Pyramidal cells in piriform cortex receive a convergence of inputs from monoamine activated GABAergic interneurons

1993 ◽  
Vol 600 (1) ◽  
pp. 63-73 ◽  
Author(s):  
Randy L. Gellman ◽  
George K. Aghajanian
Keyword(s):  
Piriform Cortex ◽  
Pyramidal Cells ◽  
Gabaergic Interneurons

scholarly journals Differential inhibition of pyramidal cells and inhibitory interneurons along the rostrocaudal axis of anterior piriform cortex

2018 ◽  
Vol 115 (34) ◽  
pp. E8067-E8076 ◽  
Author(s):  
Adam M. Large ◽  
Nathan W. Vogler ◽  
Martha Canto-Bustos ◽  
F. Kathryn Friason ◽  
Paul Schick ◽  
...  
Keyword(s):  
Sensory Processing ◽  
Spatial Representation ◽  
Piriform Cortex ◽  
Pyramidal Cells ◽  
Inhibitory Neurons ◽  
Gabaergic Interneurons ◽  
Inhibitory Circuits ◽  
Anterior Piriform Cortex ◽  
Odor Processing ◽  
Spatial Asymmetries

The spatial representation of stimuli in sensory neocortices provides a scaffold for elucidating circuit mechanisms underlying sensory processing. However, the anterior piriform cortex (APC) lacks topology for odor identity as well as afferent and intracortical excitation. Consequently, olfactory processing is considered homogenous along the APC rostral–caudal (RC) axis. We recorded excitatory and inhibitory neurons in APC while optogenetically activating GABAergic interneurons along the RC axis. In contrast to excitation, we find opposing, spatially asymmetric inhibition onto pyramidal cells (PCs) and interneurons. PCs are strongly inhibited by caudal stimulation sites, whereas interneurons are strongly inhibited by rostral sites. At least two mechanisms underlie spatial asymmetries. Enhanced caudal inhibition of PCs is due to increased synaptic strength, whereas rostrally biased inhibition of interneurons is mediated by increased somatostatin–interneuron density. Altogether, we show differences in rostral and caudal inhibitory circuits in APC that may underlie spatial variation in odor processing along the RC axis.

Characterization of synaptically mediated fast and slow inhibitory processes in piriform cortex in an in vitro slice preparation

1988 ◽  
Vol 59 (5) ◽  
pp. 1352-1376 ◽  
Author(s):  
G. F. Tseng ◽  
L. B. Haberly
Keyword(s):  
Membrane Potential ◽  
Piriform Cortex ◽  
Reversal Potential ◽  
Pyramidal Cells ◽  
Membrane Depolarization ◽  
Resting Membrane Potential ◽  
Excitatory Postsynaptic Potential ◽  
Pentobarbital Sodium ◽  
Postsynaptic Potential ◽  
Conductance Increase

1. Intracellular recordings were obtained from anatomically verified layer II pyramidal cells in slices from rat piriform cortex cut perpendicular to the surface. 2. Responses to afferent and association fiber stimulation at resting membrane potential consisted of a depolarizing potential followed by a late hyperpolarizing potential (LHP). Membrane polarization by current injection revealed two components in the depolarizing potential: an initial excitatory postsynaptic potential (EPSP) followed at brief latency by an inhibitory postsynaptic potential (IPSP) that inverted with membrane depolarization and truncated the duration of the EPSP. 3. The early IPSP displayed the following characteristics suggesting mediation by gamma-aminobutyric acid (GABA) receptors linked to Cl- channels: associated conductance increase, sensitivity to increases in internal Cl- concentration, blockage by picrotoxin and bicuculline, and potentiation by pentobarbital sodium. The reversal potential was in the depolarizing direction with respect to resting membrane potential so that the inhibitory effect was exclusively via current shunting. 4. The LHP had an associated conductance increase and a reversal potential of -90 mV in normal bathing medium that shifted according to Nernst predictions for a K+ potential with changes in external K+ over the range 4.5-8 mM indicating mediation by the opening of K+ channels and ruling out an electrogenic pump origin. 5. Lack of effect of bath-applied 8-bromoadenosine 3',5'-cyclic monophosphate (8-Br-cAMP) or internally applied ethylene glycol-bis(beta-aminoethyl ether)-N,N,N',N'-tetraacetic acid (EGTA) on the LHP and failure of high amplitude, direct membrane depolarization to evoke a comparable potential, argue against endogenous mediation of the LHP by a Ca2+ activated K+ conductance [gK(Ca)]. However, an apparent endogenously mediated gK(Ca) with a duration much greater than the LHP was observed in a low percent of layer II pyramidal cells. Lack of effect of 8-Br-cAMP also indicates a lack of dependence of the LHP on cAMP. 6. Other characteristics of the LHP that were demonstrated include: a lack of blockage by GABAA receptor antagonists, a probable voltage sensitivity (decrease in amplitude in the depolarizing direction), and an apparent brief onset latency (less than 10 ms) when the early IPSP was blocked by picrotoxin. The LHP was unaffected by pentobarbital sodium when the early IPSP was blocked by picrotoxin. 7. Both the LHP and early IPSP were blocked by low Ca2+/high Mg2+, consistent with disynaptic mediation.(ABSTRACT TRUNCATED AT 400 WORDS)

