Large, deep layer pyramid-pyramid single axon EPSPs in slices of rat motor cortex display paired pulse and frequency-dependent depression, mediated presynaptically and self-facilitation, mediated postsynaptically

1993 ◽  
Vol 70 (6) ◽  
pp. 2354-2369 ◽  
Author(s):  
A. M. Thomson ◽  
J. Deuchars ◽  
D. C. West
Keyword(s):  
Deep Layer ◽  
Short Interval ◽  
Pyramidal Cells ◽  
Postsynaptic Membrane ◽  
Paired Pulse ◽  
Paired Pulse Facilitation ◽  
Wide Range ◽  
Mean Width ◽  
The Mean ◽  
Paired Pulse Depression

1. In slices of rat sensorimotor cortex, dual intracellular recordings were obtained from 1,952 pairs of deep layer pyramidal neurons. Where action potentials in one neurone elicited excitatory postsynaptic potentials (EPSPs, n = 56) in the other, responses to different presynaptic firing rates and patterns and at different postsynaptic membrane potentials were recorded and on some occasions both neurons were filled with biocytin. 2. Slices were fixed, sectioned again at 60 microns, and incubated with Avidin horseradish peroxidase (HRP), which was then visualized using the 3,3'-diaminobenzidine tetrahydrochloride (DAB) method. All neurones reported here that were identified histologically were pyramidal cells with their somata in the deep layers (V and VI). 3. One in 70 of the tests performed revealed a synaptic connection, 25 of which were studied in detail. Mean EPSP amplitude was 1.67 +/- 1.66 (SD) mV, with some single sweep events as large as 9 mV. For some of the smaller EPSPs the amplitude distributions contained a clear peak around 0 mV, the coefficient of variation (CV) was large, and paired pulse facilitation was apparent. EPSPs with large average amplitudes displayed no apparent failures of transmission, EPSP amplitudes were fairly evenly distributed around the mean, CVs were small, and paired pulse depression was apparent in 2.5 mM extracellular Ca2+. When single sweeps were selected according to the size of the first EPSP, large second EPSPs were found to follow small first EPSPs and small second EPSPs to follow large first EPSPs. Paired pulse effects appeared, in the majority of tests, to be due to a change in presynaptic release probability. 4. Two EPSPs were recorded in three different extracellular Ca2+ concentrations. In 1 mM Ca2+, the first EPSP of a short interval pair was small and paired pulse facilitation was apparent. In 5 mM Ca2+, first EPSPs were between 2.5 and 4 times larger than in 1 mM Ca2+ and paired pulse depression was apparent. In all Ca2+ concentrations however, averaged third and fourth EPSPs of brief bursts were of similar amplitudes and smaller than second EPSPs. If presynaptic inhibition does contribute to paired pulse effects here, it is not overcome by a combination of raised extracellular Ca2+ and repetitive presynaptic firing. 5. These EPSPs displayed a wide range of time courses. The mean 10-90% rise time was 2.49 +/- 1.08 ms, the mean width at half amplitude was 15.39 +/- 5.42 ms (n = 22), and the mean EPSP latency was 1.59 +/- 0.68 ms (n = 18). (ABSTRACT TRUNCATED AT 400 WORDS)

Properties of Unitary IPSCs in Hippocampal Pyramidal Cells Originating From Different Types of Interneurons in Young Rats

1997 ◽  
Vol 77 (4) ◽  
pp. 1939-1949 ◽  
Author(s):  
Mohamed Ouardouz ◽  
Jean-Claude Lacaille
Keyword(s):  
Reversal Potential ◽  
Pyramidal Cells ◽  
Mean Amplitude ◽  
Paired Pulse ◽  
Young Rats ◽  
Different Types ◽  
The Mean ◽  
Paired Pulse Depression ◽  
Types Of Interneurons ◽  
Stimulation Of

