Anatomy, physiology, and synaptic responses of rat layer V auditory cortical cells and effects of intracellular GABA(A) blockade.
The varied extracortical targets of layer V make it an important site for cortical processing and output, which may be regulated by differences in the pyramidal neurons found there. Two populations of projection neurons, regular spiking (RS) and intrinsic bursting (IB), have been identified in layer V of some sensory cortices, and differences in their inhibitory inputs have been indirectly demonstrated. In this report, IB and RS cells were identified in rat auditory cortical slices, and differences in thalamocortical inhibition reaching RS and IB cells were demonstrated directly using intracellular GABA(A) blockers. Thalamocortical synaptic input to RS cells was always a combination of excitation and both GABA(A) and GABA(B) inhibition. Stimulation seldom triggered a suprathreshold response. IB cell synaptic responses were mostly excitatory, and stimulation usually triggered action potentials. This apparent difference was confirmed directly using intracellular chloride channel blockers. Before intracellular diffusion, synaptic responses were stable and similar to control conditions. Subsequently, GABA(A) was blocked, revealing a cell's total excitatory input. On GABA(A) blockade, RS cells responded to synaptic stimulation with large, suprathreshold excitatory events, indicating that excitation, while always present in these cells, is masked by GABA(A). In IB cells that had visible GABA(A) input, it often masked an excitatory postsynaptic potential (EPSP) that could lead to additional suprathreshold events. These findings indicate that IB cells receive less GABA(A)-mediated inhibitory input and are able to spike or burst in response to thalamocortical synaptic stimulation far more readily than RS cells. Such differences may have implications for the influence each cell type exerts on its postsynaptic targets.
Hefti
B J
BJ
Department of Anatomy and Neuroscience Training Program, University of Wisconsin Medical School, Madison, Wisconsin 53706, USA.
Smith
P H
PH
D000200:Action Potentials / Q000187:drug effects; D000818:Animals; D001303:Auditory Cortex / Q000166:cytology / Q000187:drug effects* / Q000502:physiology*; D001710:Biotin / Q000031:analogs & derivatives / Q000493:pharmacokinetics; D047250:Calixarenes; D002614:Chelating Agents / Q000494:pharmacology; D018118:Chloride Channels / Q000037:antagonists & inhibitors; D019706:Excitatory Postsynaptic Potentials / Q000187:drug effects; D058787:GABA-A Receptor Antagonists; D058788:GABA-B Receptor Antagonists; D066298:In Vitro Techniques; D010636:Phenols / Q000494:pharmacology; D051381:Rats; D020318:Rats, Long-Evans; D011930:Reaction Time; D013569:Synapses / Q000502:physiology*; D013788:Thalamus / Q000502:physiology
D002614:Chelating Agents; D018118:Chloride Channels; D058787:GABA-A Receptor Antagonists; D058788:GABA-B Receptor Antagonists; D010636:Phenols; C121325:calix(4)arene; C070614:neurobiotin; D047250:Calixarenes; D001710:Biotin