Oral Presentations - Session 2F: UC 333
Cholinergic neuromodulation of parvalbumin interneurons during hippocampal gamma oscillations and pilocarpine-induced seizures
Presentation Type
Presentation
Faculty Mentor’s Full Name
J. Josh Lawrence
Faculty Mentor’s Department
Center for Structural and Functional Neuroscience
Abstract / Artist's Statement
Epilepsy, one of the most common neurological diseases, is widely studied in the medical and scientific fields. The pilocarpine model of induced epilepsy has become a standard for studying seizures in a laboratory setting, allowing further investigation into specific mechanisms underlying seizure activity. Parvalbumin-positive (PV+) interneurons, a specialized class of inhibitory cells, are implicated in pilocarpine-induced seizures. However, the underlying mechanisms by which PV+ cells contribute to seizure generation are unknown.
The precise balance of the inhibitory and excitatory neuronal networks is critical to normal brain function. Imbalances between inhibitory PV+ cells and excitatory glutamatergic networks could contribute to seizure generation and other pathological states. Here, we test the hypothesis that pilocarpine, a nonselective muscarinic receptor agonist, activates PV+ interneurons and renders hippocampal circuits vulnerable to seizures. Our laboratory has previously demonstrated that the elimination of M1 muscarinic acetylcholine receptors (mAChRs) from PV+ cells results in a loss of cholinergic modulation of PV+ cells, learning deficits, and seizure protection. .Using pilocarpine application to hippocampal slices, I will determine whether pilocarpine activates PV+ cells through glutamatergic circuits or by direct excitation of M1 mAChRs on PV+ cells. These studies will lead to a more comprehensive understanding of the processes underlying epileptiform activity.
Cholinergic neuromodulation of parvalbumin interneurons during hippocampal gamma oscillations and pilocarpine-induced seizures
UC 333
Epilepsy, one of the most common neurological diseases, is widely studied in the medical and scientific fields. The pilocarpine model of induced epilepsy has become a standard for studying seizures in a laboratory setting, allowing further investigation into specific mechanisms underlying seizure activity. Parvalbumin-positive (PV+) interneurons, a specialized class of inhibitory cells, are implicated in pilocarpine-induced seizures. However, the underlying mechanisms by which PV+ cells contribute to seizure generation are unknown.
The precise balance of the inhibitory and excitatory neuronal networks is critical to normal brain function. Imbalances between inhibitory PV+ cells and excitatory glutamatergic networks could contribute to seizure generation and other pathological states. Here, we test the hypothesis that pilocarpine, a nonselective muscarinic receptor agonist, activates PV+ interneurons and renders hippocampal circuits vulnerable to seizures. Our laboratory has previously demonstrated that the elimination of M1 muscarinic acetylcholine receptors (mAChRs) from PV+ cells results in a loss of cholinergic modulation of PV+ cells, learning deficits, and seizure protection. .Using pilocarpine application to hippocampal slices, I will determine whether pilocarpine activates PV+ cells through glutamatergic circuits or by direct excitation of M1 mAChRs on PV+ cells. These studies will lead to a more comprehensive understanding of the processes underlying epileptiform activity.