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N-Methyl-D-aspartate and L-aspartate activate distinct receptors in piriform cortex.

The effects of ionophoretically applied N-methyl-DL-aspartate (NMDA) and aspartate on identified pyramidal neurons in rat piriform cortex were examined in isolated, submerged, and perfused brain slices. NMDA was more potent than aspartate in eliciting neuronal discharge. Perfusion of the acidic amino acid antagonists, DL-2-amino-5-phosphonovalerate (APV), 10(-6) or 10(-5) M, DL-2-amino-7-phosphonoheptanoate (APH), 10(-5) M, and gamma-D-glutamylglycine (gamma DGG), 10(-5) M, selectively blocked the response to NMDA without effect on the response to aspartate. At higher concentrations which blocked responses to both NMDA and aspartate, gamma DGG blocked kainate responses and depressed glutamate and quisqualate responses. These results suggest that in piriform neurons NMDA and aspartate act at distinct receptor sites, not a common receptor site, and that both of these sites are distinct from those that mediate responses to glutamate, quisqualate, and kainate.

2-Amino-5-phosphonovalerate↗

Imaging epileptiform discharges in slices of piriform cortex with voltage-sensitive fluorescent dyes.

Voltage imaging techniques were used to investigate epileptiform discharges in brain slices containing piriform cortex (PC). These experiments pinpointed the site of discharge onset in the endopiriform nucleus (En). Under some conditions, discharge onset also occurred simultaneously in adjoining neocortex. With slightly suprathreshold electrical stimulation, discharge generation was a two-stage process in which onset was preceded by a sustained spatially localized depolarization denoted as plateau activity. Plateau activity was seen away from the onset site, in a border region between En and layer III of PC. A similar two-stage sequence was seen for slices taken from a variety of planes, using two different interictal models as well as an ictal model. Plateau activity was found to be necessary for the generation of both kinds of discharge. Synaptic transmission at the site of onset was found to be required for the generation of interictal-like discharges, but ictal-like discharges were different in that they could still be generated when synaptic transmission at this site was impaired. These studies identify specialized regions with potentially important roles in epileptogenesis and help to elucidate the neuronal circuitry that can produce epileptiform activity.

Animals↗

Catecholamine innervation of the piriform cortex: a tracing and immunohistochemical study in the rat.

In order to determine the origin of the catecholamine innervation of the rat piriform cortex (PC), we combined retrograde transport of the B subunit of the cholera toxin (CTb) with tyrosine hydroxylase (TH) immunohistochemistry. A substantial number of CTb retrogradely labeled cells was found in the parabrachial pigmented, paranigral and interfascicular nuclei of the ventral tegmental area and the dorsal part of the locus coeruleus, whereas nearly no labeling was noted in the substantia nigra. Following TH immunohistochemistry on the same sections, most if not all of the CTb labeled cells were also TH immunoreactive. Occasional double-labeled cells were also observed in the anterior part of the raphe dorsal nucleus. As visualized with dopamine beta-hydroxylase, dopamine or TH immunohistochemistry, the noradrenaline fibers were homogeneously distributed whereas the dopamine fibers showed rostro-caudal and latero-medial differences. The distribution of TH fibers overlapped both patterns. Our report suggests that the heterogeneous distribution of the DA fibers could support a differential centrifugal modulation of the olfactory information processing throughout the PC.

Animals↗

Olfactory learning is associated with increased spine density along apical dendrites of pyramidal neurons in the rat piriform cortex.

We studied the effect of olfactory learning on the dendritic spine density of pyramidal neurons in the rat piriform (olfactory) cortex. Rats were trained to distinguish between two pairs of odours in an olfactory discrimination task. Three days after training completion, rats were killed and layer II pyramidal neurons identified by Golgi impregnation were examined with a light microscope. Counts of visible spines were performed along the secondary and tertiary branches of both the apical dendrites and the basal dendrites, which are the sites of intracortical synaptic inputs. An estimate of the true spine density was obtained using Feldman and Peters' method (1979, The Journal of Comparative Neurology, 188, 527--542). The estimated true spine density along apical dendrites was higher in neurons from trained rats than those in pseudotrained and naive rats by 15%. As length of spiny dendrites did not change significantly after learning, the learning-related increase in spine density in neurons from trained rats may indicate on an increased number of excitatory synapses interconnecting pyramidal neurons in the piriform cortex, following olfactory learning.

