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At least 127 records · Page 7Linked to original sources

PubMed2002

Temporal-to-spatial dynamic mapping, flexible recognition, and temporal correlations in an olfactory cortex model.

This paper proposes temporal-to-spatial dynamic mapping inspired by neural dynamics of the olfactory cortex. In our model the temporal structure of olfactory-bulb patterns is mapped to the spatial dynamics of the ensemble of cortical neurons. This mapping is based on the following biological mechanism: while anterior part of piriform cortex can be excited by the afferent input alone, the posterior areas require both afferent and association signals, which are temporally correlated in a specific way. One of the functional types of the neurons in our model corresponds to the cortical spatial dynamics and encodes odor components, and another represents temporal activity of association-fiber signals, which, we suggest, may be relevant to the encoding of odor concentrations. The temporal-to-spatial mapping and distributed representation of the model enable simultaneous rough cluster classification and fine recognition of patterns within a cluster as parts of the same dynamic process. The model is able to extract and segment the components of complex odor patterns which are spatiotemporal sequences of neural activity.

Animals↗

PubMed1984

Amino acid transmitter candidates in various regions of the primary olfactory cortex following bulbectomy.

The effect of bulbectomy on amino acid levels in 5 regions of the rat primary olfactory cortex has been monitored. Glutamate levels were significantly lowered in the lateral olfactory tract only. In contrast, aspartate levels were significantly reduced in all regions except the periamygdaloid cortex. The results suggest transmitter heterogeneity of the tract fibres and confirm a likely transmitter role for aspartate for some tract terminals.

Amino Acids↗

PubMed2004

Attentional modulation in human primary olfactory cortex.

Central to the concept of attention is the fact that identical stimuli can be processed in different ways. In olfaction, attention may designate the identical flow of air through the nose as either respiration or olfactory exploration. Here we have used functional magnetic resonance imaging (fMRI) to probe this attentional mechanism in primary olfactory cortex (POC). We report a dissociation in POC that revealed attention-dependent and attention-independent subregions. Whereas a temporal subregion comprising temporal piriform cortex (PirT) responded equally across conditions, a frontal subregion comprising frontal piriform cortex (PirF) and the olfactory tubercle responded preferentially to attended sniffs as opposed to unattended sniffs. In addition, a task-specific anticipatory response occurred in the attention-dependent region only. This dissociation was consistent across two experimental designs: one focusing on sniffs of clean air, the other focusing on odor-laden sniffs. Our findings highlight the role of attention at the earliest cortical levels of olfactory processing.

Adult↗

PubMedDate not supplied

The effects of corticoliberin at different concentrations on long-term potentiation in slices of rat olfactory cortex.

Experiments were performed to investigate evoked focal potentials in slices of rat olfactory cortex. The results showed that 1 microM corticotropin-releasing factor (CRF; corticoliberin) increases the frequency of posttetanic potentiation, which had a shorter delay phase than in control experiments. Posttetanic potentiation during perfusion with 0.1 microM corticoliberin had a longer delay phase than in control experiments.

Animals↗

PubMed1994

NMDA antagonists increase recovery of evoked potentials from slices of rat olfactory cortex after anoxia.

1. The role of glutamate in producing tissue damage during cerebral anoxia was investigated in brain slices using antagonists to the NMDA and AMPA receptor types. 2. Tissue function was assessed by field recordings of the synaptically evoked potentials elicited by stimulating the main afferent input to the olfactory cortex, the lateral olfactory tract. Anoxia was produced by bathing the slice in glucose-free solution equilibrated with 95% N2/5% CO2. 3. The amount of recovery of the evoked potential was inversely dependent on the period of anoxia and temperature: at 24 degrees C, 15 min of anoxia followed by reoxygenation produced a 14.6 +/- 4.1% recovery whereas there was no recovery at 35 degrees C. 4. Dizocilpine and ketamine had no effect on synaptic transmission in oxygenated media but following anoxia they produced an increased recovery of the responses: from 14.6 +/- 4.1% to 48.3 +/- 7.8% for dizocilpine (10 microM) and 21.6 +/- 7.7% to 87.2 +/- 7.1% for ketamine (200 microM); the tissue endurance to anoxia was increased by around 5 min. 5. Blockade of the AMPA receptors did not influence recovery in spite of the depressed synaptic transmission. A similar synaptic attenuation produced by lignocaine provided some increase in post-anoxic recovery. 6. The NMDA receptor antagonist, AP5, antagonized NMDA at 50 microM by 3.7 fold and at 200 microM by 15 fold but only 200 microM increased post-anoxic recovery. This suggests that a substantial degree of NMDA antagonist is required before anoxic tissue damage due to NMDA receptor activation can be nullified. The antagonist to the glycine binding site, 7-chlorokynurenic acid also increased recovery. 7. These in vitro experiments confirm the idea that NMDA receptor activation makes a substantial contribution to cerebral tissue damage and that this can be reduced by a substantial blockade of these receptors.

