neuropeptide-y and 2-amino-4-phosphonobutyric-acid

Neuropeptide Y (NPY) has been shown to depress hyperexcitable activity that has been acutely induced in the normal rat brain. To test the hypothesis that NPY can also reduce excitability in the chronically epileptic human brain, we recorded intracellularly from dentate granule cells in hippocampal slices from patients with hippocampal seizure onset. NPY had a potent and long-lasting inhibitory action on perforant path-evoked excitatory responses. In comparison, the group 3 metabotropic glutamate receptor agonist L-2-amino-4-phosphonobutyric acid (L-AP4) evoked a mild and transient decrease. NPY-containing axons were found throughout the hippocampus, and in many epileptic patients were reorganized, particularly in the dentate molecular layer. NPY may therefore play a beneficial role in reducing granule cell excitability in chronically epileptic human tissue, and subsequently limit seizure severity.

Topics: 2-Amino-5-phosphonovalerate; Aminobutyrates; Animals; Axons; Dentate Gyrus; Electric Stimulation; Electroencephalography; Epilepsy, Temporal Lobe; Evoked Potentials; Excitatory Amino Acid Agonists; Excitatory Amino Acid Antagonists; Hippocampus; Humans; In Vitro Techniques; Neuropeptide Y; Perforant Pathway; Rats; Receptors, Metabotropic Glutamate; Synapses; Synaptic Transmission; Time Factors