Inhibitory postsynaptic potentials evoked in thalamic neurons by stimulation of the reticularis nucleus evoke slow spikes in isolated rat brain slices--I.
In isolated slices of rat thalamus, inhibitory postsynaptic potentials evoked by electrical stimulation of the nucleus reticularis, were recorded intracellularly in relay neurons in the anterior part of the thalamus. These inhibitory postsynaptic potentials were found to have reversal potentials close to the resting potential of the recorded cell, to reduce neuronal excitability and to be sensitive to electrophoretic application of the GABA antagonists bicuculline and picrotoxin, indicating that they were GABA-activated, chloride mediated events. Voltage sensitive responses of relay neurons evoked by current injection and by inhibitory postsynaptic potentials were then compared. Hyperpolarizing current pulses and hyperpolarizing inhibitory postsynaptic potential trains elicited from membrane potentials positive to -70 mV resulted in rebound slow spike activation on repolarization. Depolarizing current pulses and depolarizing inhibitory postsynaptic potential trains evoked slow spikes when elicited from membrane potentials negative to -60 mV. There was, however, one major difference, the slow spikes evoked by inhibitory postsynaptic potentials were always delayed to the end of the train. Reversal potentials of evoked inhibitory postsynaptic potentials were found to depend on the potential at which the membrane was held immediately before the inhibitory postsynaptic potential was evoked, indicating that passive distribution of chloride ions contributes to their equilibrium potential. Evoked inhibitory postsynaptic potentials consisted of at least two components with different reversal potentials although current voltage relations indicated that similar decreases in membrane resistance were associated with both components and that they shifted approximately in parallel when inhibitory postsynaptic potentials were evoked from different holding potentials. Trains of GABA-mediated inhibitory postsynaptic potentials, similar to those recorded during spindling, will evoke slow spikes in almost all thalamic relay neurons irrespective of other synaptic inputs. This response will effectively synchronize burst firing in all cells receiving the same inhibitory input.
Thomson
A M
AM
Department of Physiology, University College, Cardiff, U.K.
D000818:Animals; D001640:Bicuculline / Q000494:pharmacology; D002118:Calcium / Q000378:metabolism; D004558:Electric Stimulation; D004594:Electrophysiology; D005071:Evoked Potentials; D005260:Female; D009474:Neurons / Q000187:drug effects / Q000502:physiology*; D051381:Rats; D012154:Reticular Formation / Q000502:physiology*; D013788:Thalamus / Q000166:cytology* / Q000187:drug effects / Q000502:physiology; D005680:gamma-Aminobutyric Acid / Q000494:pharmacology
D005680:gamma-Aminobutyric Acid; D002118:Calcium; D001640:Bicuculline