Animals↗

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

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)

Animals↗

Long-term potentiation of monosynaptic EPSPs in rat piriform cortex in vitro.

Induction of long-term potentiation (LTP) by burst stimulation patterned after the limbic system theta rhythm was studied in slices of piriform cortex. Monosynaptic responses were evoked by stimulation of afferent fibers of the lateral olfactory tract (LOT) or the intrinsic associational (ASSN) feedback system. LTP was difficult to elicit at LOT synapses in the presence of 2.5 mM extracellular Mg2+, and when it was induced potentiation increased for 20-30 min after burst stimulation before stabilizing. The probability of inducing LTP was increased when the extracellular Mg2+ concentration was reduced to 50 microM. In ASSN synapses LTP developed in about 1 min after burst stimulation and then remained stable. ASSN system LTP was more readily induced in slices from caudal than rostral piriform. Induction of LTP at both LOT and ASSN synapses was blocked by D-2-amino-5-phosphonopentanoate, indicating that NMDA receptor activation was required. Neither system exhibited the decremental short-term potentiation effect observed after burst stimulation of inputs to the CA1 field of hippocampus.

2-Amino-5-phosphonovalerate↗

The US3 protein kinase of herpes simplex virus attenuates the activation of the c-Jun N-terminal protein kinase signal transduction pathway in infected piriform cortex neurons of C57BL/6 mice.

Stereotaxic microinjection of herpes simplex virus (HSV) into the mouse olfactory bulb resulted in infection of neurons of the piriform cortex. Neurons infected with the wildtype HSV showed no evident phosphorylation of c-Jun N-terminal protein kinase (JNK)/c-Jun. In contrast, neurons infected with a US3 gene-disrupted mutant of the L1BR1 virus displayed phosphorylated JNK/c-Jun in a nuclear staining fashion. Induction of neuronal apoptosis by the wildtype HSV was partially suppressed when compared with that of the L1BR1 virus. A US3-rescued isolate of the L1B(-)11 virus behaved as did the wildtype virus. Collectively, the US3 protein kinase of HSV plays a role in attenuating the virus-induced activation of the JNK signal transduction pathway in the central nervous system and may contribute, at least in part, to controlling neuronal apoptosis.

Animals↗

Deep neurons in piriform cortex. II. Membrane properties that underlie unusual synaptic responses.

1. Membrane properties of deep pyramidal and multipolar cells in layer III of the rat piriform cortex and multipolar cells in the underlying endopiriform nucleus (layer IV) were studied in a slice preparation with the primary goal of elucidating the origin of the unusual synaptic responses described in the companion paper. 2. Micropipettes containing either Lucifer yellow (LY) for combined morphological-physiological analysis or potassium acetate (KAc) were used for the analysis. Comparison of membrane properties of pyramidal cells measured with these two electrolytes revealed significant differences. With LY and other Li+ salts, resting membrane potentials were more depolarized, input resistances higher, spike amplitudes lower, and spike durations longer. 3. As measured with KAc-containing electrodes, membrane properties of deep pyramidal and multipolar cells were similar to each other, but differed from those of superficial pyramidal cells. Resting membrane potentials were more depolarized, thresholds lower, input resistances higher, membrane time constants slower, and spikes smaller and slower. 4. In response to depolarizing current pulses, both deep pyramidal and multipolar cells exhibited an initial depolarizing peak of graded amplitude that fell to a steady state within 150 ms. Current-voltage (I-V) relationships displayed a large increase in slope resistance during the depolarizing peak, but were relatively linear in the depolarizing direction at steady state. In cells with relatively hyperpolarized resting membrane potentials, threshold for the depolarizing peak could be -65 mV or below. Based on a reduction by steady depolarization, reduction by Co2+ and potentiation by Ba2+, it is postulated that the peak is generated in part by a low threshold inactivating Ca2+ current. A partial blockage of this peak by tetrodotoxin (TTX) suggests that a Na+ current also contributes. 5. In response to hyperpolarizing current pulses, especially at depolarized membrane potentials, there was usually a sag from an initial maximum and a depolarizing rebound after current offset in both deep pyramidal and multipolar cells. Based on the dependence on membrane potential (Vm), insensitivity to TTX and blockage by carbamylcholine chloride (carbachol), it is postulated that an M-current contributes to the sag and rebound. 6. The depolarizing rebound that followed offset of hyperpolarizing current pulses could trigger a Ba2+-potentiated local response that resembled the depolarizing peak triggered by depolarizing current, suggesting that the postulated low-threshold inactivating Ca2+ current contributes to its generation.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

