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At least 19 recordsLinked to original sources
PubMed2002

Locus coeruleus activation modulates firing rate and temporal organization of odour-induced single-cell responses in rat piriform cortex.

Piriform cortex (PCx) is the primary cortical projection region for olfactory information and has bidirectional monosynaptic connections with olfactory bulb and association cortices. PCx neurons display a complex receptive field, responding to odours rather than their molecular components, suggesting that these neurons are involved in higher order olfactory processing. Neuromodulators, especially noradrenaline (NA), have important influences on sensory processing in other cortical regions and might be responsible for the plasticity observed in PCx during learning. The present study is the first attempt to examine in vivo the actions of NA on sensory responses in the PCx. Stimulation of the noradrenergic nucleus locus coeruleus (LC) was used to induce release of NA in the forebrain in urethane-anaesthetized rats. Extracellular recording of single units was made simultaneously in anterior and posterior PCx. The responses to an odour stimulus were measured over 25 trials. Twenty-five subsequent odour presentations were preceded by stimulation of the ipsilateral LC through a bipolar electrode, previously placed in the LC under electrophysiological control. This priming stimulation modified the activity of 77 of the 135 recorded neurons. For most cells, LC stimulation enhanced cortical responses to odour in terms of both spike count and temporal organization, with some differential effects in anterior and posterior regions. These results are the first to show enhancement of sensory responses in the olfactory cortex by LC activation. Spontaneous activation of LC neurons such as occurs during learning could serve to enhance olfactory perception and promote learning.

Action Potentials↗
PubMed1996

Layer-specific properties of the transient K current (IA) in piriform cortex.

Piriform cortex in the rat is highly susceptible to induction of epileptiform activity. Experiments in vivo and in vitro indicate that this activity originates in endopiriform nucleus (EN). In slices, EN neurons are more excitable than layer II (LII) pyramidal cells, with more positive resting potentials and lower spike thresholds. We investigated potassium currents in EN and LII to evaluate their contribution to these differences in excitability. Whole-cell currents were recorded from identified cells in brain slices. A rapidly inactivating outward current (IA) had distinct properties in LII (IA,LII) versus EN (IA,EN). The peak amplitude of IA,EN was 45% smaller than IA,LII, and the kinetics of activation and inactivation was significantly slower for IA,EN. The midpoint of steady-state inactivation was hyperpolarized by 10 mV for IA,EN versus IA,LII, whereas activation was similar in the two cell groups. Other voltage-dependent potassium currents were indistinguishable between EN and LII. Simulations using a compartmental model of LII cells argue that different cellular distributions of IA channels in EN versus LII cells cannot account for these differences. Thus, at least some of the differences are intrinsic to the channels themselves. Current-clamp simulations suggest that the differences between IA,LII and IA,EN can account for the observed difference in resting potentials between the two cell groups. Simulations show that this difference in resting potential leads to longer first spike latencies in response to depolarizing stimuli. Thus, these differences in the properties of IA could make EN more susceptible to induction and expression of epileptiform activity.

Animals↗
PubMed1997

Converging inputs to the entorhinal cortex from the piriform cortex and medial septum: facilitation and current source density analysis.

