ePoster

<B DATA-OLK-COPY-SOURCE="MESSAGEBODY">CCP1 REGULATE FUNCTIONAL PROPERTIES OF CORTICAL PARVALBUMIN INTERNEURONS </B>

Sam Jadotand 2 co-authors

Liege University

FENS Forum 2026 (2026)
Barcelona, Spain
Board PS01-07AM-059

Presentation

Date TBA

Board: PS01-07AM-059

Poster preview

<B DATA-OLK-COPY-SOURCE="MESSAGEBODY">CCP1 REGULATE FUNCTIONAL PROPERTIES OF CORTICAL PARVALBUMIN INTERNEURONS </B> poster preview

Event Information

Poster Board

PS01-07AM-059

Abstract

Microtubules are essential for axonal growth and branching, as well as for axonal transport, which is required for the maintenance of neuronal processes and their functions. These processes are tightly regulated by numerous post-translational modifications, including polyglutamylation, which is highly enriched in the brain and controlled by a set of glutamylating (glutamylases) and deglutamylating (deglutamylases) enzymes. Certain neuronal populations are highly dependent on the deglutamylase CCP1, the loss of which leads to multiple consequences, including transport defects along microtubules in parvalbumin (PV) interneurons but also neuronal degeneration in the case of Purkinje cell.
In the CCP1 cKO mouse model, in which CCP1 loss is restricted to cortical interneurons, only PV interneurons exhibit increased polyglutamylation, associated with impaired microtubule-based transport in both anterograde and retrograde directions. We investigated the consequences of these transport defects on synaptic input and neurotransmitter release in PV interneurons. Initial observations indicate that basal synaptic release of GABA from PV interneuron is not affected by CCP1 loss. In contrast, spontaneous and miniature excitatory synaptic currents are less frequent and their kinetics are prolonged, reflecting a decrease in excitatory drive and possibly changes in the subunit composition of postsynaptic glutamatergic AMPA receptors expressed by PV interneurons. Active and passive electrophysiological properties of these neurons are also impacted by CCP1 loss. Further investigations are required to determine the consequences of the loss of CCP1 in interneurons for the local circuitry.

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