PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “Olfactory Cortex”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 37 records · Page 2Linked to original sources

Neurogenesis in the rat primary olfactory cortex.

Neurogenesis in the rat primary olfactory cortex was examined with [3H]thymidine autoradiography. The experimental animals were the offspring of pregnant females given an injection of [3H]thymidine on two consecutive gestation days. Nine groups of embryos were exposed to [3H]thymidine on E13-E14, E14-E15....E21-E22, respectively. On P60, the percentage of labeled cells and the proportion of cells originating during 24 hr periods were quantified at selected anatomical levels of the anterior and posterior piriform cortex, dorsal lateral peduncular cortex, and posterior two-thirds of the ventral agranular insular cortex. Throughout most of the primary olfactory cortex, deep cells are generated earlier than superficial cells: the 'inside-out' pattern. Neurons in the anterior (prepiriform) cortex are located lateral to the caudal anterior olfactory nucleus and olfactory tubercle, and are generated mainly between E14 and E18 in a caudal (older) to rostral (younger) neurogenetic gradient. Neurons in the posterior (periamygdaloid) cortex are located lateral to the caudal olfactory tubercle and amygdala, and are generated mainly between E14 and E17 simultaneously along the rostrocaudal plane. Superficial cells in the piriform cortex have some additional neurogenetic gradients; ventromedial cells forming transition zones with either the olfactory tubercle or amygdala originate earlier than cells located dorsally and laterally. In the posterior piriform cortex, younger neurons are located at middle dorsoventral levels while older neurons lie above and below. Neurons in the dorsolateral peduncular cortex originate between E14 and E20 in a caudal to rostral gradient of neurogenesis; caudal parts also have a lateral to medial neurogenetic gradient. The most lateral part of the dorsolateral peduncular cortex is unique and does not have the typical 'inside-out' cortical neurogenetic gradient. Neurons in the ventral agranular insular cortex (area 13) originate mainly between E15 and E17 in combined caudal to rostral and ventral to dorsal neurogenetic gradients. The neurogenetic gradients in the primary olfactory cortex, along with patterns of neurogenesis throughout the olfactory projection field are related to the termination patterns of afferents from the main olfactory bulb.

Animals↗

Effect of lesions of the olfactory bulb on the levels of amino acids and related enzymes in the olfactory cortex of the guinea pig.

Olfactory bulb removal and consequential degeneration of the lateral olfactory tract led to a decrease in the levels of glutaminase and malate dehydrogenase in the ipsilateral olfactory cortex. These changes in enzyme activity may account for the well established decrease in the levels of aspartate and glutamate in the olfactory cortex following ipsilateral bulbectomy. The level of glutamine synthetase, a glial marker enzyme, was slightly increased while the activities of glutamate decarboxylase, glutamate dehydrogenase, and glutamate oxaloacetic transaminase were unchanged.

Amino Acids↗

Calcium-dependent inward currents in voltage-clamped guinea-pig olfactory cortex neurones.

Guinea-pig olfactory cortex neurones in vitro (23 degrees C--25 degrees C) were voltage clamped by means of a single microelectrode sample-and-hold technique. In most Cs+-loaded neurones (in the presence of tetrodotoxin), membrane depolarization beyond -60 mV elicited inward currents, which had rapid activation kinetics. The steady-state current-voltage relationship was N-shaped with a region of negative slope conductance between - 50 mV and - 20 mV. The rate of inactivation varied according to the holding potential and the command potential. The inward currents were maintained when external Ca2+ was replaced by Ba2+, and were blocked by Cd2+, suggesting that Ca2+ was the principal charge carrier. The results demonstrate the existence of calcium current in olfactory cortex neurones.

Animals↗

Studies on unmyelinated axons and varicosities in the olfactory cortex.

The main afferent input to the olfactory cortex from the olfactory bulbs is via the lateral olfactory tract (LOT). The axons within the lateral olfactory tract are myelinated. On leaving the LOT, they lose their myelination as they fan out over the layer immediately beneath the pial surface to make en passant synaptic connections with dendrites from neurones within the olfactory cortex. Using the guinea-pig, a semiquantitative electron micrographical study was made of the density and dimensions of these unmyelinated axons and the varicosities they create. The unmyelinated axons were very fine (0.17 +/- 0.004 micron in diameter) and punctuated at 2 microns intervals by varicosities containing a single type of vesicle. The electrophysiological consequences of this close varicosity spacing is that axonal and varicosity membranes behave electrically as single units.

