A fundamental issue in developmental science is whether ontogenetic changes in memory are caused by the development of cellular plasticity mechanisms within the brain's memory systems or maturation of sensory inputs to the memory systems. Here, we provide evidence that the development of eyeblink conditioning, a form of associative learning that depends on the cerebellum, is driven by the development of sensory inputs rather than the development of neuronal plasticity mechanisms. We find that rats as young as 12 days old show associative eyeblink conditioning when pontine stimulation is used in place of an external (e.g., a tone) conditioned stimulus. Eyeblink-conditioned responses established with pontine stimulation in 12-day-old rats were reversibly abolished by an infusion of muscimol into the cerebellar interpositus nucleus. The findings suggest that cerebellar neurons are capable of supporting associative learning-specific plasticity in vivo in very immature animals if given sufficient afferent stimulation.cerebellum ͉ eyelid conditioning ͉ learning ͉ memory I t seems reasonable to assume that the development of memory is caused by the maturation of synaptic plasticity mechanisms within the memory systems of the brain. For example, the development of declarative memory could be related to the development of long-term potentiation in the medial temporal lobe, and conditioning of discrete movements could be related to the development of cerebellar long-term depression. On the other hand, it is possible that the cerebellum and hippocampus are capable of establishing learning-related synaptic plasticity in young animals but simply do not receive sufficient sensory input during learning. We evaluated these possibilities by examining the effects of electrically stimulating a sensory input pathway to the cerebellum on eyeblink conditioning in rats that are too immature to show conditioning with external sensory stimuli.Eyeblink conditioning, a type of associative learning, typically involves the presentation of a conditioned stimulus (CS) that does not produce a blink reflex before training (e.g., a tone or light) followed by an unconditioned stimulus (US) that reliably elicits the blink reflex. Repeated presentations of the CS and US result in the acquisition of a conditioned response (CR) that precedes the onset of the US. Eyeblink conditioning emerges ontogenetically between postnatal days 17 and 24 in rats (1). Developmental changes in human eyeblink conditioning have also been documented (2).The cerebellar hemisphere that is ipsilateral to the conditioned eye is essential for acquisition and retention of eyeblink conditioning in adult and infant animals (3, 4). Neurons within the pontine nuclei (PN) are part of the mossy fiber pathway that sends CS information to the cerebellum (5-7). Cerebellar neurons are thought to develop learning-specific changes in synaptic efficacy to CS inputs, which underlies memory for the CS-US association (8). Using either cerebellar slices or cultured neurons from rodents, many ...