2-Amino-5-phosphonovalerate↗

PubMedDate not supplied

Pharmacological evidence that protein kinase C modulates monosynaptic excitations in the olfactory cortex.

The possible occurrence and role of protein kinase C at the lateral olfactory tract (LOT)-pyramidal cell synapse of the rat olfactory cortex slice has been investigated by determining the effects of both activators (4-beta-phorbol-12,13,diacetate [PDAc] and 1,2-dioctanoyl-sn-glycerol) and inhibitors (5-isoquinolinylsulphonyl)-2-methylpiperazine [H-7], sangivamycin and polymyxin B) of the enzyme on the surface field potential known as the N-wave. PDAc (0.3 to 20 mumol/l) and 1,2-dioctanoyl-sn-glycerol (25 to 250 mumol/l) increased the area and amplitude of the potential. In control slices in which a population spike was recorded, PDAc also triggered the appearance of multiple spikes. In a series of input-output experiments, PDAc (2.5 or 5 mumol/l) increased the area and amplitude of the N-wave relative to that of the action potential but did not significantly affect pyramidal cell excitability. The effects of PDAc on the N-wave were antagonised by all three protein kinase C inhibitors but not by the calmodulin antagonist calmidazolium and were greater in slices perfused with solution containing 10 rather than 1 mmol/l Mg2+ or 1.25 rather than 5 mmol/l Ca2+. The effect of PDAc on the amplitude but not area of the N-wave was blocked by the potassium channel blocker tetraethylammonium (10 mmol/l) but not by 4-aminopyridine (0.25 mmol/l). In a series of conditioning experiments, PDAc (1 to 5 mumol/l) reduced the amplitude of the N-wave evoked by a second stimulus compared to that evoked by the first conditioning pulse.(ABSTRACT TRUNCATED AT 250 WORDS)

Action Potentials↗

PubMed1968

Electrical activity observed in guinea-pig olfactory cortex maintained in vitro.

1. Electrical recordings were made from a preparation of guinea-pig olfactory cortex maintained in vitro.2. The response of the prepiriform area to a volley delivered to the lateral olfactory tract comprised a sharp negative deflexion upon which several positive notches were superimposed followed by a long-duration low-amplitude positive wave.3. Both the negative and positive waves were of maximal amplitude near the top surface of the preparation (the original cortical surface).4. Units recorded at depths of 250-350 mu showed facilitation and latency variation. The latency distribution of these spikes was very similar to that of the positive notches observed on the surface of the slice.5. The surface observed negative waves were rapidly abolished by oxygen lack.6. The negative and positive waves have been tentatively identified as the extracellular manifestations of the excitatory post-synaptic potentials (EPSPs) and inhibitory post-synaptic potentials (IPSPs) occurring in the apical dendrites.7. Some spontaneous activity was observed in a proportion of the preparations studied.8. The evidence presented here strongly supports the contention that portions of the mammalian brain may be maintained in a satisfactory functional condition when isolated from the body, provided that they are maintained in a suitable environment. We believe that such preparations will prove very useful for physiological studies of the mammalian brain.

Action Potentials↗

PubMed1978

A depolarizing inhibitory potential in neurones of the olfactory cortex in vitro.

1. Stable intracellular recordings were obtained from neurones in slices of the guinea-pig olfactory cortex maintained in vitro. 2. Single stimuli applied to the lateral olfactory tract (l.o.t.) produced an excitatory post-synaptic potential (e.p.s.p.) usually generating a single spike. 3. The e.p.s.p. was followed by a long (200-500 msec) after-depolarization (l.a.d.) of peak amplitude 5-16 mV. This was accompanied by a very large conductance increase and was associated with an inhibition of the intracellularly recorded e.p.s.p. and of spike generation. 4. The l.a.d. was more susceptible than the e.p.s.p. to depression by (i) repetitive l.o.t. stimulation and (ii) raising external [Mg2+]. The l.a.d. could be generated without a preceding spike. 5. At an average resting membrane potential of -74 mV the average reversal potential for the l.a.d. (El.a.d.) was -63 mV.El.a.d. became more positive on reducing [Cl-]out or on using KCl-filled electrodes. 6. It is concluded that the l.a.d. represents a Cl- -mediated inhibitory post-synaptic potential, generated through deep-lying recurrent inhibitory loops.