Converging inputs to the entorhinal cortex from the piriform cortex and medial septum: facilitation and current source density analysis. J. Neurophysiol. 78: 2602-2615, 1997. The entorhinal cortex receives sensory inputs from the piriform cortex and modulatory inputs from the medial septum. To examine short-term synaptic facilitation effects in these pathways, current source density (CSD) analysis was used first to localize the entorhinal cortex membrane currents, which generate field potentials evoked by stimulation of these afferents. Field potentials were recorded at 50-micron intervals through the medial entorhinal cortex in urethan-anesthetized rats and the one-dimensional CSD was calculated. Piriform cortex stimulation evoked a surface-negative, deep-positive field potential component in the entorhinal cortex with mean onset and peak latencies of 10.4 and 18.4 ms. The component followed brief 100-Hz stimulation, consistent with a monosynaptic response. CSD analysis linked the component to a current sink, which often began in layer I before peaking in layer II. A later, surface-positive field potential component peaked at latencies near 45 ms and was associated with a current source in layer II. Medial septal stimulation evoked positive and negative field potential components which peaked at latencies near 7 and 16 ms, respectively. A weaker and more prolonged surface-negative, deep-positive component peaked at latencies near 25 ms. The early components were generated by currents in the hippocampal formation, and the late surface-negative component was generated by currents in layers II to IV of the entorhinal cortex. Short-term facilitation effects in conscious animals were examined using electrodes chronically implanted near layer II of the entorhinal cortex. Paired-pulse stimulation of the piriform cortex at interpulse intervals of 30 and 40 ms caused the largest facilitation (248%) of responses evoked by the second pulse. Responses evoked by medial septal stimulation also were facilitated maximally (59%) by a piriform cortex conditioning pulse delivered 30-40 ms earlier. Paired pulse stimulation of the medial septum caused the largest facilitation (149%) at intervals of 70 ms, but piriform cortex evoked responses were facilitated maximally (46%) by a septal conditioning pulse 100-200 ms earlier. Frequency potentiation effects were maximal during 12- to 18-Hz stimulation of either the piriform cortex or medial septum. Occlusion tests suggested that piriform cortex and medial septal efferents activate the same neurons. The CSD analysis results show that evoked field potential methods can be used effectively in chronically prepared animals to examine synaptic responses in the converging inputs from the piriform cortex and medial septum to the entorhinal cortex. The short-term potentiation phenomena observed here suggest that low-frequency activity in these pathways during endogenous oscillatory states may enhance entorhinal cortex responsivity to olfactory inputs.

Animals↗
PubMed1997

Piriform cortex efferents to the entorhinal cortex in vivo: kindling-induced potentiation and the enhancement of long-term potentiation by low-frequency piriform cortex or medial septal stimulation.

The entorhinal cortex receives input from many cortical areas and mediates the flow of information between these sites and the hippocampal formation. Long-term synaptic plasticity in cortical efferents to the entorhinal cortex may contribute to the transmission of neural activity to the hippocampus, as well as the storage of information, but little is known about plasticity in these pathways. We describe here the use of evoked field potential recordings from chronically implanted electrodes in the rat entorhinal cortex to investigate synaptic plasticity in the large piriform (olfactory) cortex projection to the superficial layers of the entorhinal cortex. Both kindling-induced potentiation and long-term potentiation (LTP) were tested. In addition, we attempted to modulate LTP induction by the co-induction of frequency potentiation and by the co-activation of the medial septum. Epileptogenic kindling stimulations of the piriform cortex (1-s, 60-Hz trains 3 times/day for 5 days) were found to result in a reliable potentiation of field responses evoked by piriform cortex test pulses. Non-epileptogenic tetanization of the piriform cortex with 400-Hz 16-pulse trains reliably resulted in LTP effects. These effects could be augmented by embedding brief LTP induction stimuli within 11-pulse, 15-Hz trains that alone produce only frequency potentiation. Co-activating the medial septum with 10-Hz trains, just prior to tetanization of the piriform cortex, augmented LTP of piriform cortex inputs to the entorhinal cortex in an input-specific manner. All potentiation effects were found to last for periods of weeks. These findings demonstrate that both epileptogenic and non-epileptogenic piriform cortex stimulation induces lasting potentiation of population field responses in the entorhinal cortex of the awake rat. The LTP effects were inducible in a graded manner and were sensitive to the temporal context of stimulation. The finding that low-frequency activation of the septum can enhance plasticity in the entorhinal cortex adds to a body of data indicating a role for the medial septum in contributing to theta activity and plasticity in both the entorhinal cortex and hippocampal formation.

Animals↗
PubMed2000

Characteristics of plateau activity during the latent period prior to epileptiform discharges in slices from rat piriform cortex.

