Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Olfactory Pathways”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

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

At least 973 records · Page 54Linked to original sources
PubMed1995

Coculture of the vomeronasal organ and olfactory bulb of the fetal rat.

The vomeronasal organ and the olfactory bulb of the rat were cocultured from 15-day embryo siblings on collagen-coated membrane in Dulbecco's modified Eagle's medium containing fetal calf serum, horse serum, and antibiotics. At 4 days in vitro (DIV), vomeronasal axons forming two to three large fascicles were seen originating from the explants of the vomeronasal organ. Differential axonal growth was observed. Some fascicles made connections with the explants of the olfactory bulb. Twenty percent of the cocultures studied here showed the formation of connections. At 6-10 DIV many fascicles that did not connect with the olfactory bulb had degenerated, and large fascicles that were connected with the olfactory bulb survived for more than 10 DIV. The formation of connections between the vomeronasal organ and the olfactory bulb in coculture favors the survival of large nerve fascicles, but it could not be determined whether or not the presence of the olfactory bulb affects the initial orientation of the fibers and fascicles from the explants of the vomeronasal organ.

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↗
PubMed1995

Brain 2-deoxyglucose levels related to maternal behavior-inducing stimuli in the rat.

Levels of [14C]2-deoxyglucose (2-DG), measured autoradiographically, in the medial preoptic area (MPOA), were higher during natural parturition with concurrent maternal behavior than in non-pregnant non-maternal controls, whereas levels in the vomeronasal system were lower in virgin rats made maternal by cohabitation with young than in control and parturient rats. Previous studies have shown that lesions of MPOA disrupt maternal behavior, whereas lesions of vomeronasal structures stimulate it, and that an increase in 2-DG levels is indicative of an increase in firing activity in neuron terminals. Consequently, the present findings suggest that maternal behavior can be induced by: (a) an increase in parturition-generated sensory stimulatory input to the MPOA in response to mechanostimulation of the birth canal, and (b) a separate chemosensory vomeronasal pathway whose activity is reduced cohabitation with young, thereby disinhibiting maternal behavior.

Animals↗
PubMed1991

Contrasting neurochemical interactions of tiletamine, a potent phencyclidine (PCP) receptor ligand, with the N-methyl-D-aspartate-coupled and -uncoupled PCP recognition sites.

Neurochemical interactions of tiletamine, a potent phencyclidine (PCP) receptor ligand, with the N-methyl-D-aspartate (NMDA)-coupled and -uncoupled PCP recognition sites were examined. Tiletamine potently displaced the binding of [3H]1-(2-thienyl)cyclohexylpiperidine with an IC50 of 79 nM without affecting sigma-, glycine, glutamate, kainate, quisqualate, or dopamine (DA) receptors. Like other PCP ligands acting via the NMDA-coupled PCP recognition sites, tiletamine decreased basal, harmaline-, and D-serine-mediated increases in cyclic cGMP levels and induced stereotypy and ataxia. Tiletamine was nearly five times more potent than PCP at inhibiting the binding of 3-hydroxy[3H]PCP to its high-affinity NMDA-uncoupled PCP recognition sites. However, following parenteral administration, dizocilpine maleate (MK-801), ketamine, PCP, dexoxadrol, and 1-(2-thienyl)cyclohexylpiperidine HCl, but not tiletamine, increased rat pyriform cortical DA metabolism and/or release, a response modulated by the NMDA-uncoupled PCP recognition sites. Pretreatment with tiletamine did not attenuate the MK-801-induced increases in rat pyriform cortical DA metabolism, a result suggesting that tiletamine is not a partial agonist of the NMDA-uncoupled PCP recognition sites in this region. However, following intracerebroventricular administration (100-500 micrograms/rat), tiletamine increased pyriform cortical DA metabolism with a bell-shaped dose-response curve. These data indicate a differential interaction of tiletamine with the NMDA-coupled and -uncoupled PCP recognition sites. The paradoxical effects of tiletamine suggest that tiletamine might activate receptor(s) or neuronal pathways of unknown pharmacology.

