Abstract
Associative memory is essential for cognition, in which associative memory cells and their plasticity presumably play important roles. The mechanism underlying associative memory extinction vs. maintenance remains unclear, which we have studied in a mouse model of cross-modal associative learning. Paired whisker and olfaction stimulations lead to a full establishment of odorant-induced whisker motion in training day 10, which almost disappears if paired stimulations are not given in a week, and then recovers after paired stimulation for an additional day. In mice that show associative memory, extinction and recovery, we have analyzed the dynamical plasticity of glutamatergic neurons in layers II–III of the barrel cortex and layers IV–V of the motor cortex. Compared with control mice, the rate of evoked spikes as well as the amplitude and frequency of excitatory postsynaptic currents increase, whereas the amplitude and frequency of inhibitory postsynaptic currents (IPSC) decrease at training day 10 in associative memory mice. Without paired training for a week, these plastic changes are persistent in the barrel cortex and decayed in the motor cortex. If paired training is given for an additional day to revoke associative memory, neuronal plasticity recovers in the motor cortex. Our study indicates persistent neuronal plasticity in the barrel cortex for cross-modal memory maintenance as well as the dynamical change of neuronal plasticity in the motor cortex for memory retrieval and extinction. In other words, the sensory cortices are essential for long-term memory while the behavior-related cortices with the inability of memory retrieval are correlated to memory extinction.
Highlights
Associative learning is a common approach for information acquisition and associative memory is essential to logical reasoning and associative thinking (Wasserman and Miller, 1997; Suzuki, 2008; Wang and Cui, 2017)
Whisker retraction durations are 1.25 ± 0.2 s at day 1, 3.20 ± 0.20 s at day 10, 1.31 ± 0.20 s at day and 3.19 ± 0.2 s at day (Figure 1E; two asterisks denote p < 0.01; One-way analysis of variance (ANOVA))
As odorant-induced whisker motion is accompanied by the upregulations of glutamatergic neurons and synapses in the barrel cortices (Wang et al, 2015; Gao et al, 2016; Yan et al, 2016), we aim to study whether the upregulation, decay and re-upregulation of neuronal and synaptic activity in the barrel cortex and the motor cortex are parallel to and even correlated to the establishment, extinction and reestablishment of cross-modal associative memory
Summary
Associative learning is a common approach for information acquisition and associative memory is essential to logical reasoning and associative thinking (Wasserman and Miller, 1997; Suzuki, 2008; Wang and Cui, 2017). It has been suggested that information retrievals triggered by the cues and presented by the behaviors are fulfilled by the neuronal circuits from sensory cortices to behavior-guide cortices through their relayed brain regions (Wang et al, 2015) This suggestion is granted by the facts that the stimulations to any of these areas can trigger memory retrievals (Ehrlich et al, 2009; Pape and Pare, 2010; Liu et al, 2012; Li et al, 2013; Xu and Südhof, 2013; Otis et al, 2017; Yokose et al, 2017) as well as the responses to associated signals can be recorded in sensory cortices (Wang et al, 2015; Vincis and Fontanini, 2016; Yan et al, 2016) and their downstream brain regions (Naya et al, 2003; Takehara-Nishiuchi and McNaughton, 2008; Viskontas, 2008; Cai et al, 2016). If this is a case, we should see the persistence of neuronal plasticity in the sensory cortices and the decay of neuronal plasticity in behavior-control cortices during memory extinction, as well as the recovery of neuronal plasticity in behavior-control cortices after memory restoration
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