Ouardouz, Mohamed and Jean-Claude Lacaille. Properties of unitary IPSCs in hippocampal pyramidal cells originating from different types of interneurons in young rats. J. Neurophysiol. 77: 1939–1949, 1997. Whole cell recordings were used in hippocampal slices of young rats to examine unitary inhibitory postsynaptic currents (uIPSCs) evoked in CA1 pyramidal cells at room temperature. Loose cell-attached stimulation was applied to activate single interneurons of different subtypes located in stratum oriens (OR), near stratum pyramidale (PYR), and at the border of stratum radiatum and lacunosum-moleculare (LM). uIPSCs evoked by stimulation of PYR and OR interneurons had similar onset latency, rise time, peak amplitude, and decay. In contrast, uIPSCs elicited by activation of LM interneurons were significantly smaller in amplitude and had a slower time course. The mean reversal potential of uIPSCs was −53.1 ± 2.1 (SE) mV during recordings with intracellular solution containing potassium gluconate. With the use of recording solution containing the potassium channel blocker cesium, the reversal potential of uIPSCs was not significantly different (−58.5 ± 2.6 mV), suggesting that these synaptic currents were not mediated by potassium conductances. Bath application of the γ-aminobutyric acid-A (GABAA) receptor antagonist bicuculline (25 μM) reversibly blocked uIPSCs evoked by stimulation of all interneuron subtypes. In bicuculline, the mean peak amplitude of uIPSCs recorded with potassium gluconate was reduced to 3.5 ± 4.4% of control ( n = 7). Similarly, with cesium methanesulfonate, the mean amplitude in bicuculline was 2.9 ± 3.1% of control ( n = 13). Application of the GABAB receptor antagonist CGP 55845A (5 μM) resulted in a significant and reversible increase in the mean amplitude of uIPSCs recorded with cesium-containing intracellular solution. Thus uIPSCs from all cell types appeared under tonic presynaptic inhibition by GABAB receptors. Paired stimulation of individual interneurons at 100- to 200-ms intervals did not result in paired pulse depression of uIPSCs. For individual responses, a significant negative correlation was observed between the amplitude of the first and second uIPSCs. A significant paired pulse facilitation (154.0 ± 8.0%) was observed when the first uIPSC was smaller than the mean of all first uIPSCs. A small, but not significant, paired pulse depression (90.8 ± 4.0%) was found when the first uIPSC was larger than the mean of all first uIPSCs. Our results indicate that these different subtypes of hippocampal interneurons generate Cl−-mediated GABAA uIPSCs. uIPSCs originating from different types of interneurons may have heterogeneous properties and may be subject to tonic presynaptic inhibition via heterosynaptic GABAB receptors. These results suggest a specialization of function for inhibitory interneurons and point to complex presynaptic modulation of interneuron function.

scholarly journals Frequency‐dependent shift from paired‐pulse facilitation to paired‐pulse depression at unitary CA3‐CA3 synapses in the rat hippocampus

2002 ◽  
Vol 544 (2) ◽  
pp. 469-476 ◽  
Author(s):  
Chiara Saviane ◽  
Leonid P. Savtchenko ◽  
Giacomo Raffaelli ◽  
Leon L. Voronin ◽  
Enrico Cherubini
Keyword(s):  
Rat Hippocampus ◽  
Frequency Dependent ◽  
Paired Pulse ◽  
Paired Pulse Facilitation ◽  
Paired Pulse Depression

scholarly journals Properties of the primary somatosensory cortex projection to the primary motor cortex in the mouse

2015 ◽  
Vol 113 (7) ◽  
pp. 2400-2407 ◽  
Author(s):  
Iraklis Petrof ◽  
Angela N. Viaene ◽  
S. Murray Sherman
Keyword(s):  
Primary Motor Cortex ◽  
Metabotropic Glutamate Receptor ◽  
Pyramidal Cells ◽  
Receptor Activation ◽  
Slice Preparation ◽  
Paired Pulse ◽  
Metabotropic Glutamate ◽  
Driver Pathway ◽  
Synaptic Boutons ◽  
Paired Pulse Depression