Animals↗

Patterns of endogenous amino acid release from slices of rat and guinea-pig olfactory cortex.

A study has been made of the effects of depolarizing stimuli on the release of endogenous amino acid neurotransmitter candidates (aspartate, glutamate, GABA and taurine) from in vitro preparations of rat and guinea pig olfactory cortex. Exposure of small cubes of olfactory cortex tissue from either species to potassium chloride (50 mM) was accompanied by a calcium-dependent release of aspartate, glutamate and GABA. A similar release pattern was evoked by protoveratrine A (100 muM) although the release was largely calcium-independent. Neither agent led to increased release of taurine. Electrical stimulation of the excitatory input (lateral olfactory tract) of freshly prepared, synaptically intact olfactory cortex slices of both species induced significant release of aspartate and GABA from the uncut pial surface and of aspartate, GABA and glutamate from the cut surface. Evoked taurine release occurred from both surfaces of rat olfactory cortex slices but no release was detected from guinea pig olfactory cortex slices. These patterns of release were unaffected by changes in stimulus frequency and were mimicked by protoveratrine A (100 muM) applied to one or other surface. Preincubation of slices from rats for 2 led to loss of tissue amino acids and to changes in their release patterns; the presence of glutamine (5 mM) during preincubation prevented the loss of amino acids but did not alter their pattern of release. Because of the close similarities between both the electrophysiological properties and the patterns of amino acid release it is concluded that there is probably an identity of amino acid neurotransmitters (aspartate, glutamate and GABA) in rat and guinea pig olfactory cortex. The role of taurine in the rat olfactory cortex is unknown but would seem unlikely to be that of a neurotransmitter. The results are discussed: (i) in terms of the cellular origins of the released amino acids; and (ii) wit respect to apparent experimental discrepancies which have appeared in the literature.

Amino Acids↗

Odor maps in the olfactory cortex.

In the olfactory system, environmental chemicals are deconstructed into neural signals and then reconstructed to form odor perceptions. Much has been learned about odor coding in the olfactory epithelium and bulb, but little is known about how odors are subsequently encoded in the cortex to yield diverse perceptions. Here, we report that the representation of odors by fixed glomeruli in the olfactory bulb is transformed in the cortex into highly distributed and multiplexed odor maps. In the mouse olfactory cortex, individual odorants are represented by subsets of sparsely distributed neurons. Different odorants elicit distinct, but partially overlapping, patterns that are strikingly similar among individuals. With increases in odorant concentration, the representations expand spatially and include additional cortical neurons. Structurally related odorants have highly related representations, suggesting an underlying logic to the mapping of odor identities in the cortex.

Animals↗

Endogenous adenosine inhibits excitatory transmission in the rat olfactory cortex slice.

Excitatory neurotransmission in the rat olfactory cortex slice has been monitored by measuring the amplitude of the N-wave surface field potential evoked by stimulation of the lateral olfactory tract. Application of exogenous adenosine or aspartate depressed the N-wave amplitude and evoked synthesis of cyclic AMP. These effects were partially antagonized by theophylline and the reduction of amplitude of the N-wave was potentiated by dipyridamole. When the olfactory tract slice was stimulated, dipyridamole alone reduced the amplitude of the N-wave and increased levels of cyclic AMP, both effects being antagonized by theophylline. Exogenous adenosine significantly attenuated the K+-evoked release of [3H]D-aspartate by a mechanism insensitive to either theophylline or dipyridamole. It is concluded that synaptic activation of the olfactory cortex releases adenosine, possibly as the result of the actions of the transmitter candidate of the olfactory tract, aspartate, and that this causes sufficient adenosine to accumulate to depress excitatory transmission and elevate tissue levels of cyclic AMP although there is no positive evidence that these two effects are directly related.

1-Methyl-3-isobutylxanthine↗

Near-infrared spectroscopy of the adult human olfactory cortex.