The deep piriform region has an unusually high seizure susceptibility. Voltage imaging previously located the sites of epileptiform discharge onset in slices of rat piriform cortex and revealed the spatiotemporal pattern of development of two types of electrical activity during the latent period prior to discharge onset. A ramplike depolarization (onset activity) appears at the site of discharge onset. Onset activity is preceded by a sustained low-amplitude depolarization (plateau activity) at another site, which shows little if any overlap with the site of onset. Because synaptic blockade at either of these two sites blocks discharges, it was proposed that both forms of latent period activity are necessary for the generation of epileptiform discharges and that the onset and plateau sites work together in the amplification of electrical activity. The capacity for amplification was examined here by studying subthreshold responses in slices of piriform cortex using two different in vitro models of epilepsy. Under some conditions electrically evoked responses showed a nonlinear dependence on stimulus current, suggesting amplification by strong polysynaptic excitatory responses. The sites of plateau and onset activity were mapped for different in vitro models of epilepsy and different sites of stimulation. These experiments showed that the site of plateau activity expanded into deep layers of neighboring neocortex in parallel with expansions of the onset site into neocortex. These results provide further evidence that interactions between the sites of onset and plateau activity play an important role in the initiation of epileptiform discharges. The site of plateau activity showed little variation with different stimulation sites in the piriform cortex, but when stimulation was applied in the endopiriform nucleus (in the sites of onset of plateau activity), plateau activity had a lower amplitude and became distributed over a much wider area. These results indicate that in the initiation of epileptiform discharges, the location of the circuit that generates plateau activity is not rigidly defined but can exhibit flexibility.

Animals↗
PubMed1998

Voltage imaging of epileptiform activity in slices from rat piriform cortex: onset and propagation.

The piriform cortex is a temporal lobe structure with a very high seizure susceptibility. To investigate the spatiotemporal characteristics of epileptiform activity, slices of piriform cortex were examined by imaging electrical activity with a voltage-sensitive fluorescent dye. Discharge activity was studied for different sites of stimulation and different planes of slicing along the anterior-posterior axis. Epileptiform behavior was elicited either by disinhibition with a gamma-aminobutyric acid-A receptor antagonist or by induction with a transient period of spontaneous bursting in low-chloride medium. Control activity recorded with fluorescent dye had the same pharmacological and temporal characteristics as control activity reported previously with microelectrodes. Simultaneous optical and extracellular microelectrode recordings of epileptiform discharges showed the same duration, latency, and all-or-none character as described previously with microelectrodes. Under all conditions examined, threshold electrical stimulation applied throughout the piriform cortex evoked all-or-none epileptiform discharges originating in a site that included the endopiriform nucleus, a previously identified site of discharge onset. In induced slices, but not disinhibited slices, the site of onset also included layer VI of the adjoining agranular insular cortex and perirhinal cortex, in slices from anterior and posterior piriform cortex, respectively. These locations had not been identified previously as sites of discharge onset. Thus like the endopiriform nucleus, the deep agranular insular cortex and perirhinal cortex have a very low seizure threshold. Additional subtle differences were noted between the induced and disinhibited models of epileptogenesis. Velocity was determined for discharges after onset, as they propagated outward to the overlying piriform cortex. Propagation in other directions was examined as well. In most cases, velocities were below that for action potential conduction, suggesting that recurrent excitation and/or ephaptic interactions play a role in discharge propagation. Future investigations of the cellular and organizational properties of regions identified in this study should help clarify the neurobiological basis of high seizure susceptibility.

Animals↗
PubMed2000

Bilateral lesions of the central but not anterior or posterior parts of the piriform cortex retard amygdala kindling in rats.

