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Learning-related cellular modifications occur not only at synapses but also in the intrinsic properties of the neurons. Learning-induced enhancement in neuronal excitability is evident in hippocampal and piriform cortex pyramidal neurons following a complex olfactory-discrimination operant conditioning task. Such enhanced excitability is manifested in reduced spike frequency adaptation that results from reduction in the slow afterhyperpolarization (AHP), which develops after a burst of action potentials. AHP reduction is apparent throughout the pyramidal cells neuronal population. The AHP amplitude tends to return back to its initial value within days when training is suspended. This recovery is accompanied by reduced learning capability, but not by loss of memories for learned odors.
The post-burst AHP reduction is mediated by decreased conductance for a specific calcium-dependent potassium current, the slow IAHP. This long-lasting reduction is dependent on persistent activation of the PKC and ERK second messenger systems. Similar long-lasting AHP reduction can be induced in-vitro by repetitive synaptic stimulation or by kainate application. Such activity-dependent AHP reduction is occluded by prior learning.
Olfactory-learning induced enhanced neuronal excitability in CA1 pyramidal neurons is also accompanied by enhanced learning capability in a novel hippocampus-dependent task, the Morris water maze.
We suggested that AHP reduction is the cellular mechanism that enables neuronal ensembles to enter into a state which may be best termed "learning mode". This state lasts for up to several days and its behavioral manifestation is enhanced learning capability in tasks that depend on these particular neuronal ensembles. Specifically, enhanced neuronal excitability sets a time window in which most neurons in the relevant neuronal network are more excitable, and thus activity-dependent synaptic modifications are more likely to occur.