[WTI-trainee] FW: Announcing: Special Seminar with Dr. Chris Dulla - September 30th, 2025, 100 College St. Room 180 A/B

Fri Sep 19 10:39:52 EDT 2025

See below!

Best,
Giovanna

Giovanna Guerrero-Medina, PhD [A button for name playback in email signature] <https://www.name-coach.com/giovanna-guerrero-medina>

She/Her/Ella

Director for Professional Development & Community,

Wu Tsai Institute at Yale

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wti.yale.edu<https://wti.yale.edu/>

From: Neuroscience <neuroscience-bounces at mailman.yale.edu> on behalf of Bownes, Katherine <katherine.bownes at yale.edu>
Date: Friday, September 19, 2025 at 10:26 AM
To:
Subject: [Neuroscience] Announcing: Special Seminar with Dr. Chris Dulla - September 30th, 2025, 100 College St. Room 180 A/B

In honor of National Post-Doc Appreciation Week, we will be hosting Dr. Chris Dulla (Tufts University) to give a seminar about his work and mentoring philosophy on September 30th, 2025 at 12:00PM in 100 College Room 180 A/B. In addition to his scientific accomplishments, Dr. Dulla has been recognized for excellent post-doctoral mentorship by the glowing feedback of his trainees and his receipt of the 2018 NINDS Landis Award for Mentorship.

Warm regards,

Paras Patel, PhD
On behalf of the Yale Neuroscience Post-Doctoral Committee

Title: When your Ferrari breaks down: Metabolic-functional coupling of fast-spiking parvalbumin inhibitory neurons in the healthy and injured brain

Abstract: Parvalbumin-positive interneurons (PV-INs) are critical regulators of circuit activity and are selectively vulnerable across neurological disorders, including traumatic brain injury (TBI), epilepsy, Alzheimer’s disease, and schizophrenia. Their susceptibility is thought to stem from high metabolic demands driven by intense electrical activity. Using single-nucleus RNA-sequencing (snRNAseq) from rodent and human TBI, we show that PV-INs possess unique metabolic specializations that are lost after injury but can be restored in vivo by the glycolytic inhibitor 2-deoxyglucose. We define a PV-IN transcriptional identity module—encompassing ion channels, metabolic enzymes, and synaptic machinery—that reveals heterogeneous subsets of injury-associated PV-INs with disrupted identity. Loss of metabolic specialization is tightly coupled to this transcriptional dysfunction, with the PV-IN–enriched transcriptional co-activator Ppargc1a emerging as a key driver. We further identify a family of long non-coding RNAs enriched in dysfunctional PV-INs that inversely correlates with metabolic specialization. Finally, analysis of published human TBI snRNAseq datasets confirms nearly identical PV-IN changes, underscoring the central role of PV-IN metabolic dysfunction in TBI pathology.

[cid:174209b7-e3b4-4d34-837f-81c06e1f4090]

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