensory and motor neurons that give rise to the gill-withdrawal reflex, while sensitization involves increases in sensory-motor connectivity (Figure 22-41)

  • The hippocampus is a region of the brain that is required for the formation of long-lasting memories (Figure 22-42). Hippocampal synapses undergo activity-dependent forms of synaptic strengthening called long-term potentiation (LTP) and activity-dependent forms of synaptic weakening called long-term depression (LTD).

  • Changes in synaptic strength can be mediated by presynaptic, trans-synaptic, or postsynaptic mechanisms.

  • Activity generates a constitutively active form of CamKIIα in the postsynaptic compartment, which phosphorylates substrates in the postsynaptic density, including glutamate receptors. Mice lacking CamKIIα have defects in hippocampal LTP and memory.

  • Activity regulates the trafficking of AMPA glutamate receptors in the postsynaptic membrane. LTP is accompanied by an increase in insertion of AMPA receptors in the postsynaptic density, while LTD is accompanied by a decrease in the concentration of AMPA receptors in the postsynaptic density (Figure 22-43).

  • Short-term forms of synaptic plasticity involve changes in preexisting proteins at the synapses, but long-term forms require new mRNA and protein synthesis.

  • Synapse-specific forms of plasticity involve the local translation of synaptically localized mRNAs.

  • Fragile X syndrome is caused by null mutations in the gene encoding the RNA-binding protein FMRP. FMRP regulates local translation at synapses. Mice lacking FMRP have abnormal synapses and exhibit learning impairments and deficits in hippocampal LTD.