Action Potentials↗

PubMed1989

A phorbol diester-induced enhancement of synaptic transmission in olfactory cortex.

1. Extracellular field synaptic potentials were recorded from pial surface slices of guinea-pig olfactory cortex maintained in vitro. 2. Phorbol 12,13-dibutyrate (0.1-10 microM) enhanced the amplitude of the evoked potential (by 51.2 +/- 10.4% with 1 microM) in normal solution. When the evoked potential was partially depressed by Cd, Co, Mn or a reduced Ca concentration, phorbol 12,13-dibutyrate (1 microM) induced a much larger enhancement of the evoked potential (196.5 +/- 24.4% increase). Phorbol 12,13-diacetate and mezerein had similar effects but were less potent. 4 beta-Phorbol (10 microM) had no effect. 3. The diacylglycerol analogues, dioctanoylglycerol (100-1000 microM), 1-oleoyl-2-acetylglycerol (100-500 microM) or diolein (100 microM) had no effect on the evoked potentials, either alone or in the presence of Cd. 4. The isoquinolinylsulphonamide inhibitor (H-7) of protein kinase C slightly enhanced the e.p.s.p. and had no effect on the potentiation produced by phorbol ester. Another protein kinase C inhibitor, acridine orange (100-1000 microM), had no effect on the action of phorbol ester. 5. These results show that transmitter release, as at other synapses, is enhanced by phorbol esters but Ca did not potentiate this action. The pharmacological profile of the effect on transmitter release differed from that of protein kinase C in cell-free preparations and therefore it is unclear whether protein kinase C was involved in the present study.

Animals↗

PubMed1994

A comparison of the muscarinic response and morphological properties of identified cells in the guinea-pig olfactory cortex in vitro.

The electrophysiological and morphological characteristics of neurons in the guinea-pig olfactory cortex brain slice were investigated using a combined intracellular recording and neurobiotin-dye filling technique, in an attempt to show whether a clear relation existed between cell morphology and excitatory muscarinic response profile. Out of 46 sampled neurons, 25 (termed type 1), responded to bath-application of the muscarinic agonist oxotremorine-M (10 microM, 2-3 min) with a strong and persistent excitation coupled with the appearance of a slow depolarizing afterpotential (10-20 mV amplitude) following a large depolarizing stimulus. These neurons were identified as deep pyramidal cells located in cortical layer III, with characteristic pyramidal/ovoid shaped cell bodies, prominent apical dendrites with branches extending to the surface, and extensive basal dendritic trees. The cells showed a regular spiking pattern in response to injected depolarizing current, with no evidence of bursting behaviour. Nine cells (termed type 2), were strongly excited by oxotremorine-M, but only generated a weak depolarizing afterpotential (< 5 mV) following stimulation. These neurons (located in layer III or at layer II-III border) had a variable, non-pyramidal morphology with either a fusiform/tripolar, stellate/multipolar or bipolar/bi-tufted appearance, respectively. Apart from a more prominent post-spike afterhyperpolarization observed in some type 2 cells, their resting membrane properties and firing patterns were indistinguishable from those of type 1 responding cells. Twelve cells (termed type 3) showed little or no excitatory response to oxotremorine-M, and never generated a post-stimulus slow afterdepolarization. These cells (within compact layer II) had the morphological features of superficial pyramidal cells, typified by their short apical trunks and well-developed apical dendritic trees. They could be distinguished electrophysiologically by their ability to show spike fractionation during injection of large depolarizing current pulses. The morphology and laminar position of neurobiotin-filled cells was also compared with those of cells stained by the Golgi-Cox method. Some factors that may have contributed to the observed differences in muscarinic response profile are discussed. It is proposed that the selective muscarinic induction of the slow depolarizing afterpotential phenomenon in deep pyramidal cells may be important in olfactory cortical learning and memory processes.

Animals↗

PubMed1991

Action of general anaesthetics on unclamped Ca(2+)-mediated currents in unmyelinated axons of rat olfactory cortex.

Na+ and Ca2+ currents were monitored using a suction electrode in unclamped presynaptic axons of rat olfactory cortex pretreated with 0.1 mM 3,4-diaminopyridine and 5 mM tetraethylammonium. The effects of anaesthetics on these currents were compared with tetrodotoxin or cadmium. Ketamine (0.1-1 mM), ether (20-200 mM), diisopropylphenol (0.01-0.5 mM) and lignocaine (0.01-0.2 mmol/l) all depressed both the initial Na+ component and the Ca(2+)-mediated tail of the response. Urethane (5-100 mM), halothane (1-5 mM) and pentobarbitone (0.1-2 mM) showed slight selectivity for the axonal Ca2+ tail. Diisopropylphenol apparently enhanced the Ca2+ tail at low concentrations. The alphaxalone (1-50 microM) depression was very weak. In a few cases the depression may contribute to anaesthesia but with others, high concentrations may contribute to the toxicity of the substances in vivo.