The primary somatosensory (S1) and primary motor (M1) cortices are reciprocally connected, and their interaction has long been hypothesized to contribute to coordinated motor output. Very little is known, however, about the nature and synaptic properties of the S1 input to M1. Here we wanted to take advantage of a previously developed sensorimotor slice preparation that preserves much of the S1-to-M1 connectivity (Rocco MM, Brumberg JC. J Neurosci Methods 162: 139–147, 2007), as well as available optogenetic methodologies, in order to investigate the synaptic profile of this projection. Our data show that S1 input to pyramidal cells of M1 is highly homogeneous, possesses many features of a “driver” pathway, such as paired-pulse depression and lack of metabotropic glutamate receptor activation, and is mediated through axons that terminate in both small and large synaptic boutons. Our data suggest that S1 provides M1 with afferents that possess synaptic and anatomical characteristics ideal for the delivery of strong inputs that can “drive” postsynaptic M1 cells, thereby potentially affecting their output.

Paired-pulse facilitation of IPSCs in slices of immature and mature mouse somatosensory neocortex

1995 ◽  
Vol 73 (6) ◽  
pp. 2591-2595 ◽  
Author(s):  
I. A. Fleidervish ◽  
M. J. Gutnick
Keyword(s):  
Age Groups ◽  
Equilibrium Potential ◽  
Patch Clamp Technique ◽  
Paired Pulse ◽  
Paired Pulse Facilitation ◽  
Mature Mouse ◽  
Layer V ◽  
Immature Cells ◽  
Whole Cell Recordings ◽  
Paired Pulse Depression

1. Whole cell recordings from layer V neurons of mouse somatosensory cortex were made with the use of a "blind" patch-clamp technique. In slices from immature [postnatal days 6 to 11 (P6-P11)] and juvenile (P18-P21) animals, inhibitory postsynaptic currents (IPSCs) were evoked in all cells by extracellular stimulation at the layer V-VI border. Monosynaptic IPSCs, with latency < 2 ms, were isolated pharmacologically by blockade of ionotropic glutamatergic transmission. IPSCs were blocked by bicuculline methiodide and reversed near the predicted equilibrium potential for Cl-. 2. IPSC characteristics were not different for the two age groups. At 1.5-2 times threshold intensity (0.2 Hz), they fluctuated in amplitude with occasional failures. At -70 or -80 mV, mean amplitudes were -202 +/- 20 (SE) pA and -207 +/- 32 pA for immature (39 cells) and juvenile (13 cells) cortex, respectively. Half rise times were 0.74 +/- 0.03 ms (n = 7 cells) in neonates and 0.67 +/- 0.04 ms (n = 7 cells) in juveniles. Decays were biexponential with tau 1 = 14.8 +/- 1.3 ms and tau 2 = 59.0 +/- 7.4 ms (n = 7 cells) in neonates, and tau 1 = 11.9 +/- 1.1 ms and tau 2 = 55.5 +/- 4.2 ms (n = 7 cells) in juveniles. 3. Pairs of stimuli elicited paired-pulse facilitation (PPF) when delivered at brief interstimulus intervals (ISI), and paired-pulse depression (PPD) at long ISI. PPF, which was evident in 64% of immature cells and 38% of juvenile cells, was maximal (38 +/- 4% greater than the conditioning response) at 20-40 ms. PPD, which was evident in 82% of immature cells and 87% of juvenile cells, was maximal (29 +/- 2% smaller than the conditioning response) by 300 ms. In each age group, some animals showed PPF without PPD.(ABSTRACT TRUNCATED AT 250 WORDS)

Activity-Dependent Depression of Local Excitatory Connections in the CA1 Region of Mouse Hippocampus

2007 ◽  
Vol 97 (6) ◽  
pp. 3926-3936 ◽  
Author(s):  
Ann E. Fink ◽  
Joshua Sariñana ◽  
Erin E. Gray ◽  
Thomas J. O'Dell
Keyword(s):  
Pyramidal Cell ◽  
Adenosine Receptors ◽  
Low Frequency ◽  
Pyramidal Cells ◽  
Paired Pulse ◽  
Ca1 Pyramidal Cells ◽  
Ca1 Region ◽  
Activity Dependent ◽  
Fiber Stimulation ◽  
Paired Pulse Depression