Animals↗
PubMed1991

Kindling-induced potentiation in the piriform cortex.

At intensities sufficient to induce epileptiform afterdischarges, repeated electrical stimulation of limbic structures can lead to the development of permanent increases in the strength of the epileptiform response (kindling). Field potentials evoked by pulse stimulation are also increased in amplitude in a number of forebrain pathways following kindling. This kindling-induced potentiation effect is similar in many respects to the 'long-term potentiation' (LTP) effect which is produced by non-epileptogenic stimulation. There are, however, some interesting differences. For example, kindling-induced potentiation can far outlast LTP. In these experiments, we attempted to determine the longevity of the kindling-induced potentiation of the response evoked in the piriform cortex by olfactory bulb stimulation, following olfactory bulb kindling. This system was targeted because both the olfactory bulb and the piriform cortex are highly reactive kindling sites. In addition, we used the paired pulse technique to monitor facilitation and inhibition in this system. Kindling was found to induce a potentiation in the piriform field potential that lasted for at least 3 months (the period of the experiment) with little or no decay. Kindling also produced a decrease in paired pulse facilitation. In some animals the net facilitation was changed to a net depression. These results are consistent with the interpretation that kindling produces an increase in recurrent inhibition in the piriform cortex. The paired pulse measures, however, returned to near baseline levels over the 3-month test period.

Animals↗
PubMed2002

How do transplanted olfactory ensheathing cells restore function?

In this article, we review our work on regeneration of the corticospinal tract in rats following a lesion at upper cervical level. We outline the rationale for using olfactory ensheathing cells, and summarize the evidence for regeneration and functional recovery. The present interpretation on the mechanisms of functional recovery is partly hypothetical, and we emphasize where further experimental evidence is needed.

Animals↗
PubMed1993

GABAA and glutamate receptor involvement in dendrodendritic synaptic interactions from salamander olfactory bulb.

1. Whole-cell patch clamp and optical recording techniques were applied to the same in vitro salamander olfactory bulb preparations to study the postsynaptic responses of single mitral/tufted cells in the context of the surrounding neural activity in which they are embedded. Mitral/tufted cells were identified by intracellular filling with biocytin. 2. Single mitral/tufted cells were under a tonic GABAA receptor-mediated inhibitory influence as revealed by the recording of bicuculline methiodide (BMI)/picrotoxin-sensitive inhibitory postsynaptic currents (IPSCs) in symmetrical chloride conditions at a holding potential of -70 mV. Depolarizing voltage steps (100 ms) applied to single cells or electrical stimulation of the olfactory nerve or medial olfactory tract evoked a prolonged increase in the frequency of GABAergic IPSCs. 3. The frequency of spontaneous and driven IPSCs was reduced with application of the glutamate receptor antagonists 6-cyano-2,3-dihydroxy-7-nitro-quionoxaline (CNQX) or 2-amino-5-phosphonopentanoic acid (AP5) whereas olfactory nerve- or medial olfactory tract-driven IPSC frequency was enhanced with removal of bathing Mg2+, indicating that GABAergic interneurones were driven by mitral/tufted cells at both non-NMDA and NMDA receptors. 4. Olfactory nerve or medial olfactory tract stimulation evoked widely distributed changes in fluorescence in preparations stained with the voltage-sensitive dye RH414. The optical response predominantly consisted of a decrease in fluorescence, indicative of depolarization. The presence of the dye did not obviously affect mitral/tufted cell postsynaptic responses. 5. BMI enhanced the amplitude and duration of optical signals related to depolarization within the bulb and in regions central to the bulb. In the presence of BMI, depolarizing activity appeared to spread hundreds of micrometres into regions of the bulb not activated in control conditions showing explicitly that GABAA receptors in the bulb participate in lateral inhibition. 6. CNQX and AP5 attenuated the optical signals within the bulb supporting the contention that in these conditions, optical signals arise mainly from granule cell dendritic activity. Furthermore, AP5 or removal of bath Mg2+ reduced or enlarged the spatial distribution of activity respectively, suggesting that in some cases the NMDA receptor may be involved in generating or stabilizing spatial patterns of activity. 7. It is concluded that in the salamander olfactory bulb, both GABAA- and glutamate receptor-mediated synaptic transmission shape the different temporal and spatial patterns of neural activity associated with olfactory coding.