Anesthetics↗

PubMed1998

Inward-rectifying membrane currents activated by hyperpolarization in immature rat olfactory cortex neurones in vitro.

The properties of inward-rectifying membrane currents in immature rat olfactory cortex neurones (postnatal day (P) 10-22) were analysed using whole-cell patch-clamp recordings. In 78% of cells (40/51), injection of hyperpolarizing current pulses elicited graded electrotonic potentials showing a slowly developing sag in the membrane potential. Under voltage clamp, negative commands from -50 mV activated slow inward current (ISlow) relaxations whose amplitude and exponential rate of onset increased with increasing hyperpolarization (n=40); the ISlow activation time constant (tauon) ranged from 650+/-116 (mean+/-S.E.M.) ms at -70 mV to 177+/-18 ms at -120 mV; n=34). By contrast, in 11/51 neurones, similar negative commands revealed only fast-type inward rectification (IIR) with either rapid (n=9) or 'instantaneous' onset kinetics (n=2). ISlow activation threshold was at approximately -60 mV, with full activation at -120 mV; the half-maximal voltage (V0.5) and slope factor (k) of activation were: -85+/-0.4 mV and 11+/-0.5, respectively (n=13). The estimated reversal potential for ISlow was -28+/-2 mV (n=5). No obvious age-dependent changes in maximal ISlow current amplitude or density (at -120 mV) or in the proportion of cells showing IIR were found between P10 and P22. Islow was blocked by Cs+ (5 mM, n=6) or the specific h-current blocker ZD 7288 (50 microM, n=11) but not Ba2+ (500 microM, n=7); in contrast, IIR was blocked by Cs+ or Ba2+ but not ZD 7288. It is concluded that unlike adult olfactory cortical cells, immature olfactory neurones can exhibit both slow and fast-types of inward rectification: the more predominant ISlow component, resembled the h-current (Ih) previously identified in other central neurones.

Animals↗

PubMed2005

Synapse-specific downregulation of NMDA receptors by early experience: a critical period for plasticity of sensory input to olfactory cortex.

Olfaction is required at birth for survival; however, little is known about the maturation of olfactory cortical circuits. Here we show that in vivo sensory experience mediates the development of excitatory transmission in pyramidal neurons of rat olfactory cortex. We find a postnatal critical period during which there is an experience-dependent increase in the contribution of AMPARs versus NMDARs to transmission at primary sensory synapses but not associational inputs. The shift in receptors underlying transmission is mediated by a strong activity-dependent downregulation of NMDARs and modest increase in AMPARs. Sensory activity leads to a loss of "silent" NMDAR-only synapses and an increase in threshold for inducing long-term plasticity. These results indicate the importance of early olfactory experience in the establishment of cortical circuits and could reflect mechanisms governing early olfactory "imprinting."

Aging↗

PubMed2004

The effects of corticotropin-releasing factor on anoxia-induced changes in evoked potentials in living slices of rat olfactory cortex.

Experiments were performed to address the dynamics of evoked focal potentials in slices of rat olfactory cortex during 10-min anoxia and subsequent reoxygenation. These experiments showed that perfusion with corticotropin-releasing factor (CRF)--corticoliberin--at concentrations of 1, 10, and 100 nM had no effect on changes in EPSP parameters before or during anoxia. However, CRF (10 and 100 nM) significantly aided recovery of the amplitude and slope of EPSP during reoxygenation. Application of the competitive NMDA receptor blocker APV (50 microM) during reoxygenation did not eliminate the protective effects of CRF on neuronal activity.

Action Potentials↗

PubMed1987

Primordial synaptic structures and synaptogenesis in rat olfactory cortex.

Mature synaptic contacts and various primordial synaptic elements were studied, counted, and analyzed in rat olfactory cortex from birth to 30 days of age. Primordial structures possess one or a few, but not all, of the features of a true mature synapse and have been grouped into two major classes based upon type of apposition: 1) single or 2) partial and multiple, with vacant postsynaptic sites included in the latter. There is a classical fivefold increase in number of mature synapses between birth and 30 days, but different patterns in the primordial appositions are observed. It is suggested that single apposition contribute to early synapse formation, while partial and multiple appositions participate later on during a time of rapid growth of new afferents to the area. The results suggest a clear role for primordial synaptic structures in synaptogenesis; that the sequence may be more diverse than originally hypothesized, occurring at different stages; and that competition, synapse elimination, and replacement may be more prevalent in normal synaptogenesis than has been previously suspected.

