Elif B. Guven
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Research Subjects
Elif B. Guven has a total of 12 co-authors. Here are the top co-authors by number of shared publications:
- Dalton James Surmeier
Department of Neuroscience, Feinberg School of Medicine, Northwestern University, Chicago, Illinois, USA
1 shared publication - Ema Ilijic
Department of Neuroscience, Feinberg School of Medicine, Northwestern University, Chicago, IL 60611, USA; Aligning Science Across Parkinson's (ASAP) Collaborative Research Network, Chevy Chase, MD 20815, USA
1 shared publication - James M. Tepper
Rutgers University
1 shared publication Jay Li
Department of Internal Medicine, University of Michigan Medical School. Ann Arbor, MI, USA
1 shared publication- Marziyeh Belal
Department of Neuroscience, Feinberg School of Medicine, Northwestern University, Chicago, IL 60611, USA; Aligning Science Across Parkinson's (ASAP) Collaborative Research Network, Chevy Chase, MD 20815, USA
1 shared publication - Maxime Assous
Cardiff University, School of Biosciences, Cardiff, Wales, UK
1 shared publication
Latest Publications
- Open Access
Cholinergic interneuron control of GABAergic circuits targeting spiny projection neurons is disrupted in parkinsonian models
Parkinson's disease (PD) is known to alter the intrinsic properties of striatal cholinergic interneurons (ChIs). However, how PD shapes ChI control of intrastriatal GABAergic circuits regulating principal spiny projection neurons (SPNs) is unknown. To fill this gap, striatal circuits in healthy and parkinsonian mice were interrogated. In ex vivo brain slices from healthy mice, optogenetic stimulation of ChIs evoked GABA A receptor currents in both indirect and direct pathway SPNs that were attributable to nicotinic acetylcholine receptor (nAChR)-mediated activation of GABAergic interneurons (GIs). Simulations suggested that this circuit exerts a state-dependent control of SPN dendritic integration that was modulated by concomitant muscarinic receptor signaling. Surprisingly, in mouse models of prodromal and parkinsonian states, the ability of ChIs to engage this intrastriatal circuitry was disrupted because interneurons down-regulated nicotinic AChRs. Taken together, these studies suggest that impaired ChI control of GABAergic interneurons contributes to behavioral deficits in both prodromal and clinical PD states.
Open AccessCholinergic interneuron control of GABAergic circuits targeting spiny projection neurons is disrupted in parkinsonian models
Parkinson's disease (PD) is known to alter the intrinsic properties of striatal cholinergic interneurons (ChIs). However, how PD shapes ChI control of intrastriatal GABAergic circuits regulating principal spiny projection neurons (SPNs) is unknown. To fill this gap, striatal circuits in healthy and parkinsonian mice were interrogated. In ex vivo brain slices from healthy mice, optogenetic stimulation of ChIs evoked GABA A receptor currents in both indirect and direct pathway SPNs that were attributable to nicotinic acetylcholine receptor (nAChR)-mediated activation of GABAergic interneurons (GIs). Simulations suggested that this circuit exerts a state-dependent control of SPN dendritic integration that was modulated by concomitant muscarinic receptor signaling. Surprisingly, in mouse models of prodromal and parkinsonian states, the ability of ChIs to engage this intrastriatal circuitry was disrupted because interneurons down-regulated nicotinic AChRs. Taken together, these studies suggest that impaired ChI control of GABAergic interneurons contributes to behavioral deficits in both prodromal and clinical PD states.