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Results for “Olfactory Cortex”

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At least 73 records · Page 4Linked to original sources

PubMed2006

Pax6-dependent boundary defines alignment of migrating olfactory cortex neurons via the repulsive activity of ephrin A5.

Neuronal migration is a prerequisite event for the establishment of highly ordered neuronal circuits in the developing brain. Here, we report Pax6-dependent alignment of the olfactory cortex neurons in the developing telencephalon. These neurons were generated in the dorsal part of telencephalon, migrated ventrally and stopped at the pallium-subpallium boundary (PSB). In Pax6 mutant rat embryos, however, these neurons invaded the ventral part of the telencephalon by crossing the PSB. Ephrin A5, one of the ligands for EphA receptors, was specifically expressed in the ventral part of the telencephalon, and its expression level was markedly reduced in the Pax6 mutant. Gain- and loss-of-function studies of ephrin A5 indicated that ephrin A5 plays an important role in the alignment of olfactory cortex neurons at the PSB. Our results suggest that Pax6-regulated ephrin A5 acts as a repulsive molecule for olfactory cortex neurons in the developing telencephalon.

Animals↗

PubMed1989

Effects of pentobarbitone, ketamine and lignocaine on synaptic transmission in the rat olfactory cortex in vitro.

The effects of pentobarbitone, ketamine and lignocaine on synaptic transmission in the rat olfactory cortex were studied. All agents depressed the presynaptic spike, the excitatory postsynaptic potential (EPSP) and the population spike evoked by stimulation of the lateral olfactory tract in a concentration-dependent manner. However, each anaesthetic had different effects on the processes of excitatory synaptic transmission. Pentobarbitone depressed primarily the EPSP, ketamine primarily the excitability of the presynaptic fibres and lignocaine the excitability of the presynaptic fibres; lignocaine also reduced the release of excitatory transmitters. None of the three agents influenced the passive membrane properties or the excitability of olfactory pyramidal cells. These data indicate that these agents block synaptic transmission in the olfactory cortex by different mechanisms.

Action Potentials↗

PubMed1987

Possible presynaptic actions of 2-amino-4-phosphonobutyrate in rat olfactory cortex.

1 The effect of 2-amino-4-phosphonobutyrate (APB) on facilitation at the lateral olfactory tract (LOT)-superficial pyramidal cell synapse of the olfactory cortex has been studied by recording the relative changes in amplitude of the N-waves evoked on stimulation of the LOT by pairs of stimuli. 2 Although APB (0.01 to 5 mM) reduced the amplitude of the conditioning response there was an overall increase in facilitation over conditioning intervals of up to 1700 ms which was concentration-dependent and inversely related to the concentration of extracellular calcium (1.25 to 5 mM). 3 The L-(+)-isomer of APB was more potent than the D-(-)-form in increasing synaptic facilitation. 4 The potassium channel blockers 4-aminopyridine (0.25 mM), 3,4-diaminopyridine (0.1 mM), tetraethylammonium (10 mM) and catechol (1 mM) all reduced facilitation but failed to antagonize the increase in facilitation produced by APB (1 mM). In contrast, all 4 drugs antagonized APB-induced reductions in the amplitude of the conditioning response. 5 APB (1 mM) significantly reduced the K+-evoked release of endogenous aspartate and glutamate but not of gamma-aminobutyric acid from slices of olfactory cortex. 6 It is suggested that APB reduces the amplitude of the conditioning response and increases synaptic facilitation by reducing transmitter release from the LOT terminals. The mechanism is unlikely to involve activation of terminal potassium currents.

Amino Acids↗

PubMed1993

Presence of C-flanking peptide of neuropeptide Y(C-PON)-immunoreactive neurons in the olfactory cortex of the hedgehog (Erinaceus europaeus).