Aging↗

PubMed1988

Electron microscopy of plasticity in rat olfactory cortex.

Electron microscopy (EM) is being used to study the ultrastructural basis for the age-dependent reorganization of afferents in the olfactory cortex (OC) of rat after deafferentation of the area by removal of the ipsilateral olfactory bulb (OB). The double-lesion technique was used with a primary lesion of the OB at various postnatal (PN) ages between PN 0 and 30 and in the adult (PN 100). After appropriate survival times to remove initial lesion-degenerated terminals from the OB lesion, a second lesion was placed in the ipsilateral OC. One to 3 days later the tissue is prepared for EM with emphasis on a study of changes in the superficial and deep dendritic layer (Ia and Ib respectively) rostral to the lesion. In control litter mates with both OBs intact, but with a single OC lesion only, degenerating synaptic terminals occur onto dendritic spines and branches only in deeper Ib. However, in adults with OB lesions at PN 0-9, OC lesions produce degenerating terminals throughout Ia and Ib including immediately subjacent to the pia. In Ia degenerating terminals are greatly reduced in the PN 13 group and rare to absent in experiments with OB lesions at older ages (PN 30-100). Electron-dense debris within glia occurs throughout layer I in each double-lesion group but is greatest in experiments with OB lesions at older ages. Some transsynaptic alterations are seen throughout, especially in the PN 30-100 group even at a distance from the OC lesion. The results support earlier light microscopic (LM) findings, suggesting PN 9-13 as critical ages for developmental plasticity and prove that at least in the younger ages, synapses are involved in the phenomenon. This may be explained by either reinnervation of deafferented sites or persistence of synapses that would otherwise have been eliminated by afferents from the OB. In addition, some of the LM degeneration particles probably are engulfed masses of debris and not synaptic structures, especially in cases which were operated at older ages and survived for 3 days. The various afferent pathways involved in the events as well as factors that limit the phenomenon in older ages are discussed.

Animals↗

PubMed1982

Convulsant actions of 4-aminopyridine on the guinea-pig olfactory cortex slice.

The effects of bath-applied 4-aminopyridine on neurones and extracellular potassium and calcium concentrations were recorded in slices of guinea-pig olfactory cortex. Neurones were orthodromically activated by stimulating the lateral olfactory tract. 4-Aminopyridine (3-10 microM) had the following effects: (1) an increase in the frequency and amplitude of spontaneous postsynaptic potentials; (2) a prolongation and oscillatory behaviour of orthodromically evoked postsynaptic potentials; (3) induction of spontaneous or stimulus-evoked seizure-type discharges which were accompanied by large rises in extracellular potassium and falls in calcium concentration; (4) a prolongation of the lateral olfactory tract population fibre spike. Prior to paroxysmal depolarization, membrane potential, input resistance and soma spike duration were unaffected. In the seconds before seizure discharges, a late hyperpolarizing potential (evoked by orthodromic stimulation) was reduced in amplitude or abolished. Diphenylhydantoin (50 microM) or magnesium ions (5 mM) prevented paroxysmal activity. Our results show that 4-aminopyridine can produce seizure-type discharges in a brain slice preparation. The role of increased spontaneous potentials and possible loss of synaptic inhibition as causal factors for such discharges is discussed.

4-Aminopyridine↗

PubMed1983

Levels and synthesis of glutamate and aspartate in the olfactory cortex following bulbectomy.

Guinea pigs were unilaterally bulbectomised and the contents of aspartate, glutamate and GABA measured in slices of olfactory cortex taken from the lesioned and intact hemispheres. Two days after the operation there was a fall in the aspartate and glutamate levels, which persisted for over 120 days, whereas gamma-aminobutyric acid (GABA) showed a transient fall followed by a small rise. The fall in glutamate and aspartate was much greater in small, thin slices containing a high density of nerve terminals. The synthesis of 13C aminoacids from [13C]glucose during electrical stimulation was greater in the slices taken from the normal side than in those from the operated side. The GABA synthesis, however, was four times greater on the lesioned side. This time-course for the fall in acidic amino acids correlates with the fall in electrical responses, and this lends weight to the idea that aspartate and/or glutamate mediate synaptic transmission in the area.

Animals↗