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At least 19 recordsLinked to original sources
PubMed1980

Time-course of declining electrical activity in guinea-pig olfactory cortex after olfactory bulb removal.

An electrophysiological study has been made of the degeneration of the afferent axons of the lateral olfactory tract (L.O.T.) which give rise to excitatory synapses throughout the olfactory cortex. These fibres were severed by removing one or both olfactory bulbs. Evoked potentials were recorded from slices of olfactory cortex in vitro prepared at various times after bulbectomy. Up to 1.6 days later, all potentials were similar to those of the unoperated side. Between 1.6 and 1.8 days there was a complete loss of evoked potential from both L.O.T. axons and postsynaptic neurones, which occurred synchronously at all points along a 5-6 mm length of the tract.

Action Potentials↗
PubMed1980

Effect of intervening lesions on amino acid distributions in rat olfactory cortex and olfactory bulb.

Levels of the proposed neurotransmitter amino acids glutamate, aspartate, gamma-aminobutyric acid (GABA), and glycine were measured within the layered structures of the olfactory bulb and olfactory cortex following unilateral transections of the lateral olfactory tract or of virtually all fiber tracts of the olfactory peduncle. Distributions of the amino acids on both lesion and control sides were examined and compared by means of a mapping procedure. The results suggest: 1) Glutamate and aspartate are specifically associated with mitral (and presumably also tufted) cell axons and terminals in the piriform cortex. The distribution of aspartate in the olfactory bulb is further suggestive of a specific association of aspartate with mitral cell dendrites and somata. 2) Glutamate might be specifically associated with some centrifugal fibers traveling to the olfactory bulb in or near the anterior commissure. 3) GABA might be specifically related to some certrifugal fibers to the olfactory bulb in addition to its prominent association with granule cells of the bulb. 4) Glycine is unlikely to play a prominent neurotransmitter role in either the olfactory bulb or olfactory cortex.

Amino Acids↗
PubMed1980

Alterations in axons and synapses of olfactory cortex following olfactory bulb lesions in newborn rats.

The olfactory cortex of rats is being studied at various survival times following deafferentating olfactory bulb ablation on the day of birth. The neonatal axons and synaptic terminals undergo rapid, flocculent degeneration and fragmentation. Most are not electron-dense and therefore probably not argyrophilic at this particular age of the lesion. The degeneration and removal of debris is far more rapid than in adults, yielding a markedly enlarged extracellular space with a relative absence of glia at the vacated postsynaptic "thickenings". Denervated postsynaptic "thickenings" become occupied by neuronal and nonneuronal profiles and profiles of uncertain origin, singly or in various combinations, or the sites may remain partially vacant. One or more axons with synaptic vesicles often aggregated at the site are commonly involved. Certain terminals form contacts on progressively greater lengths of the "thickening" until typical synaptic contacts predominate by 14 days survival. The results suggest a competitive reinnervation process and provide a fine structural explanation for the events leading to alterations in this pathway following neonatal deafferentation.

Age Factors↗
PubMed2006

Strong single-fiber sensory inputs to olfactory cortex: implications for olfactory coding.

Olfactory information is first encoded in a combinatorial fashion by olfactory bulb glomeruli, which individually represent distinct chemical features of odors. This information is then transmitted to piriform (olfactory) cortex, via axons of olfactory bulb mitral and tufted (M/T) cells, where it is presumed to form the odor percept. However, mechanisms governing the integration of sensory information in mammalian olfactory cortex are unclear. Here we show that single M/T cells can make powerful connections with cortical pyramidal cells, and coincident input from few M/T cells is sufficient to elicit spike output. These findings suggest that odor coding is broad and distributed in olfactory cortex.

Action Potentials↗
PubMed1984

Changes in cytochrome oxidase activity of the rabbit olfactory cortex following unilateral olfactory bulbectomy.

