Analysis of synaptic plasticity events concerning the endocannabinoid system in the young adolescent (YA) rat media perforant pathway (MPP) following repetitive mild traumatic brain injury (r-mTBI)
| dc.contributor.author | Zejnulahovic, Emir | |
| dc.date.accessioned | 2026-02-19T23:55:00Z | |
| dc.date.available | 2026-02-19T23:55:00Z | |
| dc.date.issued | 2025 | |
| dc.description.abstract | Traumatic brain injury (TBI) is a widespread health issue, with mild TBIs (mTBI) making up to 85% of cases, often underdiagnosed due to subtle symptoms. Young adolescents are most at risk for repetitive mTBI (r-mTBI), which compounds mTBI symptoms and outcomes. These injuries can impair synaptic plasticity, including short-term potentiation (STP) and long-term potentiation (LTP), both crucial for cognition. Acute neuronal damage and chronic apoptosis underlie these deficits, especially in the dentate gyrus (DG) and its medial/lateral perforant pathways (MPP/LPP) substructures, whose electrical inputs are essential for adult neurogenesis. Cannabinoid one receptors (CB1Rs) and Transient Receptor Vanilloid Protein 1 (TRPV1), part of the endocannabinoid system (EC), regulate synaptic plasticity in MPP/LPP due to the high concentrations each receptor has in the DG. Altered EC signaling in mTBI models contributes to excitotoxicity. Pharmacological tools for targeting CB1Rs (AM251) and TRPV1 (AMG9810) reveal the receptor’s effects indirectly before and after r-mTBI. 53 Sprague Dawley rats were used for recordings, with ninety-nine slices used. Animals were split across six groups (Sham/r-mTBI controls, plus corresponding drug groups). Sham/r-mTBI controls only showed differences in LTP induction, with mechanistic properties of the synapse appearing unchanged via paired pulse and short-term potentiation (STP) recordings. Both AMG9180 and AM251 restored LTP deficits seen between Sham/r-mTBI controls, while TRPV1 also significantly enhanced STP levels, and removed paired-pulse facilitation effects seen in Shams. This suggests that both receptors can be pharmacologically manipulated to aid in synaptic plasticity deficits following r-mTBI, as well as suggesting that both receptors are downregulated following r-mTBI. | |
| dc.description.reviewstatus | Unreviewed | |
| dc.description.scholarlevel | Undergraduate | |
| dc.identifier.uri | https://hdl.handle.net/1828/23328 | |
| dc.language.iso | en | |
| dc.subject.department | Department of Biology | |
| dc.title | Analysis of synaptic plasticity events concerning the endocannabinoid system in the young adolescent (YA) rat media perforant pathway (MPP) following repetitive mild traumatic brain injury (r-mTBI) | |
| dc.type | Honours thesis |