scholarly journals Pontine stimulation overcomes developmental limitations in the neural mechanisms of eyeblink conditioning

2005 ◽  
Vol 12 (3) ◽  
pp. 255-259 ◽  
Author(s):  
J. H. Freeman
2015 ◽  
Vol 112 (45) ◽  
pp. 14060-14065 ◽  
Author(s):  
Anders Rasmussen ◽  
Riccardo Zucca ◽  
Fredrik Johansson ◽  
Dan-Anders Jirenhed ◽  
Germund Hesslow

A central tenet of Rescorla and Wagner’s model of associative learning is that the reinforcement value of a paired trial diminishes as the associative strength between the presented stimuli increases. Despite its fundamental importance to behavioral sciences, the neural mechanisms underlying the model have not been fully explored. Here, we present findings that, taken together, can explain why a stronger association leads to a reduced reinforcement value, within the context of eyeblink conditioning. Specifically, we show that learned pause responses in Purkinje cells, which trigger adaptively timed conditioned eyeblinks, suppress the unconditional stimulus (US) signal in a graded manner. Furthermore, by examining how Purkinje cells respond to two distinct conditional stimuli and to a compound stimulus, we provide evidence that could potentially help explain the somewhat counterintuitive overexpectation phenomenon, which was derived from the Rescorla–Wagner model.


2018 ◽  
Vol 4 (10) ◽  
pp. eaas9426 ◽  
Author(s):  
Henk-Jan Boele ◽  
Saša Peter ◽  
Michiel M. Ten Brinke ◽  
Lucas Verdonschot ◽  
Anna C. H. IJpelaar ◽  
...  

Pavlovian eyeblink conditioning has been used extensively to study the neural mechanisms underlying associative and motor learning. During this simple learning task, memory formation takes place at Purkinje cells in defined areas of the cerebellar cortex, which acquire a strong temporary suppression of their activity during conditioning. Yet, it is unknown which neuronal plasticity mechanisms mediate this suppression. Two potential mechanisms include long-term depression of parallel fiber to Purkinje cell synapses and feed-forward inhibition by molecular layer interneurons. We show, using a triple transgenic approach, that only concurrent disruption of both these suppression mechanisms can severely impair conditioning, highlighting that both processes can compensate for each other’s deficits.


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