Although the presence of the neuropeptide C-terminal flanking peptide of neuropeptide Y, C-PON, has been described in the central nervous system (CNS) of mammals, to date there is no information related with its involvement in brain functions. An analysis of the location of C-PON in specific neuronal circuits of known anatomy and physiological action should provide light on its physiological role. The presence, distribution and morphology of C-PON-containing neurons in the olfactory cortex of the hedgehog was studied by immunocytochemistry. Immunoreactive neurons to C-PON were widely distributed in the three layers of the olfactory cortex of this primitive mammal. These neurons were medium sized and showed two or three immunostained, poorly branched, dendrites. In some positive neurons, a fine, beaded axon-like process was also immunostained. Although direct evidence of a physiological function of C-PON in the olfactory cortex of the hedgehog cannot be accurately stated from our findings, the morphology of C-PON neurons and their distribution in the deep cortical layers, where the majority of pyramidal neurons are located, suggest that this neuropeptide may play a role in the intrinsic neuronal circuitry of the relatively well-developed hedgehog paleocortex. A regulatory vascular role of some peptide-immunoreactive neurons can be inferred since occasional C-PON-positive neurons have been located near blood vessels.

Animals↗

PubMed1982

Baclofen: effects on evoked field potentials and amino acid neurotransmitter release in the rat olfactory cortex slice.

A study has been made of the in vitro effects of (+/-)- and (-)-baclofen on the evoked field potentials and release of endogenous amino acid neurotransmitter candidates (aspartate, glutamate, GABA and possibly taurine) which accompany electrical stimulation of the excitatory input to the olfactory cortex slice, the lateral olfactory tract. Baclofen appears to reduce the excitatory input to the GABA-utilizing inhibitory interneurones; this action was manifest as a drug-induced abolition of the field potential known as the P-wave (IC50 for (-)-baclofen, 1.7 +/- 0.4 microM) together with a simultaneous reduction in the synaptically evoked release of aspartase and glutamate from the cut surface of slices. Both these actions of baclofen exhibited concentration dependence and stereospecificity and were not antagonized by picrotoxin (25 microM) thereby suggesting that they are directly related. The consequence of this action of baclofen was the abolition of GABA-mediated presynaptic and postsynaptic inhibition together with their respective field potential correlates, the late N- and I-waves. (+/-)-Baclofen (5 and 25 microM) also inhibited the potassium-evoked release of aspartate and glutamate from small cubes of tissue but, except at a high concentration (1 mM), had no effect on GABA release. Baclofen (up to 1 mM) did not affect transmission either at the lateral olfactory tract-superficial pyramidal cell synapse, a site where aspartate is the likely neurotransmitter, or at the superficial pyramidal cell collateral-deep pyramidal cell excitatory synapse. It is proposed that: (i) the actions of baclofen on the olfactory cortex are the result of inhibition of aspartate and glutamate release, probably from deep pyramidal cell collaterals; and (ii) not all neurones utilizing excitatory amino acids as their neurotransmitters are subject to the inhibitory action of baclofen.

Animals↗

PubMed1976

Possible presynaptic inhibition in rat olfactory cortex.

1. Field potentials were evoked from rat olfactory cortex slices in vitro at room temperature by lateral olfactory tract stimulation. At very slow stimulation rates (less than 0-1 Hz) a delayed negative wave (late N-wave) was found to follow the first negative wave (N-wave). This late N-wave started 30 msec after the stimulus and lasted for 50-150 msec. 2. Low Ca2+/high Mg2+ medium abolished the late N-wave more rapidly than the N-wave, suggesting a possible multisynaptic origin. 3. The GABA antagonist bicuculline (10(-6) M) abolished the late N-wave without affecting the N-wave. 4. During the late N-wave, both the tract action potential and the N-wave to a second stimulus were reduced. This was attributed, at least in part, to collision with antidromic action potentials which could be detected during the late N-wave. 5. These findings are discussed in terms of a possible presynaptic depolarizing action of a GABA-like transmitter giving rise to presynaptic inhibition and the late N-wave.

Animals↗

PubMed1985

Adenosine-induced depression of synaptic transmission in the isolated olfactory cortex: receptor identification.

