Entorhinal inputs to hippocampal CA1 and dentate gyrus in the rat: a current-source-density study

Abstract

1. Laminar profiles of the average evoked potentials and current-source-density analysis were used to study the input provided by the medial perforant path (PP) to the hippocampus in the urethan-anesthetized rat. 2. Stimulation of the PP activated an early latency sink in the middle molecular layer of the dentate gyrus (DG) and in the stratum lacunosum-moleculare in CA1. The DG current sink was generated by excitatory synaptic currents activated by the PP on dentate granule cells. In the normal rat, the peak current sink in the DG was typically five times greater than that of CA1. However, the CA1 sink could be distinguished from the DG sink in several ways: 1) it peaked when the DG sink was subsiding; 2) it showed paired-pulse facilitation, whereas the DG sink did not; and 3) in rats in which the DG was lesioned by local colchicine injection, the DG sink was reduced much more than the CA1 sink. 3. The PP afferents to CA1 required a slightly higher stimulus threshold (> 100 microA) for activation than those projecting to the DG granule cells (< 30 microA). The onset latency of the early CA1 sink (2.5 +/- 0.2 ms, mean +/- SE) was also slightly longer than that of the DG sink (1.7 +/- 0.1 ms), suggesting that the axons of entorhinal layer III cells that project to CA1 have a slightly lower conduction velocity than the axons of the layer II cells that project to the DG. 4. The short-latency current sink activated by the PP in the distal dendritic layers of CA1 was likely provided by excitatory currents at the distal apical dendrites of CA1 pyramidal cells. The accompanying current source was mainly confined to stratum radiatum and appeared not to involve the cell body layer. Thus the electrotonic current spread may not be effective enough to depolarize the cell body or axon hillock. Contribution of interneurons to the above source-sink profile is possible, with the provision that these interneurons must have dendritic processes that span strata radiatum and lacunosum moleculare. 5. Extracellular field recordings provided no evidence that PP evoked a short-latency (< 9 ms) CA1-generated population spike, even with the use of micropipettes filled with mM bicuculline. Similarly, unit recordings in CA1 revealed only long-latency (9-17 ms) unit firing after PP stimulation, corresponding to a late, di/trisynaptic excitation of CA1 via the Schaffer collaterals.(ABSTRACT TRUNCATED AT 400 WORDS)

Interaction of nucleus reuniens and entorhinal cortex projections in hippocampal field CA1 of the rat

“…However, at IPI 25 ms, EC-induced PPF was hardly noticeable (PPF 1.1 ± 0.2, n=4). These findings are in agreement with those reported in previous studies (Sloviter 1991;Leung et al 1995;Dolleman-van der Weel et al 1997;Eleore et al 2011;Ito and Schuman 2012;Gonzalez et al 2016). …”

Loss of dendritic inhibition in the hippocampus after repeated early-life hyperthermic seizures in rats

“…MPP stimulation excited the distal apical dendrites of CA1 pyramidal cells. CSD analysis revealed a current sink in the SLM of CA1, with an accompanying current source in CA1 stratum radiatum (Leung et al, 1995;Wu and Leung, 2003).…”

“…However, at 8-25 ms latency, a source in SLM (# in Fig. 6B) developed in correspondence to a stratum radiatum excitatory sink and a PS in CA1, likely mediated polysynaptically through CA3 (Leung et al, 1995). CGP35348 also increased, as compared to baseline, a mid-dendritic excitatory sink and PS in the dentate gyrus (DG PS in Fig.…”

“…For recordings made before and after icv CGP35348, the SLM sink was assessed at 4.5-7.5 ms after a MPP stimulus (fixed for each rat), relative to the baseline at 0.1 ms immediately before the MPP stimulus. The latter procedure is necessary for excluding the polysynaptic activity in CA1 induced by icv CGP35348 (below), and it measured the putatively monosynaptic SLM sink before its peak during no-drug condition (Leung et al, 1995). In all recordings, the CA1 pyramidal cell layer was assumed to be the location of the maximal PS sink, and the location of the distal source associated with the CA3-evoked pEPSP corresponded to the location of the maximal excitatory sink evoked by the MPP stimulus in SLM.…”

“…To obtain input-output data CA1 test pulse responses were recorded at various stimulus intensities ranging from 30 to 500 A, with a fixed interpulse interval (IPI) of 50 or 200 ms for paired-pulse stimuli. IPI profiles were created by varying the delay between pulses from 20 to 400 ms while keeping the intensity of stimuli fixed; CA3 stimulation was adjusted to evoke ∼70% of the maximal population spike (PS) in CA1, and MPP stimulation was adjusted to evoke ∼70% of the maximal PS in the dentate gyrus or near maximal MPP-evoked distal dendritic sinks in CA1 (Leung et al, 1995). The IPI was varied to help differentiate between an early ionotropic GABA A receptormediated inhibition at <100 ms (Steffensen and Henriksen, 1991) and a metabotropic GABA B receptor-mediated inhibition at >100 ms (Tsai and Leung, 2006;Olpe et al, 1993;Isaacson et al, 1993).…”