The plus symbols mark excitatory glutamatergic inputs and minus signs label inhibitory GABA-ergic inputs.Īn example of the parallel effects of inferior olivary NBQX infusion on CR performance and on the activity of a task-modulated IN cell. BC – brachium conjunctivum PM – nuclei containing eyeblink premotoneurons that include the red nucleus. Boxes with bold borders represent structures among which are in our view distributed plastic changes underlying eyeblink conditioning. Backslashed circles denote nodes at which inactivation during training disrupts CR acquisition. Output of eyeblink premotoneurons supplies motor commands to eyeblink motoneurons. Since all these sites (labeled with a star) receive CS and US information, they should be considered as putative sites of learning. These inputs are supplied in parallel to the serially connected pontine nuclei, cerebellar cortex, cerebellar interposed nuclei (IN) and brainstem nuclei contributing to projections to eyeblink premotoneurons and supplying motor commands to them. Information regarding the conditioned stimulus (CS) and unconditioned stimulus (US) information enters the network via auditory and sensory trigeminal systems. This diagram is a highly simplified representation of relevant structures and connectivity. Specific input interactions that induce these plastic changes as well as their cellular mechanisms remain unresolved.Ī conceptual block diagram of the cerebellum-related circuitry involved in acquisition and expression of classically conditioned eyeblinks in the rabbit. Results from these studies indicate that plastic changes underlying eye-blink conditioning are distributed across several cerebellar and extra-cerebellar regions. A possible solution to this problem is offered by several promising new approaches that minimize the effects of experimental interventions on spontaneous neuronal activity. Since eye-blink conditioning is mediated by a spontaneously active, recurrent neuronal network with strong tonic interactions, differentiating between the cerebellar learning hypothesis and the network performance hypothesis represents a major experimental challenge. However, recent evidence revealed that these manipulations could be explained by a network performance hypothesis which attributes learning deficits to a non-specific tonic dysfunction of eye-blink networks.
These experiments inactivated parts of cerebellum-related networks during the acquisition and expression of classically conditioned eye blinks in order to determine sites at which the plasticity occurred. The major evidence for this hypothesis originated from studies based on a telecommunications network metaphor of eye-blink circuits. The cerebellar learning hypothesis proposes that plasticity subserving eye-blink conditioning occurs in the cerebellum. Classical conditioning of the eye-blink reflex in the rabbit is a form of motor learning that is uniquely dependent on the cerebellum.