2-Amino-5-phosphonovalerate↗
PubMed1995

The telencephalic vesicles are innervated by olfactory placode-derived cells: a possible mechanism to induce neocortical development.

During early embryonic development, the olfactory placode is the source of different cell types migrating toward the telencephalic vesicle. Among these cell types are the ensheathing cells, the luteinizing hormone-releasing hormone-producing cells and the olfactory marker protein-immunoreactive cells. We have identified a novel group of olfactory placode-derived migratory cells using an antibody against beta-tubulin to label neurons and acetylcholinesterase histochemistry to label posmitotic cells. In this paper we describe the morphology, migration and fate of this novel group of cells. The first neurons detected in the rostral prosencephalon with acetylcholinesterase and anti-beta-tubulin antibody are localized in the olfactory placodes at embryonic day 11 in the rate. At embryonic day 12, anti-beta-tubulin antibody-positive cells were observed in the mesenchymal tissue between the olfactory pit and the rostral pole of the telencephalic vesicle. Anti-beta-tubulin antibody-positive cells were seen running superficially over the pial (dorsal) side of the telencephalic vesicle at embryonic day 13. The majority of these cells have a bipolar profile with short leading and trailing processes, suggesting that they are migratory elements. However, some of these cells showed elaborate processes extending for quite long distances, overlying the pial surface of the telencephalic vesicle. A mass of cells extending over the telencephalic vesicle from the developing olfactory epithelium were observed at embryonic day 13 using acetylcholinesterase histochemistry. Some of these acetylcholinesterase-positive cells were identified as neurons with the specific neuronal marker anti-beta-tubulin antibody. On embryonic day 12, neurons from the olfactory epithelium send axonal fibers toward the telencephalic vesicles. Most of these fibers spread over the anteroventral pole of the vesicles but others entered deep into the telencephalon, reaching the germinal ventricular zone. We also show that fibers run rostrocaudally over the surface of the telencephalic vesicles. We suggest that these cells and fibers, apparently originating in the olfactory placode and migrating through non-conventional routes, might play a significant role in the earliest stages of telencephalic vesicle development.

Acetylcholinesterase↗
PubMed1992

Anatomical and immunohistological demonstration of the primary neural connections of the vomeronasal organ in the dog.

Macro- and microdissection methods together with conventional histology and lectin immunohistochemistry have been used to identify the course of the vomeronasal nerves and their site of termination (accessory olfactory bulb; AOB) in the dog. The AOB in this species is small and variable in size, situated on the medial surface of the main olfactory bulb, and has an anatomical structure unlike that described for other mammals. The vomeronasal nerves and their terminal glomeruli in the AOB are easily identifiable by selective immunohistochemical staining using Ulex europeus agglutinin I.

Animals↗
PubMed1996

Caged compounds of hydrolysis-resistant analogues of cAMP and cGMP: synthesis and application to cyclic nucleotide-gated channels.

