ABSTRACT
We studied the ontogeny of inhibitory and excitatory processes in the rat dentate gyrus by examining paired-pulse plasticity in the hippocampal slice preparation. The mature dentate gyrus produces characteristic paired-pulse responses across a wide range of interpulse intervals (IPI). Paired-pulse effects on population excitatory postsynaptic potential (EPSP) slope and population spike (PS) amplitude were analyzed at postnatal day 6 (PN6), PN7/8, PN9/10, PN15/16, and PN > 60. The synaptic paired-pulse profile (10-5,000 ms IPI) matured by PN7/8. The triphasic pattern of short-latency depression, a relative facilitation at intermediate intervals, and long-latency depression was present at all ages tested. Paired-pulse effects on granule cell discharge indicated the presence of weak short-latency (20 ms IPI) inhibition at PN6, the earliest day that a population spike could be evoked. By PN7/8, short-latency inhibition was statistically equivalent to the mature dentate gyrus. Long-latency (500-2,000 ms IPI) PS inhibition was present, and equal to the mature dentate gyrus by PN6. The most consistent difference between the mature and developing dentate gyrus occurred at intermediate IPIs (40-120 ms) where spike facilitation was significantly depressed in the development groups. The studies indicate that short-term plasticity matures rapidly in the dentate gyrus and suggest that the inhibitory circuitry can function at a surprisingly early age.
Subject(s)
Hippocampus/growth & development , Neuronal Plasticity/physiology , Action Potentials , Animals , Rats , Reaction Time , Synapses/physiologyABSTRACT
The effects of spermine, an endogenous polyamine, were examined in area CA1 of the rat hippocampal slice preparation. Spermine, at low millimolar concentrations, rapidly and potently depressed NMDA and K/AMPA-mediated population EPSPs, and GABA-mediated monosynaptic population IPSPs. These effects contrast with its well-known potentiation of NMDA currents at lower concentrations. Our results raise the possibility that the large intracellular stores of spermine that are released after various neural insults could act as an endogenous neuroprotective mechanism by limiting excessive calcium entry.
Subject(s)
Excitatory Amino Acid Antagonists/pharmacology , Hippocampus/physiology , Spermine/pharmacology , Synapses/physiology , Synaptic Transmission/drug effects , Animals , Calcium Channels/drug effects , Evoked Potentials/drug effects , GABA-A Receptor Antagonists , Hippocampus/drug effects , In Vitro Techniques , Rats , Receptors, AMPA/antagonists & inhibitors , Receptors, N-Methyl-D-Aspartate/antagonists & inhibitors , Synapses/drug effectsABSTRACT
We examined the effects of GABAB receptor activation in the dentate gyrus of hippocampal slices prepared from 6-8-day-old rat pup. Baclofen (0.25-1.0 microM), a GABAB agonist, rapidly and potently disinhibited the developing dentate, similar to its effect in the mature organism. CGP 35348, a GABAB antagonist, quickly reversed the baclofen-induced disinhibition. However, GABAB antagonists did not reverse long-latency (500-1000 ms IPI) paired-pulse depression, suggesting that it is not caused by a late GABAB-mediated IPSP. GABAB-mediated disinhibition of the dentate gyrus can occur by postnatal day 6, providing a powerful mechanism for altering excitability in the developing hippocampus.
Subject(s)
Hippocampus/growth & development , Hippocampus/metabolism , Receptors, GABA-B/metabolism , Animals , Baclofen/analogs & derivatives , Baclofen/pharmacology , Electric Stimulation , Evoked Potentials/drug effects , GABA-A Receptor Antagonists , GABA-B Receptor Antagonists , In Vitro Techniques , Organophosphorus Compounds/pharmacology , Rats , Receptors, GABA-A/drug effects , Receptors, GABA-A/physiologyABSTRACT
This article is part of a study on cortical microcircuitry in which flash evoked potentials (FEPs) were recorded from the anesthetized rat visual cortex. The FEPs were subjected to current source density analysis (CSD). One of the limitations of the CSD method is the need for recording sites outside the sampling volume, in order to obtain a full description of the CSD distribution. This problem is acute in the neocortex where a tissue/fluid boundary exists. A simple solution is provided based on the fact that the field potentials decay minimally under the conditions of these experiments. In the neocortex the most superficial recording site and the deepest recording site are used to provide the extra recording sites necessary to obtain a full description of the CSD distribution. This approach when tested by summing the current sinks and sources across all layers of cortex produces excellent results, with significant reduction of the residual sinks and sources.