OBJECTIVE: Near-infrared spectroscopy (NIRS) is a non-invasive method for investigating activation of the human cortex. The applicability of NIRS to the olfactory cortex was investigated. MATERIAL AND METHODS: The relative oxy- and deoxy-hemoglobin levels of the orbito-frontal cortex during olfactory stimulation in healthy subjects were measured using NIRS. RESULTS: When perfumed strips containing the odorants beta-phenyl ethyl alcohol, iso-valeric acid and gamma-undecalactone were presented, the oxy-hemoglobin level increased but the deoxy-hemoglobin level did not change. The increase in the oxy-hemoglobin level was observed bilaterally. A placebo perfumed strip did not elicit a change in the hemoglobin level. It was also observed that the odorant intensity affected the oxy-hemoglobin level. Although the orbito-frontal cortices seemed to be activated bilaterally during olfaction, the right cortex was activated to a greater extent than the left. CONCLUSION: NIRS appears to be an adequate method for investigating the human olfactory cortex.

Adult↗

Effects of pentobarbitone on the synaptically evoked release of the amino acid neurotransmitter candidates aspartate and GABA from rat olfactory cortex.

1. In the rat olfactory cortex slice, sub-anaesthetic concentrations of pentobarbitone reduce the amplitude of the N-wave with a concomitant reduction in the release of the excitatory transmitter aspartate. The pentobarbitone induced potentiation of the GABA-mediated I-wave is accompanied by increased GABA release. Although the changes in transmitter release and evoked electrical activity are consistent, there is only circumstantial evidence that the phenomena are related. 2. Pentobarbitone also reduced release of taurine although the significance (if any) of this finding is obscure. 3. The results are discussed in terms of the mechanisms by which pentobarbitone induces the changes in amino acid release.

Animals↗

Functional properties of regenerated optic axons terminating in the primary olfactory cortex.

When the optic nerve of Rana pipiens is cut and deflected into the telencephalon, the regenerating fibers terminate selectively in the superficial neuropil of the primary olfactory cortex. These redirected fibers and their terminals on the dendrites of the cortical cells appear normal by LM and EM criteria. Electrical recording, done 2-16 months after surgery, shows visually evoked activity in the superficial neuropil (Layer I) of the olfactory cortex, and visually excited responses in the deep cortical cell layer (Layer II). In the normal frog, the electrical activity seen in the neuropil of the olfactory cortex consists of small transients about 2-3 x the noise level of the electrode contact. These occur spontaneously and are also excited by puffs of air to the nose. There is no such excitation by visual stimuli. Larger initially negative spikes cell above noise level are recorded in the cell layer next to the ependymal surface, and these are also spontaneous, or excited by puffs of air to the nose, but not by visual stimuli. In the operated frog, the small transients in the neuropil appear and are excited by the puffs of air and by visual stimuli. Similarly the responses in the cell layer are excited by both sorts of stimuli. But new types of electrical signals appear in the neuropil; they are driven only by visual stimuli presented to the affected eye. These are very large transients of the kind found in the tectal neuropil and have the two characteristic shapes which were classified as B and C types in the tectum. Such large transients are never seen in the neuropil of the olfactory cortex in normal frogs. The receptive fields of the small visually driven transients in the neuropil are not easy to make out because the signal levels are so close to the noise level that different units cannot be reliably distinguished from each other. But the receptive fields of the much larger B and C type unit responses are as easy to classify and plot as they are in tectum, even though on the average they are only about 2/3 as large as in tectum. The single-unit receptive fields belong to one or another of the several types of retinal ganglion cell classes distinguished in optic-nerve recordings. Four of the major classes normally project to the tectum and a fifth projects to the lateral geniculate complex. But all five are present in the ectopic projection to the olfactory cortex.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

The rules of formation of the olfactory representations found in the orbitofrontal cortex olfactory areas in primates.