Photolabile compounds which rapidly release cAMP or cGMP after photolysis are widely used for in situ studies of signaling pathways inside cells. We synthesized two novel caged compounds, 4,5-dimethoxy-2-nitrobenzyl 8-Br-cAMP (caged 8-Br-cAMP) and 4,5-dimethoxy-2-nitrobenzyl 8-Br-cGMP caged 8-BR-cGMP), which respectively release the hydrolysis-resistant analogues 8-Br-cAMP and 8-Br-cGMP. Their usefulness for physiological studies was examined in a mammalian cell line expressing the cyclic nucleotide-gated (CNG) ion channel of bovine olfactory sensory neurons. The synthesis procedure resulted in diastereomeric mixtures which were chromatographically separated into the axial and equatorial isomers of caged 8-BR-cAMP and of caged 8-BR-cGMP. The axial isomers which have a higher solubility and better solvolytic stability than the equatorial forms were used for experiments with CNG channels. Flashes of UV light produced steps in the concentration of 8-Br-cGMP which activated currents through CNG channels. Concentration steps inside the cell could be calibrated precisely using the relation between the ligand concentration and the normalized current. Similar results were obtained with caged 8-Br-cAMP. Control experiments with caged cGMP showed that flash-induced currents decayed within a few minutes because photoreleased cGMP was degraded by endogenous phosphodiesterase activity. The rise time of the 8-Br-cGMP-activated whole-cell current was consistent with a bimolecular reaction between channel and ligand.

1-Methyl-3-isobutylxanthine↗
PubMed1989

Excitatory influence of the accessory olfactory bulb on tuberoinfundibular arcuate neurons of female mice and its modulation by oestrogen.

The role of the accessory olfactory bulb in conveying pheromonal information to tuberoinfundibular arcuate neurons was examined electrophysiologically in chloral hydrate-anaesthetized, oestrogen (0.5 micrograms in silastic capsules)-treated and untreated ovariectomized Balb/c female mice. Electrical stimulation of the accessory olfactory bulb orthodromically excited part of tuberoinfundibular neurons which were antidromically stimulated from the median eminence and histologically verified as being located within the arcuate nucleus. No inhibitions followed accessory bulb stimulation. The excitatory response to accessory bulb stimulation was reversibly blocked by the local anaesthetic lignocaine infused into the amygdala. The percentage of tuberoinfundibular arcuate neurons responding to accessory bulb stimulation was significantly higher in oestrogen-treated than in untreated animals. There was no difference between the two groups for the antidromic activation threshold, spontaneous firing rate, absolute refractory period or frequency of successful antidromic propagation into the soma of tuberoinfundibular arcuate neurons. In oestrogen-treated preparations, tuberoinfundibular arcuate neurons responsive and unresponsive to accessory bulb stimulation could be distinguished by the frequency of successful antidromic propagation into the soma. These studies demonstrate that olfactory relay neurons in the accessory olfactory bulb act to enhance the activity of a subpopulation of tuberoinfundibular arcuate neurons via the amygdala and that this neural transmission is modulated by oestrogen.

Action Potentials↗
PubMed2002

The terminal nerve ganglion cells project to the olfactory mucosa in the dwarf gourami.

Single- and double-label immunocytochemical studies were conducted using antisera to salmon gonadotropin-releasing hormone (sGnRH) and molluscan cardioexcitatory peptide (FMRFamide) to determine whether terminal nerve ganglion cells project to the olfactory mucosa in the dwarf gourami, Colisa lalia. Both peptides were present in terminal nerve ganglion perikarya and fibers in brain and nasal cavity. Labeled fibers were present in the olfactory nerve and could be traced to the olfactory mucosa. All terminal nerve ganglion cells contained both sGnRH and FMRFamide-like peptides. This study suggests that the terminal nerve ganglion cells can influence both brain and chemoreceptive structures.

Animals↗
PubMed1997

[Neuropathological study on progression of the limbic degeneration in senile dementia of Alzheimer type].

