Abstract
Although the hippocampus is processing temporal and spatial information in particular context, the encoding rule creating memory is completely unknown. To examine the mechanism, we trained rats on an inhibitory avoidance (IA) task, a hippocampus-dependent rapid one-trial contextual learning paradigm. By combining Herpes virus-mediated in vivo gene delivery with in vitro patch-clamp recordings, I reported contextual learning drives GluR1-containing AMPA receptors into CA3-CA1 synapses. The molecular event is required for contextual memory, since bilateral expression of delivery blocker in CA1 successfully blocked IA learning. Moreover, I found a logarithmic correlation between the number of delivery blocking cells and learning performance. Considering that one all-or-none device can process 1-bit of data per clock (Nobert Wiener 1961), the logarithmic correlation may provides evidence that CA1 neurons transmit essential data of contextual information. Further, I recently reported critical role of acetylcholine as an intrinsic trigger of learning-dependent synaptic plasticity. IA training induced ACh release in CA1 that strengthened not only AMPA receptor-mediated excitatory synapses, but also GABA A receptor-mediated inhibitory synapses on each CA1 neuron. More importantly, IA-trained rats showed individually different excitatory and inhibitory synaptic inputs with wide variation on each CA1 neuron. Here I propose a new hypothesis that the diversity of synaptic inputs on CA1 neurons may depict cell-specific outputs processing experienced episodes after training.
Highlights
The hippocampus plays a central role to form new episodic memory in various species including humans [1]
We revealed that learning-dependent synaptic delivery of AMPA receptors into the CA3-CA1 synapses is required for hippocampal learning [9]
I found that i) cholinergic trigger drives learning-dependent synaptic plasticity at excitatory and inhibitory synapses, and ii) learning requires the diversity of synaptic inputs in CA1 pyramidal neurons [12]
Summary
The hippocampus plays a central role to form new episodic memory in various species including humans [1]. In 2006, in vivo field EPSC recording study showed that hippocampal learning induces LTP in CA1 region of hippocampus [8]. We revealed that learning-dependent synaptic delivery of AMPA receptors into the CA3-CA1 synapses is required for hippocampal learning [9]. Since there is no tetanus electrode in brain, endogenous trigger and/or the mechanism inducing the learning-dependent LTP were unknown. Without electrode for tetanus stimulation, bath treatment of ACh agonist induces specific bursts [10] and forms LTP in CA1 region of hippocampal slices [11]. I found that i) cholinergic trigger drives learning-dependent synaptic plasticity at excitatory and inhibitory synapses, and ii) learning requires the diversity of synaptic inputs in CA1 pyramidal neurons [12]. ACh seems to be necessary to strengthen the information-specific tagged CA1 synapses [13], depicted by hippocampal-cortical networks [14]
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