The effects of unilateral olfactory bulbectomy on cytochrome oxidase (CO) activity in the olfactory cortex were studied in adult rabbits. In intact rabbits, layer Ia of the olfactory cortex stained symmetrically for CO activity as a continuous brown band. In animals with unilateral lesion of the olfactory bulb (OB), a great decrease in the level of CO activity was found in layer Ia ipsilaterally. The change became prominent about 12 hr after OB lesion. Thereafter no further decrease in CO activity was observed up to 6 months. A decrease in the level of CO activity was observed in only the denervated lamina to which the OB neurons project directly, but not along the synaptic chain in the olfactory cortex.

Animals↗
PubMed1992

Functional correlates of selective long-term potentiation in the olfactory cortex and olfactory bulb.

High-frequency stimulation of the granule cell layer of the olfactory bulb (OB) has previously been shown to result in a selective long-term potentiation (LTP) of late components of potentials evoked in the OB and piriform cortex (PC). The functional impact of this potentiation was explored in male Long-Evans rats with chronically implanted electrodes by comparing the effects of paired-pulse stimulation of the OB in potentiated and control animals. Effects were examined on two components of the potential evoked in the PC: A1, which represents the population EPSP produced by OB mitral cells in PC pyramidal cells via the lateral olfactory tract (LOT), and B1, which represents the subsequent population EPSP produced by PC pyramidal cells in other pyramidal cells. Two separate functional correlates of selective LTP were found. First, there was enhanced paired-pulse depression of B1, indicating increased inhibition of PC pyramidal cells. Second, there was a shift from paired-pulse facilitation to depression of A1, which was accompanied by a decrease in amplitude of the LOT volley, indicating that fewer mitral cells were activated by the stimulation. This shift was most prominent in animals with stimulating electrodes closest to the mitral cell layer, suggesting that it is dependent upon direct stimulation of mitral cell somata. These observations, together with other results reported in the manuscript, support the conclusion that there is an enhanced inhibition of mitral cells following selective LTP. Thus a primary consequence of selective LTP appears to be enhanced inhibition of principal neurons in both the PC and OB. These findings are consistent with our previous proposal that selective LTP represents potentiation at excitatory synapses made by PC pyramidal cells on inhibitory interneurons in the PC and OB.

Animals↗
PubMed2001

Genetic tracing reveals a stereotyped sensory map in the olfactory cortex.

The olfactory system translates myriad chemical structures into diverse odour perceptions. To gain insight into how this is accomplished, we prepared mice that coexpressed a transneuronal tracer with only one of about 1,000 different odorant receptors. The tracer travelled from nasal neurons expressing that receptor to the olfactory bulb and then to the olfactory cortex, allowing visualization of cortical neurons that receive input from a particular odorant receptor. These studies revealed a stereotyped sensory map in the olfactory cortex in which signals from a particular receptor are targeted to specific clusters of neurons. Inputs from different receptors overlap spatially and could be combined in single neurons, potentially allowing for an integration of the components of an odorant's combinatorial receptor code. Signals from the same receptor are targeted to multiple olfactory cortical areas, permitting the parallel, and perhaps differential, processing of inputs from a single receptor before delivery to the neocortex and limbic system.

Animals↗
PubMed1999

Calcium-binding proteins: differential expression in the rat olfactory cortex after neonatal olfactory bulbectomy.

Calbindin, parvalbumin, and calretinin, members of EF-hand calcium-binding proteins, play important roles in buffering intracellular calcium ions. These proteins are localized in distinct populations of cells in the olfactory bulb (the primary sensory relay in the olfactory system) and its major synaptic target, the primary olfactory cortex (POC). In the present study, the postnatal expression of these calcium-binding proteins in layer III of POC was quantitatively examined 30 days after neonatal bulbectomy, a manipulation known to cause cell death and neurotransmitter changes. The numbers of both calbindin and parvalbumin-immunoreactive profiles showed significant increases (68% and 163%, respectively), while calretinin-immunoreactive profiles exhibited a 46% reduction. The data demonstrate that the expression of these calcium-binding proteins is regulated in part by the afferent input from the olfactory bulb. Furthermore, the resultant increase in calbindin and parvalbumin expression may provide neuroprotective support necessitated by possible alterations in intracellular calcium ions and other neurochemical factors that accompany neonatal bulb removal.