Approximately 35% of neurons in the orbitofrontal cortex taste and olfactory areas with olfactory responses provide a representation of odour that depends on the taste with which the odour has been associated previously. This representation is produced by a slowly acting learning mechanism that learns associations between odour and taste. Other neurons in the orbitofrontal cortex respond to both the odour and to the mouth feel of fat. The representation of odour thus moves for at least some neurons in the orbitofrontal cortex beyond the domain of physico-chemical properties of the odours to a domain where the ingestion-related significance of the odour determines the representation provided. Olfactory neurons in the primate orbitofrontal cortex decrease their responses to a food eaten to satiety, but remain responsive to other foods, thus contributing to a mechanism for olfactory sensory-specific satiety. It has been shown in neuroimaging studies that the human orbitofrontal cortex provides a representation of the pleasantness of odour, in that the activation produced by the odour of a food eaten to satiety decreases relative to another food-related odour not eaten in the meal. In the same general area there is a representation of the pleasantness of the smell, taste and texture of a whole food, in that activation in this area decreases to a food eaten to satiety, but not to a food that has not been eaten in the meal.

Animals↗

The trajectory of mitral cell axons in the rabbit olfactory cortex revealed by intracellular HRP injection.

The projection of the axon and axon collaterals of mitral cells to the olfactory cortex was studied in the rabbit by intracellular staining with horseradish peroxidase (HRP). The stained mitral cell axons were reconstructed from the soma to the most caudal portion of the anterior piriform cortex (aPC). Single mitral cells projected to cytoarchitectonically different areas of the olfactory cortex, i.e., the anterior olfactory nucleus (AON), the aPC, and the olfactory tubercle (OT). All the stained mitrall cells projected to both the AON and the aPC, and about one-fourth of the mitral cells projected to the OT. At the surface of the AON and the aPC, the main axon running in the lateral olfactory tract (LOT) gave off several thin collaterals at various intervals. The collaterals did not project evenly in each area but typically formed patchy terminal arbors which tended to be elongated anteroposteriorly. In both the AON and the aPC, each single mitral cell formed several terminal arbors in layer Ia. The axon collaterals innervating the OT showed two types of projection patterns. One type of collateral was emitted from the main axon within the olfactory bulb, coursed through the ventro-medial portion of the olfactory peduncle without joining the main mass of the LOT and terminated mainly in the medial portion of the OT. The other type of collateral emerged from the main axon in the LOT, coursed medioposteriorly, and projected to the lateral portion of the OT. Although individual mitral cells projected to several parts of the olfactory cortex, the fact that they made dense terminal arbors in specific places in each area suggests that the bulbocortical connections are not diffuse but highly selective.

Animals↗

Action of alpha-dendrotoxin on K+ currents in nerve terminal regions of axons in rat olfactory cortex.

1. In the rat olfactory cortex, unmyelinated axons give rise to synapses en passant. This tissue was used to study the pharmacology of axonal K(+)-currents. Responses were measured from a group of these axons as unclamped field currents, with a polarizable suction electrode. 2. A single stimulus to the axons elicited a tetrodotoxin-sensitive Na(+)-dependent transient K(+)-currents were revealed by positive polarization of the suction electrode and were manifest as a negative current following the Na(+)-component. 3. In the presence of tetraethylammonium (TEA, 5 mM) and Cd2+ (100 microM), the K(+)-component was depressed by 3,4-diaminopyridine (3,4-DAP; 1 to 20 microM; IC50 2.0 +/- 0.4 microM). alpha-Dendrotoxin (DTX; 15-1500 nM) also attenuated the aminopyridine-sensitive component (IC50 93 +/- 4 nM). At the highest DTX concentration, depression of the K(+)-current was incomplete, the residual K+ current being reduced by 3,4-DAP (0.1 to 5 microM). 4. These results indicate the presence of two aminopyridine-sensitive K+ currents in this preparation distinguished by their susceptibility to DTX.

4-Aminopyridine↗

Developmental factors affecting regeneration in the central nervous system: early but not late formed mitral cells reinnervate olfactory cortex after neonatal tract section.