Neuropathological study on the limbic lesion of 33 autopsy cases with senile dementia of Alzheimer type (SDAT) showed as follows. 1) The entorhinal cortex was more atrophied than the hippocampus. 2) Neuronal loss was found in the 2nd and 3rd layers of the entorhinal cortex, irrespective of the different numbers of senile plaques and neurofibrillary tangles (NFTs). 3) Fibrillary gliosis occurred in the stratum lacunosum of the hippocampus, irrespective of the different degrees of neuronal loss in the stratum pyramidale of the hippocampus. 4) The prosubiculum showed gliosis disproportional to neuronal loss. 5) The degree of fibrillary gliosis in the stratum lacunosum of the hippocampus and in the prosubiculum was proportional to that of the entorhinal cortical degeneration. 6) The shape of the hippocampus of the cases with SDAT was different from that in the cases with anoxic encephalopathy in which neuronal loss in the CA1 occurred primarily: 7) Distribution pattern of the lesion in the hippocampus of SDAT cases was almost the same as that found in the cases with infarct in the collateral sulcus involving the entorhinal cortex. It is assumed that the hippocampal atrophy is a primary degeneration attributable to appearance of senile plaques and NFTs. However, our present observations and previous report (Neurosci Lett 184: 141-144 1995) suggest that degeneration of the entorhinal cortex and its efferent fibres (perforant pathway) plays a considerable part of role in development of the hippocampal atrophy. The present study could contribute to understanding of progression of the limbic lesion in SDAT.

Aged↗
PubMed1982

Postnatal proliferation and maturation of olfactory bulb neurons in the rat.

Mitral cells are formed prenatally whereas most granule cells originate postnatally. Material was taken from 2-day-old, 14-day-old, 28-day-old, and adult rat olfactory bulbs and processed for rapid Golgi or Cresyl Violet staining. We show that the number of granule cell bodies/mitral cell body increases from 7.0 to 46.3 during the first two weeks of life; most mitral cells appear morphologically functional during the first postnatal week; few granule cells appear to be functional until the second postnatal week; and the number of short axon interneurons increases dramatically during the second postnatal week. We conclude the newborn rats have an intact afferent pathway from olfactory receptors to primary cortex that lacks the extensive interneuronal circuitry characteristic of adults.

Animals↗
PubMed1986

Amphibian terminal nerve: distribution revealed by LHRH and AChE markers.

Immunocytochemical and histochemical studies in the tiger salamander and bullfrog demonstrated the presence of luteinizing hormone-releasing hormone-like immunoreactive (LHRH-ir) material and acetylcholinesterase (AChE) in the terminal nerve (TN). Immunoreactive perikarya and processes were found within the olfactory, vomeronasal and trigeminal nerves and in the nasal epithelium. Central TN projections consisted of fibers terminating in the olfactory bulb and bundles that projected to another group of LHRH-ir perikarya in the preoptic region. Up to 4 weeks following hypophysectomy, the labeling intensity and number of TN-immunoreactive neurons were not altered. Acetylcholinesterase histochemistry in the salamander revealed two distinct groups of neurons associated with the TN: a lightly labeled group of fusiform perikarya was located in the olfactory nerve proper and a more heavily labeled group of larger oval perikarya was found within AChE-positive trigeminal fascicles in the ventral mucosa. This study has demonstrated that the amphibian TN follows olfactory, vomeronasal and trigeminal nerves to reach peripheral targets in the nasal mucosa. The projection of TN fibers to discrete olfactory bulb glomeruli, especially evident in the bullfrog, suggests that the TN functions in odor processing. The TN projection to the preoptic region in both of these amphibians implicates the TN in reproductive processes.

Acetylcholinesterase↗
PubMed1986

Petit mal seizure spikes in olfactory bulb and cortex caused by runaway inhibition after exhaustion of excitation.

