Brain and Behaviour Seminar
2024-2025

​​

10:30 AM, January 14th

In-person: Sidney Smith Hall Room 1087 (100 St. George Street)

​

Dr. Kei M Igarashi

Department of Anatomy and Neurobiology, School of Medicine,
University of California, Irvine

​

"Circuit mechanisms of item memory and its disruption in Alzheimer’s disease"

​

    Memory has multiple components: “what” memory (item/object), “when” memory (time) and “where” memory (space). Research in the past decades revealed neurons involved in spatial memory, including place cells in the hippocampus and grid cells in the medial entorhinal cortex (MEC). However, circuit mechanisms of memory about item and time remain largely unclear. Our lab focuses on identifying neural circuits for item memory, and how these circuits become impaired in the disease of memory – Alzheimer’s disease. We previously reported the encoding of item-outcome associative memory in the lateral entorhinal cortex (LEC) (Igarashi et al., Nature, 2014), and this encoding is controlled by dopamine signals from the ventral tegmental area (Lee et al., Nature, 2021). We recently found that neuronal populations of both the LEC (layer 5/6) and their major target, the medial prefrontal cortex, formed an internal map of pre-learned and novel items, classified into dichotomic rewarded vs. punished groups (Jun et al., Nature 2024). The formation of this internal map was mutually dependent. Our result suggests that the LEC and mPFC encodes a cognitive map of item-outcome rules.

    In the second part of the talk, I will share our recent finding of dysfunctional dopamine in the LEC of Alzheimer’s disease mouse models (Nakagawa et al., bioRxiv 2024), which further suggests the critical role of dopamine in Alzheimer’s disease.

​

​

4 PM, February 10th

Hybrid format, In-person Psychology Lounge​​

​

Dr. Caleb Browne

The Centre for Addiction and Mental Health

​​

"Neural mechanisms underlying the development of substance use disorder and relapse vulnerability"

​​​

​Substance use disorder (SUD) devastates lives and places a significant burden on the healthcare system. Despite its prevalence, effective treatment options remain limited, and the chronically relapsing nature of SUD makes long-term abstinence exceptionally difficult to achieve. This talk will present a series of preclinical studies aimed at deepening our understanding of neural mechanisms that drive the development and maintenance of SUD. First, I will describe a neural substrate within the nucleus accumbens – a crucial hub of the brain’s reward circuit – that enables drugs of abuse to hijack neural function and disrupt naturalistic goal-directed behavior. I will then outline molecular adaptations that support long-lasting relapse vulnerability in a mouse model of opioid use disorder, with a focus on an epigenetic mechanism in the ventral hippocampus – an important interface between memory and motivation. These studies integrate in vivo two-photon calcium imaging, intravenous drug self-administration, RNA sequencing, bioinformatic analyses, and CRISPR-mediated gene regulation, forming a comprehensive pipeline that has enbled us to generate new insights into how drugs of abuse access and disrupt brain circuits and behaviour. Further, our findings offer novel avenues for developing much-needed therapeutic interventions to combat SUD.

​

The link to virtual seminars will be sent one week before the seminar date. Please sign up below to receive the seminar link.

​