Diagonal band stimulation increases piriform cortex neuronal excitability in vivo.

The effects of diagonal band (NDB) stimulation on the spontaneous discharge of pyramidal cells and evoked field potentials (FPs) in piriform cortex (PC) were investigated in vivo. NDB stimulation increased the spontaneous firing rate of PC cells, and increased the disynaptic excitatory (B1) and decreased the disynaptic inhibitory (P2) FP components following lateral olfactory tract (LOT) stimulation. NDB stimulation decreased the P2 component following activation of association fibers in caudal PC. NDB stimulation reduced the paired-pulse inhibition of the P2 component following LOT and caudal PC shocks. The effects of NDB stimulation were reversed by scopolamine, suggesting the involvement of muscarinic receptors. These results suggest that activation of cholinergic inputs to PC increases the excitability of pyramidal cells, probably by a disinhibitory mechanism.

Afferent Pathways↗

Cholinergic modulation of activity-dependent synaptic plasticity in the piriform cortex and associative memory function in a network biophysical simulation.

The effect of activation of cholinergic receptors on long-term potentiation (LTP) in rat piriform cortex pyramidal cells was studied using extracellular and intracellular recordings in brain slice preparations. The functional role of this modulation was studied in a realistic network biophysical stimulation. Repetitive stimuli were applied in two paradigms: one in which the recorded cell was held at its resting potential and one in which synaptic activity was superimposed on a depolarizing pulse strong enough to evoke four action potentials. In the absence of cholinergic modulation, stimulation at 5 Hz induced LTP primarily in the second condition (13.7%, n = 6 out of 9, measured at 10 min after tetanus). When stimuli were applied in the presence of the muscarinic agonist carbachol (20 microM), LTP of greater amplitude was induced in both paradigms (resting: 41.5%, n = 11 out of 16, depolarized: 36%, n = 5 out of 7, measured at 10 min after tetanus). Increases in excitatory postsynaptic potential (EPSP) amplitudes in the presence of carbachol were gradual, starting at the time 5 Hz stimuli were applied and continuing until an action potential was evoked synaptically. In the presence of the NMDA receptor antagonist 2-amino-5-phosphonovaleric acid (APV), LTP could not be induced. The muscarinic antagonist atropine also prevented LTP induction in the presence of carbachol. Cholinergic modulation of synaptic plasticity was examined in a previously developed realistic biophysical network simulation. In simulations, use of a gradual rate of synaptic modification prevented excessive strengthening of synapses, which could cause interference between stored patterns. The effect of excess synaptic strengthening can be avoided by introducing activity dependent depression of synaptic strength. Coactivation of learning and depression rules results in a stable system where no interference occurs, at any rate of learning. Implementing the depression rule only during recall does not improve the network's performance. This implies that reduction in the strength of synaptic connections should occur in the presence of ACh, more than in normal conditions. We propose that two effects of ACh--enhancement of LTP and enhancement of LTD--should act together to increase the stability of the cortical network in the process of acquiring information.

Acetylcholine↗

Nerve gas-induced seizures: role of acetylcholine in the rapid induction of Fos and glial fibrillary acidic protein in piriform cortex.

