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Mild traumatic brain injury affects cholecystokinin interneuron physiology Adriana Hernandez Vasquez
- Format:
- Book
- Thesis/Dissertation
- Author/Creator:
- Hernandez Vasquez, Adriana, author.
- Language:
- English
- Subjects (All):
- Neurosciences.
- Cellular biology.
- Biochemistry.
- Physiological psychology.
- Cognitive psychology.
- 0317.
- 0379.
- 0487.
- 0633.
- 0989.
- Local Subjects:
- Neurosciences.
- Cellular biology.
- Biochemistry.
- Physiological psychology.
- Cognitive psychology.
- 0317.
- 0379.
- 0487.
- 0633.
- 0989.
- Genre:
- Academic theses
- Physical Description:
- 1 online resource (84 pages)
- Contained In:
- Dissertations Abstracts International 87-12B
- Place of Publication:
- Ann Arbor : ProQuest Dissertations and Theses, 2026
- Language Note:
- English
- Summary:
- Traumatic brain injury (TBI) affects nearly two million people a year and is a leading cause of death and disability. An estimated 70-90% of all TBIs are classified as mild (mTBI), yet mTBIs are not benign. TBI survivors often report cognitive impairment, such as deficits in learning and memory, that can last long after the initial injury. The hippocampus, a brain structure critically involved in learning and memory, is particularly vulnerable to TBI. Area CA1, the main output region of the hippocampus, has shown augmented inhibition after mTBI, as demonstrated by decreased stimulus-evoked action potential (AP) firing from pyramidal neurons (PNs). The injury-induced alteration to area CA1 created a network excitatory-inhibitory (E/I) imbalance, resulting in a net decline in hippocampal network activation and output. It is well known, however, that local GABAergic interneurons, like cholecystokinin basket cells (CCK BCs), modulate the firing rate of CA1 PNs through perisomatic synapses. Yet the effects of injury on CCK BCs remains to be investigated. This work aimed to address this gap in knowledge using whole-cell patch clamp techniques to investigate how mTBI affects CCK BC synaptic plasticity and physiology in a mouse model of TBI. Our results demonstrate that CCK IN synaptic plasticity is unchanged by lateral fluid percussion injury (LFPI), as shown by the ability to transiently suppress CCK IN GABAergic signaling with a strong depolarization in both the injured and uninjured groups, a process known as depolarization induced suppression of inhibition. Further analysis of CCK IN physiology revealed that CCK INs are less excitable after injury, characterized by decreased AP threshold and firing rate, while showing a decrease in frequency of miniature inhibitory current. This work provides insight into the contribution of CCK INs in hippocampal circuit dysfunction after mTBI and further our understanding of the precise mechanisms by which injury drives learning and memory deficits to aid in the development of therapies for TBI survivors
- Notes:
- Source: Dissertations Abstracts International, Volume: 87-12, Section: B.
- Advisors: Cohen, Akiva S. Committee members: Goldberg, Ethan; Ma, Minghong; Chanaday, Natali L.; Cullen, Kacy
- Ph.D. University of Pennsylvania 2026
- Vendor supplied data
- Local Notes:
- School code: 0175
- ISBN:
- 9798247979135
- Access Restriction:
- Restricted for use by site license
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