The existence of recurrent excitatory synapses between pyramidal cells in the hippocampal CA1 region has been known for some time yet little is known about activity-dependent forms of plasticity at these synapses. Here we demonstrate that under certain experimental conditions, Schaffer collateral/commissural fiber stimulation can elicit robust polysynaptic excitatory postsynaptic potentials due to recurrent synaptic inputs onto CA1 pyramidal cells. In contrast to CA3 pyramidal cell inputs, recurrent synapses onto CA1 pyramidal cells exhibited robust paired-pulse depression and a sustained, but rapidly reversible, depression in response to low-frequency trains of Schaffer collateral fiber stimulation. Blocking GABAB receptors abolished paired-pulse depression but had little effect on low-frequency stimulation (LFS)-induced depression. Instead, LFS-induced depression was significantly attenuated by an inhibitor of A1 type adenosine receptors. Blocking the postsynaptic effects of GABAB and A1 receptor activation on CA1 pyramidal cell excitability with an inhibitor of G-protein-activated inwardly rectifying potassium channels had no effect on either paired-pulse depression or LFS-induced depression. Thus activation of presynaptic GABAB and adenosine receptors appears to have an important role in activity-dependent depression at recurrent synapses. Together, our results indicate that CA3-CA1 and CA1-CA1 synapses exhibit strikingly different forms of short-term synaptic plasticity and suggest that activity-dependent changes in recurrent synaptic transmission can transform the CA1 region from a sparsely connected recurrent network into a predominantly feedforward circuit.

Somatosensory Corticothalamic Projections: Distinguishing Drivers From Modulators

2004 ◽  
Vol 92 (4) ◽  
pp. 2185-2197 ◽  
Author(s):  
Iva Reichova ◽  
S. Murray Sherman
Keyword(s):  
Lateral Geniculate Nucleus ◽  
Ampa Receptor ◽  
Metabotropic Glutamate Receptor ◽  
Cortical Layer ◽  
Paired Pulse ◽  
Paired Pulse Facilitation ◽  
Medial Nucleus ◽  
Lateral Geniculate ◽  
Posterior Medial Nucleus ◽  
Paired Pulse Depression

We used a juvenile mouse thalamocortical slice preparation with whole cell recording to investigate synaptic properties of corticothalamic inputs from somatosensory cortex to the ventral posterior medial and posterior medial nuclei (98 cells). We compared these data to those obtained from activating retinal and cortical inputs to the lateral geniculate nucleus (8 cells), the former representing a prototypical driver input and the latter, a typical modulator. Retinogeniculate activation evoked large, all-or-none excitatory postsynaptic potentials (EPSPs) that showed paired-pulse depression antagonized by N-methyl-d-aspartate (NMDA) and AMPA receptor blockers but with no sign of a metabotropic glutamate receptor (mGluR) component. Corticogeniculate activation evoked small, graded EPSPs showing paired-pulse facilitation, and the EPSPs showed both NMDA and AMPA receptor component plus an mGluR1 component. In the somatosensory thalamic relays, cortical stimulation elicited glutamatergic EPSPs in all thalamic cells, and these EPSPs fell into two groups. One, elicited from cortical layer 6 to cells of both nuclei, involved small, graded EPSPs with paired-pulse facilitation, and most also showed an mGluR1 component. The other, elicited from layer 5 to cells only of the posterior medial nucleus, involved large, all-or-none EPSPs with paired-pulse depression, and none showed an mGluR component. By analogy with results from the lateral geniculate nucleus, we conclude that the input from layer 6 to both nuclei acts as a modulator but that the layer 5 input to the posterior medial nucleus serves as a driver. Our data extend a common organizing principle from first-order nuclei to higher-order thalamic relays and further implicate the latter in corticocortical communication.

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