We have investigated the type of purine receptor in the guinea-pig olfactory cortex, using pial surfaces slices maintained in vitro. Adenosine (0.1 to 100 mumol/l) bath applied in the presence of the uptake inhibitor nitrobenzylthioinosine, depressed the evoked potentials in a dose related fashion. Synthetic and uptake resistant adenosine analogues had the same effect as adenosine and the order of potency of these was: 5'-N-ethylcarboxamide adenosine greater than L-N6-phenylisopropyl adenosine (L-PIA) = N6-cyclohexyladenosine = 2-chloroadenosine greater than adenosine greater than D-N6-phenylisopropyladenosine (D-PIA). The D-stereoisomer of PIA was 45 times less potent than L-PIA. The methylxanthine compounds 8-phenyltheophylline (3 mumol/l) and 3-isobutyl-1-methylxanthine (50 mumol/l) antagonised the depression produced by L-PIA. Rolipram, a phosphodiesterase inhibitor, in concentrations up to 100 mumol/l had no effect on the evoked potentials or on adenosine action. Forskolin, a cAMP stimulant, slightly increased the amplitude of the evoked potential, and partly reversed the depressant effect of adenosine. Noradrenaline had no effect either alone or in the presence of adenosine. The results of these experiments indicate the existence of A1 subtype adenosine receptors in the guinea pig olfactory cortex probably linked to a depression of intracellular cAMP.

Adenosine↗

PubMed1997

A compartment-based, asymmetric representation of the retina in an induced projection to the olfactory cortex.

Displacing the optic nerve into the telencephalon in adult Rana pipiens induces a projection to olfactory cortex. We have examined the topographic organization of this projection anatomically by injecting a mixture of biotin dextran (BDA) with 3H-amino acids into the affected eye immediately after making cuts across defined sectors of the nerve fiber layer to trace the complementary patterns of anterograde migration of BDA and 3H label in the cut and intact retinal axons, respectively. Fibers from the temporal side of the optic disc terminated in an oblique band along the posterior two-thirds or more of the ectopic projection field. In contrast, fibers arising in the nasal retina terminated in a parallel strip occupying the anterior one-third or less of the field. Varying the location of the cuts within each hemiretina did not reveal any further organization along the nasotemporal or dorsoventral axes of the retina. The retinal location of the cells involved in this projection was further studied with injections of wheat germ agglutinin conjugated to horseradish peroxidase into the olfactory cortex. Ganglion cells labeled by retrograde transport were found throughout the retina, but they were much more numerous on the temporal side, having a mean spatial density 3.7-7.4 times greater in the temporal hemiretina, whereas the overall ganglion cell density (labeled plus unlabeled) was roughly the same in the two halves of the retina. These data provide an example of a permanent projection in which the overall representation of the retina, though nontopological, is polarized in one axis (nasotemporal) and, therefore, compartmentally organized.

Animals↗

PubMed1994

Development and early postnatal maturation of the primary olfactory cortex.

Tritiated thymidine autoradiography was used to study the origin and distribution of neurons in the primary olfactory cortex of the rat. The principal interest was devoted to animals injected at embryonic day 12 (E12) and sacrificed at different pre- and postnatal ages. The first generated neurons appearing at E12 were studied from E15 to P63. Animals sacrificed at E15 show a group of heavily labeled cells occupying a large area of the ventro lateral region of the telencephalic vesicle. At E16 this group differentiates into the principal cells of the accessory olfactory bulb and cells of the prospective primary olfactory cortex (POC). At E18-E20 the ventral tip of the cortical plate apparently divides this group into a superficial part corresponding to layer I and a deep part, corresponding to cells located in the adult in layer III. Labeled cells in layer I were found flanking the lateral olfactory tract (TOL), but rarely in the adult suggesting that they disappear or transform postnatally. Golgi observations were carried out from E15 to postnatal day 8. The morphology of different cells were studied. Layer I contains polymorphic cells resembling Cajal-Retzius cells. Among other cell types, layer II includes kinds of pyramidal cells lacking basal dendrites known as semilunar cells and intrinsic neurons. Layer III contains pyramidal cells having more than one apical dendrite ascending to the surface.

Animals↗

PubMed1984

Excitatory and inhibitory effects of noradrenaline on synaptic transmission in the rat olfactory cortex slice.