Animals↗
PubMed2005

Sniffing Out NMDA Receptors in the Olfactory Cortex.

Selective olfactory learning is essential for survival in most newborn mammals. Findings by Franks and Isaacson in this issue of Neuron suggest that early olfactory learning might be selective, in part because olfactory experience downregulates NMDA receptors at primary inputs to the olfactory cortex.

Animals↗
PubMed1986

Effects of adenosine uptake blockers and adenosine on evoked potentials of guinea-pig olfactory cortex.

The olfactory cortex slice preparation from guinea-pig has been used to test compounds which inhibit the cellular uptake of adenosine. The uptake inhibitors dipyridamole (0.1-10 mumol/l), dilazep (1-10 mumol/l) nitrobenzylthioguanosine (1-10 mumol/l), nitrobenzylthioinosine (0.1-5 mumol/l), and hexobendine (1-100 mumol/l) increased the potency of adenosine (0.1-30 mumol/l) by up to 5-fold but did not potentiate cyclohexyladenosine (0.01-10 mumol/l). The benzodiazepine, diazepam (1 mumol/l) slightly increased the potency of adenosine (by 1.7-fold) whereas flurazepam (3 mumol/l) had no effect, suggesting that inhibition of adenosine uptake is probably not the major therapeutic action of these compounds. The uptake inhibitors depressed the amplitude of the monosynaptic epsp when added alone, an effect reversed by adenosine deaminase (1 unit/ml) whereas the adenosine deaminase inhibitor, erythro-9-(2-hydroxy-3-nonyl)adenine (10 mumol/l) had no effect on adenosine action. These results show that in this preparation (a) adenosine action is attenuated by an uptake mechanism and (b) endogenous adenosine release normally has no apparent effects on synaptic transmission at low stimulus rates. Nitrobenzylthioinosine and nitrobenzylthioguanosine are probably the best uptake blockers.

Adenosine↗
PubMed2001

Parallel-distributed processing in olfactory cortex: new insights from morphological and physiological analysis of neuronal circuitry.

A working hypothesis is proposed for piriform cortex (PC) and other olfactory cortical areas that redefines the traditional functional roles as follows: the olfactory bulb serves as the primary olfactory cortex by virtue of encoding 'molecular features' (structural components common to many odorant molecules) as a patchy mosaic reminiscent of the representation of simple features in primary visual cortex. The anterior olfactory cortex (that has been inappropriately termed the anterior olfactory nucleus) detects and stores correlations between olfactory features, creating representations (gestalts) for particular odorants and odorant mixtures. This function places anterior olfactory cortex at the level of secondary visual cortex. PC carries out functions that have traditionally defined association cortex--it detects and learns correlations between olfactory gestalts formed in anterior olfactory cortex and a large repertoire of behavioral, cognitive and contextual information to which it has access through reciprocal connections with prefrontal, entorhinal, perirhinal and amygdaloid areas. Using principles derived from artificial networks with biologically plausible parallel-distributed architectures and Hebbian synaptic plasticity (i.e. adjustments in synaptic strength based on locally convergent activity), functional proposals are made for PC and related cortical areas. Architectural features incorporated include extensive recurrent connectivity in anterior PC, predominantly feedforward connectivity in posterior PC and backprojections that connect distal to proximal structures in the cascade of olfactory cortical areas. Capabilities of the 'reciprocal feedforward correlation' architecture that characterizes PC and adjoining higher-order areas are discussed in some detail. The working hypothesis is preceded by a review of relevant anatomy and physiology, and a non-quantitative account of parallel-distributed principles. To increase the accessibility of findings for PC and to advertise its substantial potential as a model for experimental and modeling analysis of associative processes, parallels are described between PC and the hippocampal formation, inferotemporal visual cortex and prefrontal cortex.

Animals↗
PubMed2001

Olfactory learning modifies predisposition for long-term potentiation and long-term depression induction in the rat piriform (olfactory) cortex.