Soman (pinacolymethylphosphonofluoridate), a highly potent irreversible inhibitor of acetylcholinesterase (AChE), causes seizures and rapidly increases Fos and glial fibrillary acidic protein (GFAP) staining in piriform cortex (PC). This suggests that the inhibition of AChE by soman leads to increased acetylcholine (ACh) and neuronal excitability in PC. The sole source of cholinergic input to PC is from the nucleus of the diagonal band (NDB). To investigate the role of ACh in soman-induced seizures, we lesioned cholinergic neurons in NDB unilaterally with 192-IgG-saporin. By 10 d, saporin eliminated staining for choline acetyltransferase (ChAT), the synthetic enzyme for ACh, in NDB ipsilateral to the lesion. Staining for AChE, the degradative enzyme for ACh, was eliminated in PC ipsilateral to the lesioned NDB. By 45-60 min after soman, increased Fos and GFAP staining in PC was evident only ipsilateral to the unlesioned NDB. By 90-120 min after soman, Fos and GFAP staining increased bilaterally in PC. In a second experiment, electrical stimulation electrodes were implanted unilaterally in the NDB to activate focally the projections to PC in unanesthetized rats. Within 5 min of NDB stimulation, there were clear behavioral and EEG signs of convulsions. After 45-60 min of NDB stimulation, there was increased Fos and GFAP staining in layer II of PC ipsilateral to the stimulation site. Pretreatment with the selective muscarinic receptor antagonist scopolamine blocked the convulsions and prevented increased Fos and GFAP staining in PC. These results suggest that ACh release in PC triggers the initiation of seizures and gliosis after soman administration, predominantly by the activation of muscarinic receptors.

Acetylcholine↗

Repeated tetanic stimulation in piriform cortex in vitro: epileptogenesis and pharmacology.

1. Focal cortical epilepsy was investigated by applying tetanic stimulation repeatedly (100 Hz. 2 s in duration, once every 10 min, 10 episodes) to layer III association fibers in rat piriform cortex slices and recording both extracellular and intracellular responses from the endopiriform nucleus. To promote excitability, piriform slices were incubated in artificial cerebrospinal fluid (ACSF) containing 0.9 mM Mg2+ and 5 mM K+, at an initial temperature of 10-12 degrees C, which was allowed to warm passively to room temperature. 2. Responses recorded extracellularly in the endopiriform nucleus consisted of two types: weak stimulation evoked an early-occurring, small-amplitude, negatively deflecting potential; strong stimulation evoked a more complex response comprising both an early potential of maximal amplitude and a later-occurring epileptiform potential of greater amplitude and longer duration. Late-occurring epileptiform potentials were not observed in slices incubated in ACSF at room temperature. 3. Both the early potential and the late-occurring epileptiform responses were abolished by the non-N-methyl-D-aspartic acid (non-NMDA) subtype of glutamate receptor blocker, 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX; 10 microM). Application of D(-)-2-amino-5-phosphonopentanoic acid (APV; 50 microM) to block NMDA receptors was without effect on the early potential but diminished the late-occurring epileptiform potential. The late-occurring potential was unable to follow stimulation delivered at a frequency of 1 Hz. These results suggest that the early potential was generated monosynaptically and dependent solely on the activation of non-NMDA receptors, whereas the late-occurring epileptiform potential was polysynaptic in origin and possessed both a CNQX- and an APV-sensitive component. 4. Responses increased progressively in both amplitude and duration after tetanic stimulation. The threshold intensity required to evoke the complex dual-component potential was reduced by tetanic stimulation. An increase in multiunit spiking activity, indicating an increase in synchronous discharges, was also observed. A residual potential could be evoked in the presence of CNQX (10 microM) after the tetanic stimulation procedure. 5. Spontaneous discharges occurred as early as after the first episode of tetanic stimulation and persisted for the duration of the experiment. Spontaneous discharges were abolished by either CNQX or by a fourfold increase in extracellular Mg2+ concentration, the latter reversibly. APV reduced the frequency of spontaneous discharges by 38.6 +/- 9.3% (mean +/- SE). The conventional anticonvulsant drug 5,5-diphenylhydantoin, the benzodiazepine receptor agonist midazolam, and the benzodiazepine receptor antagonist flumazenil were without effect on the frequency of spontaneous discharges. Evoked responses were also unaffected by either 5,5-diphenylhydantoin or midazolam. Slices not exposed to cold ACSF, although demonstrating potentiation of evoked responses after tetanization did not produce spontaneous epileptiform discharges. 6. Intracellular recordings from endopiriform neurons revealed the cellular correlates of the extracellular responses. Weak stimulation evoked a small-amplitude depolarizing potential. Increasing the intensity of stimulation increased the amplitude of this response and also evoked a second depolarizing potential of greater amplitude occurring at variable latencies. Maximal stimulation evoked an action potential. After tetanic stimuli, responses resembling a paroxysmal depolarizing shift consisting of a depolarizing potential with superimposed multiple action potentials were evoked reliably. Passive membrane properties after repeated tetanic stimulation were not different when compared with control. 7. This novel model of in vitro focal cortical epilepsy has many features characteristic of conventional kindling including 1) progressive nature; 2) reduced threshold to evoke discharges; and 3) persist