If the lateral olfactory tract (LOT) of the golden hamster is transected in the first week of postnatal life, axons will grow back through the cut and reinnervate the terminal regions. Functional recovery occurs only when the terminal regions are reinnervated. The experiments reported here tested the hypothesis that reinnervation is due to neogenesis: the continued growth of newly formed axons which were not severed by the lesion. In the first experiment the birth dates of the mitral and tufted cells were determined in the hamster. It was found that mitral cells are formed on gestational days 11 and 12 (E11 and E12) and tufted cells on E11 to E14. Experiment 2 involved the combination of [3H]thymidine labeling, for the time of cell formation, with the retrograde transport of horseradish peroxidase (HRP), at a time when the LOT projections are not yet complete. The axons of early formed cells were found to reach the olfactory cortex before those of later formed cells. Experiment 3 examined the possibility that the axons which grow through an early LOT transection are new axons that had not yet reached the level of the cut. Animals were given [3H]thymidine to label the times of formation of mitral and tufted cells and then were given a transection of the LOT on postnatal day 3 (P3). After a recovery period sufficient to allow axonal regrowth and reinnervation, HRP was placed in the olfactory projection region caudal to the prior LOT section. The original hypothesis was not supported. Cells that are formed early and send out their axons early are able to reinnervate the olfactory cortex, whereas late formed cells do not. The results of this experiment suggest that the factors which prevent the regrowth of axons when the LOT is cut after P7 may depend on the stage of development of the tissue into which the axons are growing, rather than in the cells of origin and their axons.

Animals↗

Pharmacological evidence that NMDA receptors contribute to mono- and di-synaptic potentials in slices of mouse olfactory cortex.

Experiments have been carried out using slices of olfactory cortex of the mouse perfused in solution containing Mg2+ (1 mM) and in which the lateral olfactory tract was stimulated at a frequency of 1 pulse/5 sec to avoid polysynaptic activity. Application of the N-methyl-D-aspartate antagonist D-(-)-2-amino-5-phosphonopentanoic acid (APP, 25 microM) suppressed a low amplitude component of the potential, the latency to onset of which corresponded with that of the monosynaptically evoked N-wave in 14 of the 17 slices tested and duration of which exceeded that of the N-wave. A residual potential, recorded in slices to which the quisqualate-/kainate-selective antagonist 6,7-dinitroquinoxaline-2,3-dione (DNQX) had been applied at a concentration of 10microM, was identical to the potential suppressed by APP. The residual potential in the presence of DNQX was blocked by APP, 7-chlorokynurenate (25 microM) and (+)-5-methyl-10,11-dihydro-5H-dibenzo[a,d]cyclohepten-5,10-imine maleate (MK801, 0.125-2 microM). It was potentiated in area by exogenous D-serine (1 mM) and in slices preincubated and perfused with Mg(2+)-free solution. It is concluded that, in addition to receptors of the quisqualate/kainate categories, N-methyl-D-aspartate receptors also contribute to both mono- and di-synaptic excitations in the olfactory cortex.

2-Amino-5-phosphonovalerate↗

M-current in voltage-clamped olfactory cortex neurones.

The soma of olfactory cortex neurones in vitro was voltage-clamped by means of a single microelectrode sample-and-hold technique. In most neurones, hyperpolarizing voltage commands from relatively positive holding potentials (-40 to -50 mV) elicited a slow inward current relaxation with voltage-dependent and kinetic properties similar to the non-inactivating K+-current (M-current; IM), first described in amphibian sympathetic neurons. Deactivation of IM at negative potentials probably accounts for the slow sag of the hyperpolarizing electrotonic potential measured during current-clamp experiments. IM was inhibited by the cholinergic agonist muscarine or barium ions.

Animals↗

State-dependent sensory gating in olfactory cortex.

Sensory systems show behavioral state-dependent gating of information flow that largely depends on the thalamus. Here we examined whether the state-dependent gating occurs in the central olfactory pathway that lacks a thalamic relay. In urethane-anesthetized rats, neocortical EEG showed a periodical alternation between two states: a slow-wave state (SWS) characterized by large and slow waves and a fast-wave state (FWS) characterized by faster waves. Single-unit recordings from olfactory cortex neurons showed robust spike responses to adequate odorants during FWS, whereas they showed only weak responses during SWS. The state-dependent change in odorant-evoked responses was observed in a majority of olfactory cortex neurons, but in only a small percentage of olfactory bulb neurons. These findings demonstrate a powerful state-dependent gating of odor information in the olfactory cortex that works in synchrony with the gating of other sensory systems. They suggest a state-dependent switchover of signal processing modes in the olfactory cortex.

Animals↗