Learning-related modifications in predisposition for long-term potentiation (LTP) and long-term depression (LTD) were studied in brain slices of the rat piriform cortex following olfactory learning. Rats were trained to discriminate between pairs of odors until they demonstrated rule learning. We have previously shown that such training is accompanied by enhanced neuronal excitability and increased synaptic transmission in the intrinsic synaptic pathway. Here we show that the susceptibility for further enhancing synaptic connectivity by inducing LTP in slices from trained rats is markedly reduced after training, compared with slices from pseudo-trained and naive rats. Accordingly, while 900 stimuli at 1 Hz did not induce LTD in slices from control rats, it induced significant LTD in slices from trained rats. Post-tetanic potentiation (PTP) was also reduced after training, indicating that synaptic release is enhanced after odor learning, as previously suggested. We suggest that learning-related cellular modifications and activity-dependent synaptic plasticity share a common mechanism in the primary olfactory cortex. Our data also support the prediction generated according to the sliding modification threshold theory that learning should be accompanied by reduced capability of inducing LTP and increased susceptibility for LTD induction.

Animals↗
PubMed1983

Baclofen blocks postsynaptic inhibition but not the effect of muscimol in the olfactory cortex.

1 The olfactory cortex slice preparation from the guinea-pig brain was used to study the effects of baclofen on inhibition using intracellular recording. Stimulation of the lateral olfactory tract activities sequentially excitatory and inhibitory pathways. Inhibition is manifest as a period of increased membrane conductance (termed postsynaptic inhibitory conductance, IPSC). 2 Bath application of baclofen (0.2-500 muM) reversibly blocked the IPSC. Baclofen also produced a secondary increase in the amplitude and duration of the initial excitatory postsynaptic potential. 3 Baclofen (0.5-500 muM) slightly augmented the ability of bath-applied muscimol to increase the resting membrane conductance. Baclofen had no effect on cell excitability and membrane potential and no effect on the action of gamma-aminobutyric acid (GABA), noradrenaline, glycine, taurine or 5-hydroxytrypamine. 4 These results confirm previous suggestions that baclofen at low concentrations acts outside the GABA receptor mediating the IPSC perhaps by reducing the release of the excitatory transmitter activating the inhibitory interneurones.

Animals↗
PubMed1981

The effects of chlordiazepoxide on synaptic transmission and amino acid neurotransmitter release in slices of rat olfactory cortex.

The rat olfactory cortex slice has been used to investigate the effects of chlordiazepoxide on evoked field potentials and the release of endogenous amino acid neurotransmitters (aspartate, glutamate, GABA and possibly taurine) which accompany electrical stimulation of the lateral olfactory tract. When single, low frequency stimuli were employed, chlordiazepoxide (2 microM-1 mM) depressed the amplitude of the field potential correlate of the depolarizing actions of the lateral olfactory tract excitatory transmitter (aspartate?) although aspartate release was unaffected. The field potential correlate of GABA-mediated presynaptic inhibition (late N-wave) was also depressed in amplitude but low drug concentrations (between approximately 2 and 50 microM) increased its peak duration . Effects of chlordiazepoxide on evoked inhibition were analyzed by giving paired stimuli such that the second stimulus occurred during the field potentials evoked by the first stimulus. Chlordiazepoxide (1-20 microM) increased the depression in amplitudes of the presynaptic massed action potential and late N-wave evoked by the second of a pair of stimuli compared with those evoked by the first stimulus suggesting that presynaptic inhibition was potentiated. These effects of chlordiazepoxide were accompanied by a significant reduction in aspartate release from the lateral olfactory tract terminals. Moreover, the drug effects on presynaptic inhibition and aspartate release were antagonized by picrotoxin (5 microM). On the other hand, chlordiazepoxide (1-50 microM) had no significant effect on postsynaptic inhibition. The results are discussed in terms of both the sites (presynaptic or postsynaptic) and mechanisms of action of chlordiazepoxide.

4-Aminobutyrate Transaminase↗
PubMed1988

Presynaptic K-channel blockade counteracts the depressant effect of adenosine in olfactory cortex.