Action Potentials↗

Electrophysiological connections of neurons in ventral pallidal regions of the olfactory tubercle with the main olfactory bulb and piriform cortex.

Field potential and single unit recordings were used to assess the connections of the olfactory tubercle (OT) with the main olfactory bulb (MOB) and the piriform cortex (PC) in urethane-anesthetized rats. Current generators of depth profiles evoked in OT following MOB stimulation were localized 300 microns superficial to those elicited by PC shocks, suggesting that afferents from the MOB and PC end in different regions of the OT. Following MOB and PC stimulation antidromically invaded neurons were recorded in the ventral pallidal regions of the OT and in the vicinity of the islands of Calleja, respectively. These results demonstrate that the OT, which receives a monosynaptic input from the MOB, projects back to the bulb and that the PC seems to be also reciprocally linked with differentiated structures in the OT.

Animals↗

Postsynaptic metabotropic glutamate receptor mGluR1 mediates the late component of signal propagation in the guinea pig piriform cortex: optical imaging study.

Metabotropic glutamate receptors (mGluRs) were previously shown to mediate a postsynaptic late propagation component elicited by layer Ib stimulation in guinea pig piriform cortex slices. In the present study, the effects of some group specific or subtype specific mGluR antagonists on the late propagation component were investigated using an optical imaging method, in order to identify mGluR subtypes mediating it. A selective mGluR1 antagonist (RS)-1-aminoindan-1,5-dicarboxylic acid most effectively suppressed the late component whereas a selective mGluR5 antagonist, selective group II or group III antagonists showed little or no suppressive effect. These results suggest that the late propagation component is mediated by mGluR1.

Animals↗

Evoked epileptiform discharges in the rat anterior piriform cortex: generation and local propagation.

The purpose of this study was to identify cellular and synaptic properties of neurons in a small region within the anterior piriform cortex (aPC), termed the area tempestas (AT), responsible for triggering forebrain seizures in rats. Using a brain slice preparation, we performed whole-cell patch recordings from neurons in the regions overlapping the functionally defined AT. Local electrical stimulation activated synaptic inputs to neurons in these regions, collectively termed the deep aPC (daPC). Synaptic inputs were blocked by selective ionotropic glutamate receptor antagonists. Excitatory bursts were evoked from 59% of daPC neurons as the stimulus intensity was raised above a precise threshold. Secondary bursts (6-15 Hz) occurred in 34% of daPC neurons. Evoked bursts were synaptically driven, as they were blocked by TTX (1 microM) or 2, 3-dihydroxy-6-nitro-7-sulfamoyl-benzo(f)quinoxaline (NBQX, 1 microM), but not by inclusion of cesium and N-(2, 6-dimethylphenylcarbamoylmethyl) triethylammonium (QX-314) in the internal patch solution. Neither augmentation of excitatory nor suppression of inhibitory transmission were required to evoke bursts from daPC neurons. However, bicuculline (20 microM) lowered the threshold intensity for evoking discharges and increased the incidence and duration of evoked bursts, indicating active inhibitory control of daPC neurons. Stimulation in the daPC evoked epileptiform field potentials from layer II of the adjacent PC and bursts from layer II pyramidal neurons. This work demonstrates that synaptically dependent excitatory burst discharges can be evoked from daPC neurons without altering the balance between synaptic excitation and inhibition. Stimuli that trigger bursts in daPC neurons also generate epileptiform activity in layer II pyramidal cells, indicating that propagation of excitatory activity triggered from the daPC to the pyramidal neurons of the aPC can contribute to the initiation of seizures induced by disinhibition of the AT in vivo.