The piriform cortex is thought to be involved in temporal lobe seizure propagation, such as that occurring during kindling of the amygdala or hippocampus. A number of observations suggested that the circuits of the piriform cortex might act as a critical pathway for limbic seizure discharges to assess motor systems, but direct evidence for this suggestion is scarce. Furthermore, the piriform cortex is not a homogeneous structure, which complicates studies on its role in limbic epileptogenesis. We have previously reported data indicating that the central part of the piriform cortex might be particularly involved during amygdala kindling. In order to further evaluate the role of different parts of the piriform cortex during kindling development, we bilaterally destroyed either the central, anterior or posterior piriform cortex by microinjections of ibotenate two weeks before onset of amygdala kindling. Lesions of the anterior piriform cortex hardly affected kindling acquisition, except that fewer animals exhibited stage 3 (unilateral forelimb) seizures compared to sham controls. Lesions of the central piriform cortex significantly retarded kindling, which was due to a decreased progression from stage 3 to stage 4/5 seizures, i.e. the lesioned rats needed significantly longer for the acquisition of generalized clonic seizures in the late stages of kindling development. Lesions of the posterior piriform cortex did not significantly affect kindling development. The data demonstrate that different parts of the piriform cortex mediate qualitatively different effects on amygdala kindling. The central piriform cortex seems to be a neural substrate involved in the continuous development of kindling from stage 3 to stages 4/5, indicating that this part of the piriform cortex may have preferred access, either directly or indirectly, to structures capable of supporting generalized kindled seizure expression.

Amygdala↗
PubMed1997

Optical recording of the rat piriform cortex activity.

The piriform cortex (PCx) is a phylogenetically old brain structure which presents characteristics of a content-addressable memory. Taking into account its particular anatomo-functional organization, we hypothesized that this cortex could behave rather as an assembly of different functional units than as a functionally homogeneous structure. This hypothesis was tested by using both anatomical and functional approaches. Immunohistological and tracing experiments demonstrated that both the connections of the PCx with the higher nervous centres, and its monoaminergic and cholinergic modulatory afferents exhibited a heterogeneous distribution. Then, optical monitoring of its neuronal activity with a voltage-sensitive dye pointed out that the PCx is a functionally heterogeneous structure. Electrical stimulations of the olfactory bulb showed that the inhibitory processes which control the cortical responsiveness were not identical in all the PCx area. Two different functional areas at least could be distinguished: in the ventromedial PCx, the afferent activity is privileged since the level of inhibition of disynaptic activation remained large during repetitive stimuli. Contrarily, in the posterior PCx, the disynaptic activity remained unchanged in response to successive stimulations and the responses of neighbouring sites were statistically more synchronized than in its anterior part. Moreover, a late depolarization wave was significantly larger in the posterior PCx. These data are in good agreement with the results provided by computational models of the PCx. In the future, theoretical and experimental investigations of this cortex will be useful for understanding olfactory information processing and as a model of brain functioning at the neocortical level as well.

Animals↗
PubMed1998

Synaptic correlates of odor habituation in the rat anterior piriform cortex.

Responses of anterior piriform cortex layer II/III neurons to both odors and electrical stimulation of the lateral olfactory tract (LOT) were measured with intracellular recordings in urethan-anesthetized, freely breathing rats. Odor-evoked, respiration-entrained postsynaptic potentials (PSPs) rapidly habituated during a 50-s odor stimulus, then spontaneously recovered within 2 min of odor termination. Associated with the decrease in odor-evoked PSP amplitude was a decrease in the monosynaptic excitatory postsynaptic potentials (EPSPs) evoked by electrical stimulation of the LOT. The decrement in LOT-evoked EPSPs recovered with a time course similar to the odor response recovery. These results demonstrate that odor habituation is associated with a decrease in afferent synaptic efficacy in the anterior piriform cortex.

Action Potentials↗
PubMed1999

Modulation of inhibitory synaptic potentials in the piriform cortex.

