Dataset Information

A mechanism for differential control of axonal and dendritic spiking underlying learning in a cerebellum-like circuit.

ABSTRACT: In addition to the action potentials used for axonal signaling, many neurons generate dendritic "spikes" associated with synaptic plasticity. However, in order to control both plasticity and signaling, synaptic inputs must be able to differentially modulate the firing of these two spike types. Here, we investigate this issue in the electrosensory lobe (ELL) of weakly electric mormyrid fish, where separate control over axonal and dendritic spikes is essential for the transmission of learned predictive signals from inhibitory interneurons to the output stage of the circuit. Through a combination of experimental and modeling studies, we uncover a novel mechanism by which sensory input selectively modulates the rate of dendritic spiking by adjusting the amplitude of backpropagating axonal action potentials. Interestingly, this mechanism does not require spatially segregated synaptic inputs or dendritic compartmentalization but relies instead on an electrotonically distant spike initiation site in the axon-a common biophysical feature of neurons.

SUBMITTER: Muller SZ

PROVIDER: S-EPMC10524478 | biostudies-literature | 2023 Jul

REPOSITORIES: biostudies-literature

ACCESS DATA

Publications

A mechanism for differential control of axonal and dendritic spiking underlying learning in a cerebellum-like circuit.

Muller Salomon Z SZ Abbott L F LF Sawtell Nathaniel B NB

Current biology : CB 20230612 13

In addition to the action potentials used for axonal signaling, many neurons generate dendritic "spikes" associated with synaptic plasticity. However, in order to control both plasticity and signaling, synaptic inputs must be able to differentially modulate the firing of these two spike types. Here, we investigate this issue in the electrosensory lobe (ELL) of weakly electric mormyrid fish, where separate control over axonal and dendritic spikes is essential for the transmission of learned predi ...[more]

PMID: 37311457

Similar Datasets

Project description:Dystonia is a movement disorder characterized by sustained or intermittent muscle contractions causing abnormal, often repetitive movements, postures, or both. Although dystonia is traditionally associated with basal ganglia dysfunction, recent evidence has been pointing to a role of the cerebellum, a brain area involved in motor control and learning. Cerebellar abnormalities have been correlated with dystonia but their potential causative role remains elusive. Here, we simulated the cerebellar input-output relationship with high-resolution computational modeling. We used a data-driven cerebellar Spiking Neural Network and simulated a cerebellum-driven associative learning task, Eye-Blink Classical Conditioning (EBCC), which is characteristically altered in relation to cerebellar lesions in several pathologies. In control simulations, input stimuli entrained characteristic network dynamics and induced synaptic plasticity along task repetitions, causing a progressive spike suppression in Purkinje cells with consequent facilitation of deep cerebellar nuclei cells. These neuronal processes caused a progressive acquisition of eyelid Conditioned Responses (CRs). Then, we modified structural or functional local neural features in the network reproducing alterations reported in dystonic mice. Either reduced olivocerebellar input or aberrant Purkinje cell burst-firing resulted in abnormal learning curves imitating the dysfunctional EBCC motor responses (in terms of CR amount and timing) of dystonic mice. These behavioral deficits might be due to altered temporal processing of sensorimotor information and uncoordinated control of muscle contractions. Conversely, an imbalance of excitatory and inhibitory synaptic densities on Purkinje cells did not reflect into significant EBCC deficit. The present work suggests that only certain types of alterations, including reduced olivocerebellar input and aberrant PC burst-firing, are compatible with the EBCC changes observed in dystonia, indicating that some cerebellar lesions can have a causative role in the pathogenesis of symptoms.

Dataset Information

A mechanism for differential control of axonal and dendritic spiking underlying learning in a cerebellum-like circuit.

Publications

A mechanism for differential control of axonal and dendritic spiking underlying learning in a cerebellum-like circuit.

Similar Datasets

OmicsDI is part of the ELIXIR infrastructure

Tweets