Animals↗

The rapid anorectic response to a threonine imbalanced diet is decreased by injection of threonine into the anterior piriform cortex of rats.

Rats quickly recognize and reject diets deficient in an essential amino acid. The purpose of this study was to determine whether the anterior piriform cortex (APC), the site traditionally recognized as the amino acid chemosensor, plays a role in this early behavior. Rats had cannulae implanted bilaterally into the APC, and were injected with either saline vehicle or 2 nmoles of threonine (n = 6 per group). All rats were then fed a diet imbalanced with respect to threonine. The threonine-injected group had first meals of longer duration and consumed more food. These data conformed to expectations derived from earlier studies of responses to the first meal of an amino acid imbalanced diet. We conclude that the concentration of the dietary limiting amino acid in the APC regulates acceptance and rejection of amino acid deficient diets.

Amino Acids↗

Ultrastructure of synaptic remodeling in piriform cortex of adult rats after neonatal olfactory bulb removal: an immunocytochemical study.

The purpose of this investigation was to study possible remodeling in synaptic structures of the piriform cortex (PC) of adult rats following neonatal deafferentation by removal of the olfactory bulb (OB) at birth. Emphasis was placed on possible qualitative changes in the ultrastructure and immunocytochemical localization of cholecystokinin (CCK, a possible excitatory neurotransmitter or modulator) and glutamic acid decarboxylase (GAD, precursor enzyme to the inhibitory transmitter GABA) in axons, terminals, and synaptic complexes. Light microscopic results in normal adult material show that GAD-positive terminals form a dense band subjacent to the lateral olfactory tract (LOT), become less dense in deeper Ib, and are rare in layer II. Following deafferentation, GAD-positive terminals appear denser and more homogeneously distributed throughout layer I and are also more prevalent in layer II. Ultrastructural results of normals and controls indicate GAD-positive terminals normally contain pleomorphic or flattened vesicles and form symmetric contacts onto dendritic shafts and branches throughout layer I. In deafferented layer I not only do there appear to be greater numbers of symmetric GAD-positive contacts, but in contrast to normals, asymmetric contacts mainly onto spines are now present. Light microscopic results from deafferented material also show an apparent proliferation with spread or sprouting of CCK-positive fibers or axonlike structures mainly into layer Ia, whereas these fibers are normally observed only in the LOT and are generally few in number. Also in normals the few CCK-positive terminals in the area subjacent to the LOT contain flattened or pleomorphic vesicles and form symmetric contacts. Deafferentation results in CCK-positive terminals throughout layer I with a greater frequency of synaptic contacts which now also include a few asymmetric contacts onto spines. The findings clearly show modifications in synaptic patterns of immunocytochemical-labeled terminals that might be compatible with the process of atypical reinnervation of deafferented postsynaptic sites and possible ingrowth of new axons.

Animals↗

A large-scale simulation of the piriform cortex by a cell automaton-based network model.

An event-driven framework is used to construct a physiologically motivated large-scale model of the piriform cortex containing in the order of 10(5) neuron-like computing units. This approach is based on a hierarchically defined highly abstract neuron model consisting of finite-state machines. It provides computational efficiency while incorporating components which have identifiable counterparts in the neurophysiological domain. The network model incorporates four neuron types, and glutamatergic excitatory and GABA(A) and GABA(B) inhibitory synapses. The spatio-temporal patterns of cortical activity and the temporal and spectral characteristics of simulated electroencephalograms (EEGs) are studied. In line with previous experimental and compartmental work, 1) shock stimuli elicit EEG profiles with either isolated peaks or damped oscillations, the response type being determined by the intensity of the stimuli, and 2) temporally unpatterned input generates EEG oscillations supported by model-wide waves of excitation.

Action Potentials↗