Title

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.

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Apr 12th, 1:40 PM Apr 12th, 2:00 PM

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.