The olfactory bulb (OB), anterior olfactory nucleus (AON) and prepyriform cortex (PC) maintain 3 kinds of feedback among their populations of excitatory and inhibitory neurons: negative feedback, mutual excitation, and mutual inhibition. At normal levels of synaptic input these are balanced and give rise to chaotic and near-sinusoidal oscillatory EEG activity. Under intense repetitive electrical stimulation of the lateral olfactory tract (LOT), there is failure of the afferent excitatory terminals, perhaps due to transmitter depletion. In this circumstance there is deficient excitatory input under the condition of a high level of sustained activity among mutually inhibitory neurons. An instability develops in which some inhibitory neurons become more disinhibited (excited) and others more inhibited (less active) to the point of a paroxysmal discharge that is manifested in a massive compound IPSP of the excitatory neurons. The paroxysm terminates abruptly, but by mechanisms still unclear repeats at a rate of about 3/s for 10-70 s. It is accompanied by simultaneous ipsilateral twitching of the eyelids and muzzle, salivation, tearing, arrest, and lack of responding to sensory stimuli but without loss of posture, resembling absence in humans. It does not result from runaway mutual excitation, and it rarely culminates in full-blown convulsions. Similar spikes usually also occur in the OB and AON; the sequences of spikes appear to entrain. These normal and seizure EEGs are simulated with a network of non-linear differential equations, that is designed in conformance with the anatomy and physiology of the olfactory system. The seizure appears as an emergent property of the OB, AON and PC interactive system, that is due to an induced asymmetry in the feedback network that controls normal background activity.

Animals↗
PubMed2004

Repeated low level formaldehyde exposure produces enhanced fear conditioning to odor in male, but not female, rats.

Multiple chemical sensitivity (MCS) is an ill-defined disorder in humans attributed to exposure to volatile organic compounds. This study draws on apparent parallels between individuals with posttraumatic stress disorder (PTSD) and panic disorder and a subset of those reporting MCS, using a conditioned fear task in rats. Male and female Sprague-Dawley rats were given repeated exposure to 2 ppm formaldehyde (Form) (1 h/day x 5 days/week x 4 week) or air, and after 2-3 weeks, rats were trained on the conditioned fear task. One half of Air and Form rats were given odor (orange oil, the conditioned stimulus, CS) paired with footshock (PRD) and the other half was given the same stimuli in an unpaired manner (UNP). After 24 h, rats were placed into the same context without the CS or footshock. Male and female PRD groups demonstrated contextual freezing 5-15% of the time, while the UNP groups showed freezing 30-50% of the time, with no effect of Air or Form pretreatment. For the next 5 days, rats were placed into a novel context and tested for freezing in the absence or presence of the CS. In male rats, Form pretreatment produced a significantly greater freezing response in both UNP and PRD groups in the presence of the CS, with no differences in freezing in the absence of the CS. In female rats, no significant differences between Form pretreated rats and Air controls were observed in either the PRD or UNP groups. The increase in conditioned fear responding to the CS after Form exposure in males suggests that repeated low-level Form may act as a stressor to produce sensitized responding within olfactory/limbic pathways, and may help explain the panic-like responses observed in a subset of individuals reporting MCS. Furthermore, the male/female differences suggest a gonadal hormonal contribution to this behavior.

Analysis of Variance↗
PubMed1999

The development of brain sex differences: a multisignaling process.

In order to account for the development of sex differences in the brain, we took, as an integrative model, the vomeronasal pathway, which is involved in the control of reproductive physiology and behavior. The fact that brain sex differences take place in complex neural networks will help to develop a motivational theory of sex differences in reproductive behaviors. We also address the classic genomic actions in which three agents (the hormone, the intracellular receptor, and the transcription function) play an important role in brain differentiation, but we also point out refinements that such a theory requires if we want to account of the existence of two morphological patterns of sex differences in the brain, one in which males show greater morphological measures (neuron numbers and/or volume) than females and the opposite. Moreover, we also consider very important processes closely related to neuronal afferent input and membrane excitability for the developing of sex differences. Neurotransmission associated to metabotropic and ionotropic receptors, neurotrophic factors, neuroactive steroids that alter membrane excitability, cross-talk (and/or by-pass) phenomena, and second messenger pathways appear to be involved in the development of brain sex differences. The sexual differentiation of the brain and reproductive behavior is regarded as a cellular multisignaling process.

Animals↗