An investigation has been made of the effects of noradrenaline on excitatory transmission at the lateral olfactory tract (LOT)-superficial pyramidal cell synapse of the rat olfactory cortex slice by measuring the effects of bath-applied noradrenaline on the amplitudes and latencies of the field potentials evoked on LOT stimulation. Low concentrations of noradrenaline (0.1-5 microM) facilitate transmission whereas higher doses (20-250 microM) depress transmission. Both these effects were completely blocked by non-selective alpha- and beta-adrenoceptor antagonists, by 2-amino-5-phosphonovaleric acid (an antagonist of excitatory amino acid receptors of the N-methyl-D-aspartate type) and by the methylxanthine theophylline. The depressant effects of noradrenaline were mimicked by bath application of GABA or adenosine and specifically antagonized by bicuculline and picrotoxin. In parallel experiments, noradrenaline (100 microM) significantly increased the potassium-evoked release of endogenous aspartate, glutamate and GABA, proposed transmitters of the olfactory cortex, although the effect on GABA release was specifically antagonized by 2-amino-5-phosphonovaleric acid. Noradrenaline (100 microM) also significantly increased the potassium-evoked release of D-[3H]aspartate, an effect antagonized by a number of alpha- and beta-adrenoceptor antagonists. It is concluded that at low concentrations, noradrenaline facilitates transmission at the LOT-superficial pyramidal cell synapse by increasing excitatory amino acid neurotransmitter release. This effect is mediated by both alpha- and beta-adrenoceptors although the primary site of release is unknown. At higher concentrations of noradrenaline, the increased levels of excitatory transmitters release sufficient endogenous GABA (and possibly adenosine) to cause an overall depression of transmission. These conclusions are supported by the results of a series of experiments in which the effects of noradrenaline on stimulus input-evoked field potential output relationships were assessed. It is not possible to exclude additional direct effects of noradrenaline on membrane excitability.

Adenosine↗

PubMed1982

Effects of baclofen on the olfactory cortex slice preparation.

Baclofen has been shown to be ineffective against first order excitatory synaptic transmission in the olfactory cortex slice, whereas it is known that GABA-mediated inhibition depresses this transmission in a bicuculline-sensitive manner. In contrast, second and third order synaptic transmission, excitatory and inhibitory respectively, were depressed by baclofen. This suggests that the distribution of baclofen (GABAB) receptors differs from that of bicuculline-sensitive GABAA receptors in the olfactory cortex.

Animals↗

PubMed1994

Selective suppression of intrinsic but not afferent fiber synaptic transmission by baclofen in the piriform (olfactory) cortex.

The GABAB agonist baclofen has been shown to suppress synaptic transmission in subregions of the hippocampus and in the piriform (olfactory) cortex. Here we report a laminar selectivity of suppression of synaptic potentials in the olfactory cortex. In brain slice preparations, baclofen suppresses extracellularly recorded field potentials at the intrinsic fiber synapses proximal to the superficial pyramidal cell bodies (layer Ib) while leaving the afferent fiber synaptic potentials recorded at the distal dendrites (layer Ia) little affected. This dose-dependent selective suppression of intrinsic fiber synaptic transmission is also correlated with an increase of paired-pulse facilitation. These results suggest that afferent and intrinsic synaptic inputs may be differentially modulated by the activation of GABAB receptors and that this selective suppression is at least partially mediated via a presynaptic mechanism.

Afferent Pathways↗

PubMed1993

4-Aminopyridine causes reduction of cytochromes partly originated in glia with enhanced evoked potentials in the olfactory cortex slice.

Enhanced electrical and metabolic activities with addition of 4-aminopyridine (4-AP) were investigated in the olfactory cortex slice by recording evoked potentials, the redox state of cytochromes and the rate of oxygen uptake. During perfusion with 4-AP (0.01-0.1 mM), the late N-wave was dose-relatedly elicited in the evoked potential, concomitant with reduction of cytochromes and acceleration of oxygen uptake. These enhanced responses by 4-AP (0.1 mM) depended on the extracellular Ca2+. When the slice was subject to 2-deoxy-D-glucose (2-DG) (10 mM), initiation of the late N-wave by 4-AP (0.1 mM) was delayed, and both the reduction of cytochromes and the raised oxygen uptake prompted by the same dose of 4-AP were also significantly attenuated. Nevertheless, the presynaptic potential and N-wave, which markedly diminished by 2-DG, became tolerant to glycopenia after addition of 4-AP. By prior exposure to fluoroacetate (1 mM), the N-wave was gradually increased, but the late N-wave was rapidly decreased in amplitude by adding 4-AP (0.1 mM). The cytochrome reduction and the accelerated oxygen uptake by 4-AP (0.1 mM) were suppressed in the presence of fluoroacetate (1 mM). These results indicate that cytochromes become reduced by 4-AP, concomitant with the enhanced evoked potentials and oxygen uptake in a Ca(2+)-dependent manner, and that glial cells probably contribute to the enhanced electrical and metabolic activities in the olfactory cortex slice.