Slices of isolated olfactory cortex from guinea-pig have been used to study the action of adenosine at synapses between axons of the lateral olfactory tract and neurons in the olfactory cortex. Adenosine depressed the excitatory postsynaptic potential, and, with paired or multiple stimuli, the reduced excitatory postsynaptic potentials in adenosine showed more synaptic facilitation. Very small excitatory postsynaptic potentials which were estimated not to be affected by postsynaptic membrane conductance changes were highly sensitive to adenosine. Both observations indicate a presynaptic action of adenosine. To test whether a conductance increase to potassium ions mediated adenosine action, the K-channel blockers, 3,4-diaminopyridine (1-100 mumol/l) or 4-aminopyridine (100-500 mumol/l) were applied or Cs partially substituted for K. These substances reduced or prevented adenosine from having its depressant effect on synaptic transmission. These particular K-channel blockers also prolonged the action potential propagating along the lateral olfactory tract. When the increased excitability was counteracted by high Mg or low concentrations of tetrodotoxin, 3,4-diaminopyridine still blocked adenosine action. UO2 ions prolonged the lateral olfactory tract action potential without blockade of K-conductance, but still supported an adenosine depression of the excitatory postsynaptic potential. Veratridine also supported the adenosine depression. These observations suggest that the action of 3,4-diaminopyridine on adenosine was not solely the result of increased tissue excitability. In contrast, tetraethylammonium (20 mmol/l), Ba (0.5-4 mmol/l) or Rb replacement for K had a negligible effect on the duration of the presynaptic action potential and had no effect on the depressant action of adenosine. These data are compatible with the idea that adenosine enhances an aminopyridine-sensitive potassium conductance in nerve terminals and changes in Ca influx are consequential to this.

4-Aminopyridine↗
PubMed1983

Ro 15-1788 is a potent antagonist of benzodiazepines in the olfactory cortex slice.

The olfactory cortex slice from the guinea pig has been used to test the benzodiazepine antagonist, Ro 15-1788. Bath application of muscimol has a GABA-mimetic effect on the resting input conductance of these neurones. Benzodiazepines increase the potency of muscimol and increase the duration of postsynaptic inhibitory conductance. To measure the effect of muscimol, the input conductance was measured either directly using intracellular microelectrodes or by measuring its effect on the amplitude of the evoked compound potentials recorded from the slice surface after stimulating the lateral olfactory tract. The potentiation of postsynaptic inhibition produced by benzodiazepines was measured indirectly by their effect on the amplitude of the second of two evoked compound potentials. All of the potentiating effects of diazepam, clonazepam, flurazepam and chlordiazepoxide were blocked by Ro 15-1788 (0.01-10 mumol/l). Ro 15-1788 up to a concentration of 10 mumol/l had no effect on any of the synaptic or electrical responses when applied alone. General anaesthetics which also potentiate inhibition were unaffected by Ro 15-1788. It is concluded that Ro 15-1788 is a highly potent and specific benzodiazepine antagonist in this preparation.

Anesthetics↗
PubMed2002

Mosaic development of the olfactory cortex with Pax6-dependent and -independent components.

The olfactory cortex is the target area of olfactory bulb axons and is suggested to be derived from neuroepithelial progenitors of various ventricular domains during development. In the present study, we examined the development of the olfactory cortex, using the newly developed monoclonal antibody (mAb) 9-4c, which recognizes reticulon 1-A and -B. The mAb labeled neuroepithelial progenitors at the pallio-subpallial boundary (PSB) and their putative descendants in the deep layers of the olfactory cortex. In the Pax6 mutant embryo, labeling at the PSB was specifically lacking, and the number of immunopositive cells in the olfactory cortex was markedly reduced. In contrast, the guidepost neurons of olfactory bulb axons, lot cells, developed relatively normally in the superficial layer of the olfactory cortex in the mutant embryo. These guidepost neurons have been recently shown to originate in the pallium and eventually guide the initial projection of olfactory bulb axons. The olfactory bulb projection in the Pax6 mutant embryo also suggested the dualistic nature of the olfactory cortex development; the initial projection of olfactory bulb axons developed relatively normally, whereas the final projection of their collateral branches was severely defective.

Animals↗