title: GABA-induced potentiation of neuronal excitability occurs during contiguous pairings with intracellular calcium elevation.
abstract: The temporal convergence of neuronal signals is commonly considered as a likely prerequisite for enhanced neuronal excitability underlying the induction of associative memories. Here we report that transmitter application on presynaptic terminals of the Hermissenda Type B photoreceptors, when paired with depolarization, results in a potentiation of the excitability of the B-cell which derives from an increase in input resistance across the B-cell soma membrane. Pressure microapplication of gamma-aminobutyric acid (GABA) (12.5 microM) on the terminal branches of the Hermissenda Type B photoreceptors results in the fast (less than 1 s) activation of an inward Cl- conductance, characterized by a decrease in neuronal membrane resistance and an accompanying hyperpolarization (3-6 mV) of the B-cell. A slower effect of GABA, characterized by a slight depolarization (2-4 mV) and increase in resistance was observed approximately 2 min after GABA application. Following bath application of the Cl- channel blocker picrotoxin (100 microM), this increase in resistance was observed within 20 s of GABA application, suggesting that it was normally masked by the faster Cl- conductance. The magnitude of the resistance increase in response to GABA was enhanced when the B-cell was held at depolarized membrane potentials (-40 to -20 mV), but was eliminated if Ca2+ was removed from the extracellular bath, or if the non-specific protein kinase inhibitor H7 (100 microM) was added to the extracellular bath. In a final experiment, GABA application was paired with a transient (10 s) depolarization of the B-cell (to -20 mV).(ABSTRACT TRUNCATED AT 250 WORDS)
authors.affiliation: Department of Psychology, Rutgers University, New Brunswick, NJ 08903.
authors.forename: L D
authors.initials: LD
authors.lastname: Matzel
authors.forename: D L
authors.initials: DL
authors.lastname: Alkon
mesh_terms: D019307:1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine; D000818:Animals; D003386:Brachyura; D002118:Calcium / Q000502:physiology*; D018118:Chloride Channels; D066298:In Vitro Techniques; D007473:Ion Channels / Q000502:physiology*; D007546:Isoquinolines / Q000494:pharmacology; D007700:Kinetics; D008564:Membrane Potentials / Q000187:drug effects; D008565:Membrane Proteins / Q000187:drug effects / Q000502:physiology*; D009474:Neurons / Q000187:drug effects / Q000502:physiology*; D010786:Photoreceptor Cells / Q000187:drug effects / Q000502:physiology*; D010852:Picrotoxin / Q000494:pharmacology; D010879:Piperazines / Q000494:pharmacology; D011493:Protein Kinase C / Q000037:antagonists & inhibitors; D013569:Synapses / Q000187:drug effects / Q000502:physiology; D013997:Time Factors; D005680:gamma-Aminobutyric Acid / Q000494:pharmacology*
chemical_list: D019307:1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine; D002118:Calcium; D018118:Chloride Channels; D007473:Ion Channels; D007546:Isoquinolines; D008565:Membrane Proteins; D010852:Picrotoxin; D010879:Piperazines; D011493:Protein Kinase C; D005680:gamma-Aminobutyric Acid