4-Aminopyridine↗

PubMed1980

Intracellularly-recorded effects of glutamate and aspartate on neurones in the guinea-pig olfactory cortex slice.

The effects of bath-applied glutamate, aspartate (and some related amino acids) on neurones of the guinea pig olfactory cortex slice were recorded intracellularly. Neurones were activated either by intracellularly-applied current or orthodromically by stimulating the lateral olfactory tract. In response to orthodromic stimuli several neurones displayed a late hyperpolarizing potential (LHP) after the usual sequence of EPSP, spike and IPSP. Glutamate and aspartate evoked 3 types of response: (a) a depolarization with apparent increase in input conductance; (b) a depolarization with no detectable conductance change; and (c) a hyperpolarization with conductance increase. Some possible mechanisms by which these 3 response-types could be generated are discussed. Depolarizations evoked by the glutamate analogue, kainate, were usually irreversible. Our results emphasize that glutamate and aspartate can evoke a variety of neuronal responses from olfactory cortex neurones. Several of these responses were previously undetected in experiments based on extracellular recordings.

Animals↗

PubMed1986

The topographical organization of neurons in the rat medial frontal, insular and olfactory cortex projecting to the solitary nucleus, olfactory bulb, periaqueductal gray and superior colliculus.

In 19 rats two different retrograde tracers (Fast Blue, Diamidino Yellow, Rhodamine-labeled latex microspheres, or wheat germ agglutinin conjugated with HRP) were injected into the solitary nucleus (NTS) and either the olfactory bulb (OB), periaqueductal gray (PAG) or superior colliculus (SC). The pattern of retrogradely labeled neurons in the medial frontal, insular and olfactory cortices was examined to determine the topographical organization of the cell populations projecting to these subcortical targets and the extent to which they overlapped. In the medial frontal cortex (MFC) SC projections originated most dorsally, while NTS and OB projections originated most ventrally and exhibited slight overlap. PAG projections originated from virtually the entire MFC and overlapped with cells projecting to the OB, NTS and SC. These results are consistent with the role of dorsal MFC as the rat's frontal eye field and the ventral MFC as a visceral motor area. Laterally, in the insular cortex there was virtually complete overlap between cells projecting to the NTS and PAG. The extensive overlap of PAG projections with NTS projections medially and laterally and with SC projections medially suggests the PAG is involved in a variety of brain visceral and somatic functions. In the piriform cortex there was overlap between cells projecting to the OB and cells projecting to the SC; the cells projecting to the SC were located in the endopiriform nucleus, and may provide a substrate for orienting responses to odors.

Animals↗

PubMed1985

Adenosine A1 receptors mediate the inhibitory effects of exogenous adenosine in the rat olfactory cortex slice.

A study has been undertaken to identify the category of receptors mediating the inhibitory effects of adenosine on evoked activity in slices of olfactory cortex in the rat. The approach has been to measure the relative potencies of adenosine and a range of structural analogues [2-chloroadenosine, 2' deoxyadenosine, cyclohexyladenosine, (-)-5'N-ethyl-carboxamide adenosine and N6(L-2-phenylisopropyl)adenosine] required to: inhibit excitatory transmission at the lateral olfactory tract-pyramidal cell synapse; inhibit the specific binding of [3H]cyclohexyladenosine to membrane preparations and evoke formation of cyclic AMP. In contrast to the relative concentrations of the analogues necessary to increase levels of cyclic AMP, those required to inhibit synaptic transmission were characteristic of a selectivity for adenosine A1 receptors. The presence of adenosine A1 receptors has been demonstrated directly by characterizing the binding of [3H]cyclohexyladenosine to membranes prepared from slices of olfactory cortex. It is concluded that inhibition of transmission at the lateral olfactory tract-pyramical cell synapse by adenosine is mediated by receptors of the A1 category.

