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K J Canning

Publications and source records attributed to K J Canning.

6 recordsLinked to original sources
PubMed2000

Excitability of rat dentate gyrus granule cells in vivo is controlled by tonic and evoked GABA(B) receptor-mediated inhibition.

Tonic or evoked gamma-aminobutyric acid(B) (GABA(B)) receptor-mediated modulation of dentate gyrus excitability was evaluated in vivo in urethane-anesthetized rats. Two stimuli at an interpulse interval (IPI) of 10-9000 ms were given to the medial perforant path. Population excitatory postsynaptic potentials (pEPSPs) and population spikes (PSs) were recorded in the dentate gyrus using a glass micropipette or a multichannel silicon probe. The GABA(B) receptor antagonist CGP35348, delivered intracerebroventricularly (i.c.v.) or locally, caused a significant increase in the PS amplitude evoked by the first pulse (PS1) without an increase in either the slope or current sink of the population EPSP evoked by the first pulse (pEPSP1). The average spontaneous firing rate of putative granule cells was also increased following i. c.v. CGP35348. The PS evoked by the second pulse (PS2) relative to PS1 (PS2/PS1) was consistently suppressed at IPIs from 30 to 70 ms, even when PS1 was matched before and after CGP35348. CGP35348 increased PS1 mainly by blocking tonic postsynaptic GABA(B) receptors and decreased PS2 at 30-70 ms IPI by blocking presynaptic GABA(B) autoreceptors. These data suggest that GABA(B) receptors are tonically active in the dentate gyrus in vivo.

Action Potentials↗
PubMed2000

Physiology of the entorhinal and perirhinal projections to the hippocampus studied by current source density analysis.

Evoked field potentials and current-source-density analysis were used to study the olfactory, entorhinal, and perirhinal projections to the hippocampus. In urethane-anesthetized rats, various structures were electrically stimulated, and evoked potentials were mapped using glass micropipettes or multichannel silicon probes. Stimulation of the olfactory bulb, lateral olfactory tract, piriform cortex, amygdala-entorhinal transition, lateral entorhinal cortex, or lateral perforant path (LPP) evoked an outer molecular layer sink (inferred distal dendritic excitation) in the dentate gyrus, with progressively decreasing onset latency. Medial perforant path (MPP) stimulation evoked a middle molecular layer sink (mid-dendritic excitation) in the dentate gyrus. LPP and MPP were also inferred to monosynaptically excite the distal dendrites of CA3, often resulting in a population spike in CA3. CA3 spiking, in turn, was often followed by excitation at the inner molecular layer of the dentate gyrus. LPP and MPP evoked distal dendritic sinks but no population spikes in CA1. Stimulation of the perirhinal cortex activated a sink in the subiculum/CA1 border without activating the dentate gyrus. In addition, reverberatory activity through a hippocampal-entorhinal-hippocampal pathway may be activated by MPP or CA3 stimulation. It is suggested that the parallel projections of the entorhinal and perirhinal inputs to the distal dendrites of hippocampal principal neurons enhance local and distributed processing as characterized by CA3 to dentate gyrus feedback, and hippocampal-entorhinal reverberation.

Afferent Pathways↗
PubMed1998

Functional interconnections between CA3 and the dentate gyrus revealed by current source density analysis.

The physiological interactions between the dentate gyrus (DG) and CA3 were studied in urethane-anesthetized rats by using field potential recording and current source density (CSD) analysis. Stimulation of CA3b resulted in a short-latency (<2.5-ms onset latency) antidromic population spike in both the DG and CA3c. An excitation (current sink) at the middle molecular layer (MML) was observed at 3-ms latency, possibly mediated by the backfiring of perforant path fibers that projected to both DG and CA3. CA3 stimulation also resulted in a sink at the dendritic layers of CA3c, which was likely mediated by excitatory CA3 recurrent collaterals. It was inferred that the DG was excited at the inner molecular layer (IML) after stimulation near the CA3b/CA3c border. This IML excitation (sink) probably resulted from orthodromic CA3 or hilar projections to the IML and not from mossy fiber backfiring. The IML and the CA3c dendritic sinks were blocked by an intracerebroventricular injection of a non-N-methyl-D-aspartate receptor antagonist, 6-cyano-7-nitroquinoxaline-2, 3-dione, but not by a gamma-aminobutyric acid type A (GABA(A)) receptor antagonist, bicuculline. CA3b stimulation evoked population spike bursts (3-7-ms latency) in both DG and CA3c when GABA(A) inhibition was suppressed by bicuculline, thus confirming that the excitatory afferents project from CA3b to DG and CA3c. A CA3 conditioning stimulus pulse given 30-200 ms before a perforant-path test pulse increased the amplitude of the perforant-path-evoked DG population spike (as compared with the test response without conditioning). After a moderate-intensity stimulation of CA3, a late (<20-ms latency) excitation of the MML of the DG was found. The late DG excitation was blocked by procaine injection at the medial perforant path, suggesting its origin from the medial entorhinal cortex. In conclusion, rich interactions between CA3 and other hippocampal structures were studied quantitatively by CSD analysis in vivo. We infer that CA3 provides an early excitatory feedback path to DG through recurrent collaterals or hilar interneurons and a late feedback through the medial entorhinal cortex.

Animals↗
PubMed1997

Lateral entorhinal, perirhinal, and amygdala-entorhinal transition projections to hippocampal CA1 and dentate gyrus in the rat: a current source density study.

In urethane-anesthetized rats, cortical regions which provide distal dendritic excitation of the dentate gyrus and CA1 of the dorsal hippocampus were studied using current source density analysis. Electrical stimulation of the lateral perforant path (LPP) in the lateral angular bundle, lateral entorhinal cortex (LEC), and amygdala-entorhinal transition (TR) resulted in a current sink in the outer molecular layer of the dentate gyrus accompanied by proximal sources; this sink-source pattern is distinctly different from the source-sink-source pattern evoked by medial perforant path stimulation. The progressive decrease of the sink latency following stimulation of the TR, LEC, and LPP (11.6, 7.8, and 3.6 ms, respectively, at the dorsal blade of the dentate gyrus) suggests a possible sequence of orthodromic activation of these structures. Stimulation of the LEC or TR (collectively termed cortical stimulation) differed from LPP (fiber) stimulation. A low threshold and small chronaxie were characteristic of fiber rather than cortical stimulation. In addition, cortical stimulation, possibly through excitation of intracortical circuits, evoked larger paired-pulse facilitation of the excitatory postsynaptic currents in dentate gyrus and more symmetric excitation of the dorsal and ventral blades of the dentate gyrus as compared to fiber stimulation. Stimulation of the perirhinal cortex (PRh) evoked a short-latency sink in the outer molecular layer of the dentate gyrus with no paired-pulse facilitation, similar to fiber stimulation. A distal dendritic CA1 sink was observed after LPP but not after PRh stimulation. An ibotenic acid injection that lesioned almost all the cells in the perirhinal cortex confirmed the hypothesis that PRh stimulation activated fibers of passage, perhaps in the rostral ventrolateral angular bundle. We conclude that the PRh does not provide a significant excitatory input to the DG or CA1. We have found distinct dendritic excitation of the dentate gyrus by the lateral versus medial perforant paths, and by fiber (LPP and MPP) versus cortical (LEC and TR) stimulation. We also emphasize that processing in the entorhinal cortex is important in the temporal shaping of the signals afferent to the hippocampus.

Amygdala↗
PubMed1995

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

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)

Animals↗