GABAA-Mediated IPSCs in Piriform Cortex Have Fast and Slow Components With Different Properties and Locations on Pyramidal Cells

1997 ◽  
Vol 78 (5) ◽  
pp. 2531-2545 ◽  
Author(s):  
A. Kapur ◽  
R. A. Pearce ◽  
W. W. Lytton ◽  
L. B. Haberly
Keyword(s):  
Time Course ◽  
Feedback Inhibition ◽  
Slow Component ◽  
Piriform Cortex ◽  
Pyramidal Cells ◽  
Long Term Potentiation ◽  
Companion Paper ◽  
Protective Role ◽  
Functional Roles ◽  
Term Potentiation

Kapur, A., R. A. Pearce, W. W. Lytton, and L. B. Haberly.GABAA-mediated IPSCs in piriform cortex have fast and slow components with different properties and locations on pyramidal cells. J. Neurophysiol. 78: 2531–2545, 1997. A recent study in piriform (olfactory) cortex provided evidence that, as in hippocampus and neocortex, γ-aminobutyric acid-A (GABAA)-mediated inhibition is generated in dendrites of pyramidal cells, not just in the somatic region as previously believed. This study examines selected properties of GABAA inhibitory postsynaptic currents (IPSCs) in dendritic and somatic regions that could provide insight into their functional roles. Pharmacologically isolated GABAA-mediated IPSCs were studied by whole cell patch recording in slices. To compare properties of IPSCs in distal dendritic and somatic regions, local stimulation was carried out with tungsten microelectrodes, and spatially restricted blockade of GABAA-mediated inhibition was achieved by pressure-ejection of bicuculline from micropipettes. The results revealed that largely independent circuits generate GABAA inhibition in distal apical dendritic and somatic regions. With such independence, a selective decrease in dendritic-region inhibition could enhance integrative or plastic processes in dendrites while allowing feedback inhibition in the somatic region to restrain system excitability. This could allow modulatory fiber systems from the basal forebrain or brain stem, for example, to change the functional state of the cortex by altering the excitability of interneurons that mediate dendritic inhibition without increasing the propensity for regenerative bursting in this highly epileptogenic system. As in hippocampus, GABAA-mediated IPSCs were found to have fast and slow components with time constants of decay on the order of 10 and 40 ms, respectively, at 29°C. Modeling analysis supported physiological evidence that the slow time constant represents a true IPSC component rather than an artifactual slowing of the fast component from voltage clamp of a dendritic current. The results indicated that, whereas both dendritic and somatic-region IPSCs have both fast and slow GABAA components, there is a greater proportion of the slow component in dendrites. In a companion paper, the hypothesis is explored that the resulting slower time course of the dendritic IPSC increases its capacity to regulate the N-methyl-d-aspartate component of EPSPs. Finally, evidence is presented that the slow GABAA-mediated IPSC component is regulated by presynaptic GABAB inhibition whereas the fast is not. Based on the requirement for presynaptic GABAB-mediated block of inhibition for expression of long-term potentiation, this finding is consistent with participation of the slow GABAA component in regulation of synaptic plasticity. The lack of susceptibility of the fast GABAA component to the long-lasting, activity-induced suppression mediated by presynaptic GABAB receptors is consistent with a protective role for this process in preventing seizure activity.

scholarly journals Connectivity and network state-dependent recruitment of long-range VIP-GABAergic neurons in the mouse hippocampus