Adenosine↗

PubMed1982

The distribution of axon collaterals from the olfactory bulb and the nucleus of the horizontal limb of the diagonal band to the olfactory cortex, demonstrated by double retrograde labeling techniques.

Three different pairs of double retrograde axonal tracers have been used to study the distribution of axon collaterals from individual cells in the olfactory bulb and the nucleus of the horizontal limb of the diagonal band: (1) horseradish peroxidase (HRP) and tritiated apo-HRP (3H-HRP), (2) HRP and 125I-wheat germ agglutinin (I-WGA), and (3) the fluorochromes true blue (TB) and bisbenzimide (BB) or nuclear yellow (NY). With each combination of tracers, paired injections were made into different parts of the olfactory system, and the olfactory bulb and the nucleus of the diagonal band were examined for the presence and arrangement of cells labeled with one or both retrograde tracers. In the olfactory bulb both single and double retrogradely labeled mitral cells were found following injections in disparate parts of the olfactory cortex. Furthermore, no consistent pattern was found in the distribution of single- or double-labeled cells in the olfactory bulb; that is, the distribution of cells labeled from one area of the cortex was not consistently different from the distribution of cells labeled from other parts of the cortex. Therefore, it was concluded that individual mitral cells project to widely spaced parts of the olfactory cortex, and that there is no apparent correspondence between the location of a given cell in the olfactory bulb and the distribution of its axon in the cortex. In contrast to this, cells in the nucleus of the horizontal limb of the diagonal band were only rarely double-labeled from nonoverlapping injections into the olfactory cortex or olfactory bulb, although overlapping injections produced a high proportion of double-labeled cells. Cells which were single-labeled from different injection sites were extensively intermixed within the nucleus. Therefore, in this case it was concluded that individual cells projects to relatively restricted areas, although there was again no apparent correspondence between the position of a cell in the nucleus and the terminal field of its axon.

Animals↗

PubMed1986

Age-dependent cell death in the olfactory cortex: lack of transneuronal degeneration in neonates.

Adult olfactory cortical neurons in layer IIa undergo fulminant transneuronal degeneration after removal of afferent olfactory bulb fibers (Price, '76, Neurosci Abst. 2:161; Heimer and Kalil, '78, J. Comp. Neurol. 178:559-609). This provides an unusual example of dependence of a mature population of neurons on axonal input. In order to investigate whether similar transneuronal degeneration occurs in immature animals, a series of rats were subjected to unilateral olfactory bulb removal at various ages during the first 3 postnatal weeks. The brains were examined for degeneration after short survivals by use of the de Olmos cupric silver method, which selectively stains degenerating neurons. In addition, animals with long survivals were examined with the HRP retrograde tracing method, in order to determine if cells that survive the acute effects of deafferentation develop normal patterns of connections. Young neurons are more resistant to the effects of olfactory bulb removal than more mature neurons. There was little degeneration of cortical neurons after bulb ablation during the first 2 postnatal weeks. Although layer IIa does not become distinct from layer IIb in these experimental animals, cells that have connections normally characteristic of the cells of layer IIa, and are situated at the superficial edge of layer II, were identified with the HRP method. The severity of transneuronal degeneration increases and becomes adultlike between the second and third postnatal weeks. This increase in transneuronal degeneration is temporally associated with a progressive reduction in axonal sprouting following deafferentation during the first 3 postnatal weeks, as described in the companion paper (Friedman and Price, '86). Thus, axon sprouting may "protect" the immature IIa neurons from the effects of removal of the fibers from the olfactory bulb. A period of normal cell death has also been identified in olfactory cortex by the use of the de Olmos cupric silver method. This cellular degeneration is much less severe and has a different time course and laminar distribution than the transneuronal degeneration produced by olfactory bulb ablation in adults. Although normal cell death appears to be potentiated by removal of the olfactory bulb on postnatal day 1, it is clearly a different process from the transneuronal reaction.

Age Factors↗