Modulation of inhibitory synaptic potentials in the piriform cortex. Intracellular recordings from pyramidal neurons in brain slice preparations of the piriform cortex were used to test results from a computational model about the effects of cholinergic agonists on inhibitory synaptic potentials induced by stimulation of afferent fibers in layer Ia and association/intrinsic fibers in layer Ib. A simple model of piriform cortex as an associative memory was used to analyze how suppression of inhibitory synaptic transmission influenced performance of the network. Levels of suppression of excitatory synaptic transmission were set at levels determined in previous experimental work. Levels of suppression of inhibitory synaptic transmission were then systematically varied within the model. This modeling work demonstrated that suppression of inhibitory synaptic transmission in layer Ib should be stronger than suppression of inhibitory synaptic transmission in layer Ia to keep activity levels high enough for effective storage. Experimental data showed that perfusion of the cholinergic agonist carbachol caused a significant suppression of inhibitory postsynaptic potentials (IPSPs) in the pyramidal neurons that were induced by stimulation of layer Ib, with a weaker effect on IPSPs induced by stimulation of layer Ia. As previously described, carbachol also selectively suppressed excitatory postsynaptic potentials (EPSPs) elicited by intrinsic but not afferent fiber stimulation. The decrease in amplitude of IPSPs induced by layer Ib stimulation did not appear to be directly related to the decrease in EPSP amplitude induced by layer Ib stimulation. The stimulation necessary to induce neuronal firing with layer Ia stimulation was reduced in the presence of carbachol, whereas that necessary to induce neuronal firing with layer Ib stimulation was increased, despite the depolarization of resting membrane potential. Thus physiological data on cholinergic modulation of inhibitory synaptic potentials in the piriform cortex is compatible with the functional requirements determined from computational models of piriform cortex associative memory function.

Animals↗
PubMed1995

Associative synaptic potentials in the piriform cortex of the isolated guinea-pig brain in vitro.

The involvement of local and remote associative fibres in the generation of piriform cortex synaptic potentials was investigated in the isolated guinea-pig brain maintained in vitro by arterial perfusion by implementing current source density analysis (CSD) on cortical field potential profiles. Previous hypotheses were verified using acute surgical isolation of piriform cortical areas to study different synaptic events separately. Stimulation of the lateral olfactory tract activated associative potentials throughout the piriform cortex. In the anterior piriform cortex, the current sinks responsible for the generation of associative potentials were located in the superficial portion of layer Ib and in layer III. In the posterior piriform cortex, two associative events were observed: an early sink located in the superficial part of layer Ib, followed by a sink in the deep part of the same layer. In the anterior piriform cortex, local associative synaptic potentials were separated from the component carried by long projective fibres by surgically isolating a small area of cortex monosynaptically activated by lateral olfactory tract stimulation. In this patch of lateral olfactory tract-connected anterior piriform cortex, local associative sinks were observed in the superficial Ib layer and in layer III. Monosynaptic activation of the isolated patch of anterior piriform cortex induced purely associative potentials throughout the piriform cortex. These potentials were mediated by the synaptic activation of apical dendrites in the superficial Ib layer and selectively abolished by severing the long associative fibres. The anterior piriform cortex layer III sink and the posterior piriform cortex deep Ib associative component were evoked by the activation of large population spikes in the monosynaptic anterior piriform cortex and the disynaptic posterior piriform cortex response respectively. These two sinks are presumably generated locally through a polysynaptic circuit, whose activation depends on the degree of cortical excitation. Olfactory signal processing in the guinea-pig piriform cortex during states of normal excitability is supported by the interactions between associative inputs impinging on the synapses located separately on the dendrites of pyramidal neurons. An increase in the synchronization of piriform cortex neuron discharge activates usually silent local circuit synapses.

Afferent Pathways↗
PubMed1995

Susceptibility of different cell layers of the anterior and posterior part of the piriform cortex to electrical stimulation and kindling: comparison with the basolateral amygdala and "area tempestas".

