Five students graduate from Neuroscience Graduate Program

Three PhD students and two MSc students graduated from the Neuroscience Graduate Program in the 2019/2020 academic year. Read on to meet Cristina, Juan, Bridget, Mohammad, and Ben and to learn more about their theses and dissertations.


imageCristina Pinar, PhD

“Effects of mild traumatic brain injury on hippocampal synaptic plasticity and behaviour in juvenile rats”

(Supervisor: Brian Christie; Home department: Division of Medical Sciences)

Pinar’s dissertation focused on the effects of repeated mild traumatic brain injury (TBI; also known as concussion) on an individual’s behaviour and brain function. She specifically looked the effects on synaptic plasticity in the hippocampus, a region of the brain important for learning and memory processes. Synaptic plasticity refers to changes in the efficacy of neural communication as a result of prior experience or patterns of activation and include processes such as long-term potentiation (LTP) and long-term depression (LTD). Both LTP, LTD, and other forms of plasticity are thought to underlie learning and memory.

Through her research, Pinar found that repeated mild TBI impairs hippocampal-dependent spatial learning and memory, as well as significantly impairs the capacity for LTD in both sexes. Her data are the first to describe the negative impact of this type of injury on LTD in the dentate gyrus region of the hippocampus in both juvenile males and females, and they provide evidence for the delayed development of neurological deficits with repeated mild TBI.

Mild TBI accounts for up to 75 per cent of all brain injuries, and there is a growing awareness that repeated mild TBI can result in cumulative learning and memory deficits and neuropathology. However, there isn’t much preclinical data on the extent that these deficits manifest. Repeated mild TBI in juvenile populations is of special interest; not only is this a high-risk group, but juvenile human brains are not finished maturing. The hippocampus is a brain region important for learning and memory processes, and repeated mild TBI during the juvenile period may particularly disrupt the development of cognitive processes.


imageJuan Sanchez-Arias, PhD

“Pannexin 1 Regulates Dendritic Spines in Developing Cortical Neurons”

(Supervisor: Leigh Anne Swayne; Home department: Division of Medical Sciences)

Sanchez-Arias’ dissertation examined how Pannexin 1 (Panx1) regulates the formation of connections between nerve cells in the brain. More specifically, it explored the role of Panx1 in the development of dendritic spines and neuronal networks.

Our brains rely on synapses to transmit information through large networks of brain cells. The vast majority of these synapses are located at dendritic spines, minuscule structures at the receptive ends of brain cells. These dendritic spines form as our brain continues to develop after we are born. Abnormal dendritic spine development is a hallmark of multiple neurodevelopmental, neuropsychiatric, and neurodegenerative disorders.

Panx1 is a channel protein, meaning it forms regulated doorways into nerve cells. Sanchez-Arias’ work furthers our understanding on cortical development and places Panx1 as a novel regulator of structural and functional plasticity in the brain. It also has important implications for understanding how nerve cell connections are formed in the development of healthy brains vs. brains with disorders like those on the autism spectrum and schizophrenia.

Sanchez-Arias’s most recent research suggests that Panx1 regulation of dendritic spines development is rooted in the protein’s influence on spiny protrusions, the highly dynamic spine precursors.


imageBridget Ryan, PhD

“Investigating direct and cooperative microRNA regulation of Pax6 in vivo using a genome engineering approach”

(Supervisor: Bob Chow; Home department: Biology)

Ryan’s dissertation focused on an approach that cells employ to fine-tune the quantity of Pax6 that they make.

The mature brain is composed of a huge number of different neuronal cell, which all perform different roles in the normal functioning of the adult brain. During brain development, all of these cell types are produced from neuronal stem cells, and they must be formed in the correct numbers, migrate to the correct locations, and connect up with the correct partners. This incredibly complex process is orchestrated by factors internal to the cells themselves, and factors present in the immediate environment surrounding the cells.

Many of the factors important for directing different aspects of development are coded for in the genome, with different genes containing the instructions needed to manufacture different factors. One such factor, Pax6, is critical for normal development of the eyes and brain, and cells must manufacture it at the correct level for proper development. Generally, this can be thought of as a Goldilocks effect: if cells make too much or too little Pax6, development of the eyes and brain can be adversely affected. 

Ryan’s findings suggest that if this fine-tuning is disrupted in neuronal stem cells during development, the quantity of Pax6 that they make is elevated and the types of neurons that they produce is altered relative to normal.          


imageMohammad Motaharinia, MSc

“Longitudinal calcium imaging of VIP interneuron circuits reveals shifting response fidelity dynamics in the stroke damaged brain”

(Supervisor: Craig Brown; Home department: Division of Medical Sciences)

Motaharinia’s thesis examined the effects of stroke on inhibitory cortical interneurons. These neurons play a critical role in regulating brain excitability and function. In particular, interneurons expressing vasoactive intestinal peptide (VIP) specialize in inhibiting other types of inhibitory neurons, thus helping to control cortical sensory processing.

Motaharinia’s research showed that VIP interneurons become significantly less responsive in the first week after stroke. The loss of responsiveness was most evident in highly active VIP neurons (i.e., those that were more responsive before the stroke), whereas less active neurons were minimally affected. In fact, a small fraction of VIP neurons that were minimally active before the stroke became more responsive afterwards. This suggests that a stroke could actually unmask sensory responses in some neurons and recruit them into the sensory circuit.

Though VIP responses generally improved two to five weeks after the stroke, their responsiveness remained less predictable than that observed before the stroke. This could have vital consequences for sensory perception.


benschager_2020.jpgBen Schager, MSc

“Determinants of brain region-specific age-related declines in microvascular density in the mouse brain”

(Supervisor: Craig Brown; Home department: Division of Medical Sciences)

Schager’s thesis focused on age-related brain blood vessel loss. Capillary loss in the brain is a natural occurrence as we age. Capillaries deliver nutrients to brain tissue, so it’s possible blood vessel loss is the reason cognitive functions degrade over time, causing a lot of the behaviours associated with aging, dementia and Alzheimer’s.

Until recently, however, it wasn’t clear if these losses occurred uniformly or in specific areas. In his research, Schager found that blood vessel losses are more likely to occur in certain brain regions: white matter, the hippocampus, and sensory-motor related grey matter. Regions including the visual cortex, amygdala, and insular cortex, however, showed little loss.

One of the reasons we lose vessels in the brain is due to routine clogs, or stalls, caused by cells and other debris in the blood. Most stalls clear within seconds, but about 30 per cent of clogged capillaries are pruned from the blood vessel network and never replaced. Schager found that the regions of the brain more prone to vessel loss are also those more prone to clogging