2018 ◽  
Author(s):  
Ruggiero Francavilla ◽  
Vincent Villette ◽  
Xiao Luo ◽  
Simon Chamberland ◽  
Einer Muñoz-Pino ◽  
...  
Keyword(s):  
Molecular Diversity ◽  
Pyramidal Cells ◽  
Functional Specialization ◽  
Gabaergic Interneurons ◽  
Long Distance ◽  
State Dependent ◽  
Mouse Hippocampus ◽  
Ca1 Area ◽  
New Evidence

AbstractGABAergic interneurons in the hippocampus provide for local and long-distance coordination of neurons in functionally connected areas. Vasoactive intestinal peptide-expressing (VIP+) interneurons occupy a distinct niche in circuitry as many of them specialize in innervating GABAergic cells, thus providing network disinhibition. In the CA1 hippocampus, VIP+ interneuron-selective cells target local interneurons. Here, we discovered a novel type of VIP+ neuron whose axon innervates CA1 and also projects to the subiculum (VIP-LRPs). VIP-LRPs showed specific molecular properties and targeted interneurons within the CA1 area but both interneurons and pyramidal cells within subiculum. They were interconnected through gap junctions but demonstrated sparse spike coupling in vitro. In awake mice, VIP-LRPs decreased their activity during theta-run epochs and were more active during quiet wakefulness but not coupled to sharp-wave ripples. Together, the data provide new evidence for VIP interneuron molecular diversity and functional specialization in controlling cell ensembles along the hippocampo-subicular axis.

Spike Coding in Pyramidal Cells of the Piriform Cortex of Rat

2001 ◽  
Vol 86 (3) ◽  
pp. 1504-1510 ◽  
Author(s):  
Alexander D. Protopapas ◽  
James M. Bower
Keyword(s):  
Cognitive Function ◽  
Piriform Cortex ◽  
Pyramidal Cells ◽  
Spike Trains ◽  
Gamma Range ◽  
Cortical Oscillations ◽  
Cell Recording ◽  
Spike Coding ◽  
Theta Range

The study of cortical oscillations has undergone a renaissance in recent years because of their presumed role in cognitive function. Of particular interest are frequencies in the gamma (30–100 Hz) and theta (3–12 Hz) ranges. In this paper, we use spike coding techniques and in vitro whole cell recording to assess the ability of individual pyramidal cells of the piriform cortex to code inputs occurring in these frequencies. The results suggest that the spike trains of individual neurons are much better at representing frequencies in the theta range than those in the gamma range.

Transient synaptic modifications in piriform cortex pyramidal cells associated with odor learning

1997 ◽  
Vol 237 ◽  
pp. S43
Author(s):  
D. Saar ◽  
D. Lebel ◽  
Y. Grossman ◽  
E. Barkai
Keyword(s):  
Piriform Cortex ◽  
Pyramidal Cells ◽  
Odor Learning

scholarly journals Differential coupling of adult-born granule cells to parvalbumin and somatostatin interneurons

2019 ◽  
Author(s):  
Ayelén I. Groisman ◽  
Sung M. Yang ◽  
Alejandro F. Schinder
Keyword(s):  
Granule Cells ◽  
Pyramidal Cells ◽  
Feedback Loops ◽  
Gabaergic Interneurons ◽  
Connectivity Map ◽  
Efficient Control ◽  
Adult Born Neurons ◽  
Ca3 Pyramidal Cells ◽  
Differential Coupling ◽  
Inhibitory Networks

ABSTRACTThe dentate gyrus of the hippocampus is dominated by a strong GABAergic tone that maintains sparse levels of activity. Adult neurogenesis disrupts this balance through the continuous addition of new granule cells (GCs) that display high excitability while develop and connect within the preexisting host circuit. The dynamics of the connectivity map for developing GCs in the local inhibitory networks remains unknown. We used optogenetics to study afferent and efferent synaptogenesis between new GCs and GABAergic interneurons expressing parvalbumin (PV-INs) and somatostatin (SST-INs). Inputs from PV-INs targeted the soma and remained immature until they grew abruptly in >4-week-old GCs. This transition was accelerated by exposure to enriched environment. Inputs from SST-INs were dendritic and developed slowly until reaching maturity by 8 weeks. Synaptic outputs from GCs onto PV-INs matured faster than those onto SST-INs, but also required several weeks. In the mature dentate network, PV-INs exerted an efficient control of GC spiking and were involved in both feedforward and feedback loops, a mechanism that would favor lateral inhibition and sparse coding. Our results reveal a long-lasting transition where adult-born neurons remain poorly coupled to inhibition, which might enable a parallel streaming channel from the entorhinal cortex to CA3 pyramidal cells.

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