Several lines of evidence suggest that the piriform cortex functions as a generator in the development and propagation of forebrain (limbic type) seizures, particularly in the kindling model of epilepsy. It is, however, not clear where, within the rather large piriform cortex region, the generator resides, and how much tissue is involved. Highly sensitive loci to chemical or electrical stimulation have been described both in the deep anterior and posterior parts of the piriform cortex. Furthermore, data from piriform cortex slice preparations indicated that epileptiform potentials originate in deep structures, particularly the endopiriform nucleus that underlies the piriform cortex. In the present study, in rats, we implanted stimulation and recording electrodes in various rostrocaudal locations of the piriform cortex and endopiriform nucleus, including the "area tempestas", i.e. a structure in the anterior part of the piriform cortex previously proposed to be critically involved in the generation of convulsive seizures of limbic origin. Within the piriform cortex, electrodes were aimed at different cellular layers of this structure. For comparison, additional animals received electrodes in different parts of the basolateral amygdala. A total of 19 different locations was obtained in this way. The susceptibility of these locations to electrical stimulation was characterized by determining the threshold for induction of afterdischarges. The afterdischarge threshold was lowest in layer III of the posterior piriform cortex and some locations in the endopiriform nucleus, whereas amygdala and "area tempestas" displayed higher values. In several animals, particularly those with electrodes in layer III of the posterior piriform cortex, spontaneous spiking was seen in prestimulation recordings, whereas this was never observed in recordings from the amygdala. Subsequent kindling by repeated stimulation of the various locations demonstrated marked differences in afterdischarge threshold reduction and kindling rate. The most marked decreases in afterdischarge threshold were seen in locations within layer III of the piriform cortex, whereas several other locations, including the "area tempestas", exhibited only moderate decreases or no decrease at all. In contrast to previous observations with only few locations in the piriform cortex region, the posterior piriform cortex was not in general slower to kindle than the anterior piriform cortex, although some locations in the posterior piriform cortex exhibited significantly lower kindling rates than the amygdala. The highest kindling rate was seen in the dorsal endopiriform nucleus.(ABSTRACT TRUNCATED AT 400 WORDS)

Amygdala↗
PubMed2000

Kindling causes persistent in vivo changes in firing rates and glutamate sensitivity of central piriform cortex neurons in rats.

The present experiments were undertaken to study whether amygdala kindling induces persistent alterations in the functional status of neurons of the central piriform cortex, a subregion of the piriform cortex identified previously as a site involved in the kindling process. Extracellular, single-unit recordings of piriform cortex neurons were made in anesthetized fully kindled rats at an interval of at least five weeks after the last seizure. Electrode implanted but not kindled rats served as sham controls. An additional group of non-implanted rats was used as naive controls. Spontaneously firing piriform cortex neurons were characterized in all groups by smooth, sharp, biphasic (i.e. positive/negative) action potentials with a duration of 0.8-1.8 ms, and were primarily located at the border between piriform cortex layers II and III. In kindled rats, neurons in the central piriform cortex exhibited a significantly higher firing rate compared to controls. Based on median group values, the increase in basal activity in kindled rats averaged about 90%. The responsiveness of piriform cortex neurons to neurotransmitters was tested by microiontophoretic application of glutamate, N-methyl-D-aspartate and GABA. Piriform cortex neurons of kindled rats exhibited a significantly lower responsiveness to the excitatory effect of glutamate than naive controls. A lowered glutamate responsiveness was also seen in sham controls. No significantly altered transmitter sensitivities of piriform cortex neurons from kindled rats were seen with N-methyl-D-aspartate or GABA. The data indicate that amygdala kindling causes persistent interictal changes in both basal activity and glutamate responsiveness of central piriform cortex neurons which could contribute to the abnormal hyperexcitability characteristic of kindling.

Action Potentials↗
PubMed1998

Differences in the distribution of GABA- and GAD-immunoreactive neurons in the anterior and posterior piriform cortex of rats.

There is accumulating evidence of anterior-posterior differences in the susceptibility of the piriform cortex to seizure induction and to functional alterations in response to seizures elicited from other limbic brain regions, but the reasons for such differences along the anterior-posterior axis of the piriform cortex are not clear. In the present study, GABAergic neurons have been identified in the piriform cortex of the rat at light microscopic level by immunocytochemical localization of GABA and the GABA-synthesizing enzyme glutamic acid decarboxylase. A monoclonal antibody to GABA and, for comparison, polyclonal antibodies to GABA and glutamic acid decarboxylase were used for this purpose. In both anterior and posterior piriform cortex, the highest number and density of GABA-immunoreactive cells was found in layer II. Lower density of GABAergic cells was found in layers I and III and the subjacent endopiriform cortex. When cells were quantified in 19 corresponding sections of the piriform cortex, covering most of anterior-posterior extension of this region, there appeared to be an increased density of GABAergic neurons in sections near to or within the transition zone between anterior and posterior piriform cortex. A more detailed analysis at 4 section levels in the anterior and posterior piriform cortex and the transition zone between the 2 parts substantiated a significantly higher density of GABAergic neurons in the transition zone, which was predominantly due to increased numbers of cells in layers II and III. We propose that the transition zone between anterior and posterior piriform cortex is a location where numerous GABAergic interneurons regulate the activity of neighbouring deep pyramidal cells which receive dense excitatory input from both the olfactory bulb and distant pyramidal cells in the more anterior and posterior parts of the piriform cortex at the same time, thus increasing the risk of paroxysmal activation within this restricted area. This proposal is in line with recent observations of increased susceptibility to epileptiform activation and to kindling-induced neurochemical alterations within the transition zone between anterior and posterior piriform cortex.

Animals↗
PubMed1993

Membrane currents evoked by afferent fiber stimulation in rat piriform cortex. I. Current source-density analysis.

1. The membrane currents evoked by afferent fiber stimulation in the piriform cortex were derived by the use of current source-density (CSD) analysis in the rat under urethan anesthesia. The primary goals were to test hypotheses concerning the sequence of synaptic events evoked by afferent fiber stimulation and to derive data required for development and testing of the model presented in the companion paper. 2. In confirmation of previous studies, it was found that afferent fiber stimulation evokes a monosynaptic excitatory postsynaptic current (EPSC) in distal segments of pyramidal cell apical dendrites (layer Ia) followed by a strong disynaptic EPSC in adjacent middle segments (superficial layer Ib). 3. Given the central importance of the strong disynaptic EPSC in models for operation of the piriform cortex, the hypothesis that it is mediated by long association fibers from the anterior piriform cortex was tested by comparing its latency in response to stimulation at anterior and posterior locations. The results confirmed the hypothesis and ruled out a significant contribution from local connections in the posterior piriform cortex. 4. Intensification of pyramidal cell activity by spatially restricted disinhibition with picrotoxin confirmed the hypothesis that associational projections from the posterior piriform cortex can mediate a long-latency disynaptic EPSC in proximal dendritic segments (mid to deep layer Ib) in the anterior piriform cortex. 5. Analysis of the time course of the monosynaptic EPSC in different areas revealed that activation of the anterior piriform cortex from afferent fiber stimulation is fast and nearly synchronous throughout its extent as a result of the relatively high conduction velocities of afferent fibers in the lateral olfactory tract (LOT). By contrast, the posterior piriform cortex is sequentially activated by this EPSC as a consequence of the slow propagation velocity of afferent fiber collaterals that course across its surface. This activation is sufficiently slow that a large phase lag is present between rostral and caudal regions. 6. The time courses of the monosynaptic and principal disynaptic EPSCs changed in characteristically different ways with increasing distance from the LOT within the posterior piriform cortex. Simulations in the companion paper indicate that initiation and propagation patterns for activity in fiber systems rather than differences in synaptic conductance waveforms are responsible for these differences. 7. Although the laminar distribution of the active inward current component of the monosynaptic EPSC remained constant over time, the peak outward current associated with this EPSC shifted from the depth of proximal apical dendrites (layer Ib) to the depth of superficial pyramidal cell somata (layer II).(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1994

Connections of the piriform cortex in homing pigeons (Columba livia) studied with fast blue and WGA-HRP.

The piriform cortex in homing pigeons receives a projection from the olfactory bulb and is necessary for the operation of those aspects of the navigational map based on olfactory stimuli in these animals. The afferent and efferent projections of the piriform cortex were studied using retrograde migration of wheat-germ agglutinin horseradish peroxidase (WGA-HRP) and Fast Blue, and anterograde migration of WGA-HRP. The piriform cortex was found to receive projections from, and send projections to, numerous regions and nuclei in the telencephalon, diencephalon and lower brainstem. A reciprocal connection with the parahippocampal region suggests that the piriform cortex and hippocampal formation may be part of a neural system that regulates navigational map learning. The piriform cortex also connects reciprocally with a large portion of the anterior telencephalon, including the cortex prepiriformis and hyperstriatum dorsale. In general, the pathway connections of the piriform cortex in homing pigeons are similar to those of the piriform cortex in mammals.

Animals↗
PubMed1997

Evidence for synchronised responses in the piriform cortex by using Gibbs potential analysis.

The piriform cortex is a large paleocortical area which receives direct projections from the olfactory bulb. In order to study the spatiotemporal distribution of the piriform cortex activity, we chose optical recording of the responses evoked by olfactory bulb electrical stimulation. Such a stimulation elicited a large signal corresponding to cortical reactivation (disynaptic activity) via intrinsic association fibres. As the disynaptic activity was observed over the entire piriform area, we wondered whether or not this redistribution contributes to a synchronisation of the activity in the piriform cortex. In order to answer this question, we developed a statistical approach which allows us to take the temporal dimension into account. The analysis was performed by using the Gibbs potential analysis. The neural response of the diode is represented by a stochastic point process (occurrence of latency peak), and the response of the diode array is given as successive realisations of a binary random field defined on a finite set. The Gibbs measure associated with this field is then estimated through the interaction potentials of the field's configurations, which provide a quantitative evaluation of the interaction and the synchronisation between the neural sites. The analysis was performed on the latency of the peak of disynaptic activity, which was determined from signals from 60 different acquisitions realised with the same stimulus parameters. From these 60 files of latency values, we estimated the Gibbs interaction potential of singletons and pairs. The former gave an image of the spatiotemporal distribution of the disynaptic activity, which appears to propagate from the anterior to the posterior part of the area recorded. The estimation of the interaction potential of pairs allows us to characterise the degree of synchronisation between two neighbouring recording sites. It appeared that, in the anterior half of the area recorded, the disynaptic activity was statistically desynchronised whereas, in the posterior part the disynaptic activity appeared strongly synchronised. The functional implications of such a spatiotemporal distribution of the activity are discussed.

Models, Biological↗
PubMed2000

New features of connectivity in piriform cortex visualized by intracellular injection of pyramidal cells suggest that "primary" olfactory cortex functions like "association" cortex in other sensory systems.

Associational connections of pyramidal cells in rat posterior piriform cortex were studied by direct visualization of axons stained by intracellular injection in vivo. The results revealed that individual cells have widespread axonal arbors that extend over nearly the full length of the cerebral hemisphere. Within piriform cortex these arbors are highly distributed with no regularly arranged patchy concentrations like those associated with the columnar organization in other primary sensory areas (i.e., where periodically arranged sets of cells have common response properties, inputs, and outputs). A lack of columnar organization was also indicated by a marked disparity in the intrinsic projection patterns of neighboring injected cells. Analysis of axonal branching patterns, bouton distributions, and dendritic arbors suggested that each pyramidal cell makes a small number of synaptic contacts on a large number (>1000) of other cells in piriform cortex at disparate locations. Axons from individual pyramidal cells also arborize extensively within many neighboring cortical areas, most of which send strong projections back to piriform cortex. These include areas involved in high-order functions in prefrontal, amygdaloid, entorhinal, and perirhinal cortex, to which there are few projections from other primary sensory areas. Our results suggest that piriform cortex performs correlative functions analogous to those in association areas of neocortex rather than those typical of primary sensory areas with which it has been traditionally classed. Findings from other studies suggest that the olfactory bulb subserves functions performed by primary areas in other sensory systems.

Animals↗