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At least 19 recordsLinked to original sources
PubMed1992

Neural cell adhesion molecules are present in the fetal human primary olfactory pathway.

Olfactory tissues from human fetuses (17.5-28 weeks of gestation) were stained by immunofluorescence for neural cell adhesion molecules (N-CAMs). Staining for N-CAMs was most prominent in the olfactory nerve bundles in the lamina propria, while in the olfactory epithelium, it was present on the olfactory receptor neurons and globose basal cells. The basal cells proper and supporting cells lacked N-CAMs. In the olfactory bulb, only the olfactory nerve and glomerular layers showed moderate labeling for N-CAMs. Western blot analysis showed that the N-CAMs of the fetal human primary olfactory pathway consisted of three molecular isoforms, N-CAM180, N-CAM140 and N-CAM120.

Cell Adhesion Molecules, Neuronal↗
PubMed1978

Denervation of the primary olfactory pathway in mice. V. Long-term effect of intranasal ZnSO4 irrigation on behavior, biochemistry and morphology.

Intranasal irrigation of mice with 0.17 M ZnSO4 solution results in the immediate and total loss of the ability to find a buried food pellet. This anosmia persists for 6 weeks in at least 80% of the treated mice and for 4 months in half of the animals. This marked behavioral effect is matched by a long-term reduction of the levels of carnosine synthesis and transport in the primary olfactory pathway. These biochemical parameters are virtually undetectable at two weeks after treatment and even at one year after treatment do not exceed 5-10% of average control values. Light microscopic observations of tissues of the primary olfactory pathway at various times after treatment are consistent with these observations and indicate a substantial destruction of the olfactory epithelium with subsequent atrophy of the olfactory bulb. At very long intervals after treatment, some receptor regeneration is apparent with accompanying reinnervation of the olfactory bulb. Estimates from microscopy and biochemistry suggest that much less than 10% of the normal complement of functioning receptor cells is adequate to give apparently normal food-finding behavior.

Alanine↗
PubMedDate not supplied

Oestrogenic influences on the electrical activity of the olfactory pathway.

The influence of the oestrogenic hormones over the spontaneous and induced activity of the olfactory pathway was studied in normal female cats. Electrodes were placed chronically or acutely in the olfactory bulb (OB), olfactory tubercle (OT) and in the prepyriform cortex (PPC). Oestrogenic hormones were applied locally in the posterior hypothalamic region. Recordings were made during the two different phases of the oestral cycle. In addition, another group of castrated animals was studied. The oestral phase was induced in these cats by the subcutaneous administration of 17-beta-oestradiol. Results indicate that the pattern of the electroencephalographic spontaneous activity as well as the response induced by hypothalamic stimulation changed. The number of the bursts for each 10 sec trace was higher in oestrus than in anoestrus for all the structures studied. The duration of each burst also changed, being shorter in oestrus than in anoestrus cats. The threshold for significant bursting in the olfactory structures following hypothalamic stimulation was lower in oestrus than in anoestrus. The evoked potentials recorded in the same three olfactory structures by hypothalamic stimulation exhibited changes in correlation with the hormonal administration. In all the structures studied the amplitude of the different components of the evoked potentials increased immediately after the hormones were administered. However, the most dramatic increase was observed in the olfactory tubercle. In order to further investigate these changes in acute preparations, a study evaluating the excitability changes was conducted. Applied pulse pairs, with different interpulse intervals between 200 to 1000 msec, were delivered in the hypothalamus before and after 200 micrograms of the hormone were administered into the posterior hypothalamus.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1976

Denervation in the primary olfactory pathway of mice. III. Effect on enzymes of carnosine metabolism.

Carnosine (beta-Ala-L-His) is localized within the receptor neurons of the primary olfactory system. Carnosine synthetase, the enzyme responsible for its synthesis, is found in the primary olfactory pathway of the mouse at activities higher than that found in other body tissues and brain regions. Carnosinase, the degradative enzyme, is present at high activities, only in the olfactory epithelial portion of this pathway. Peripheral deafferentation or central denervation cause a selective decrease in the activity of carnosine synthetase in the reciprocal portion of the primary olfactory system implying specific localization within the receptor neurons. These data are consistent with a role for the dipeptide carnosine in olfactory neural transmission.

Animals↗
PubMed1975

Denervation in the primary olfactory pathway of mice. II. Effects on carnosine and other amine compounds.

Carnosine (beta-alanyl-histidine) is present in the olfactory bulb and olfactory eqithelium of mice and rats at 1-2 nmole/mg tissue. Peripheral deafferentation or central denervation causes a rapid, selective decrease of this depeptide from the reciprocal portion of the primary olfactory pathway. These data demonstrate the localization of carnosine within the primary olfactory chemoreceptor neurons and suggest a possible role for this compound in neural transmission.

Alanine↗
PubMedDate not supplied

Hypothalmic influences on the electrical activity of the olfactory pathway.

By means of evoked potentials a direct efferent connection was found to run from the posterior hypothalmus and medial forebrain bundle to primary olfactory structures (olfactory bulb, olfactory tubercle and prepyriform cortex). The pathway from the hypothalmus to the olfactory bulb follows in the lateral olfactory tract at a conduction velocity 5-10 m/sec. The olfactory tubercle functions as a relay station for the efferent fibers from various sources, running to the olfactory bulb. In animals with electrodes chronically implanted in the olfactory structures, hypothalamic stimulation gives rise to a prolonged train of hypersynchronous bursts of activity (40-50 Hz), which resemble the arousal reaction. This response is modified by transecting the cervical sympathetic trunk. By pathways still to be defined, potentials are evoked in the olfactory bulb by stimulation of the cervical sympathetic trunk and the termination of these sympathetic fibers shows a common postsynaptic neuronal pool with axons of hyopothalmic origin. Epinephrine topically applied to the olfactory mucosa induced hypersynchronous activity in olfactory structures, quite similar to that consequent to hypothalmic stimulation. These results suggest a multichanneled hypothalmic modulation of olfactory input.

Animals↗
PubMedDate not supplied

Olfactory pathway evoked potentials in response to hypothalamic stimulation.

Ipsilateral and contralateral stimulation of lateral, ventromedial and posterior hypothalamic nuclei produced evoked responses in the olfactory bulb and in the prepyriform cortex. No differences in the latencies were found by stimulation of each nucleus in the homo and contralateral olfactory structures. The high amplitude of the fast component (N1) was obtained with stimuli applied to the ventral zones and the slow components (N2, N3) were obtained with more dorsal stimulation. An ipsilateral pathway is indicated at the supramammillary and posterior commissure level, since severing these structures abolishes the evoked responses. A bilateral projection is proposed for the olfactory bulb.

Animals↗
PubMed1977

Denervation in the primary olfactory pathway of mice. IV. Biochemical and morphological evidence for neuronal replacement following nerve section.

Unilateral olfactory nerve section was performed in the mouse. Three biochemical markers of the olfactory chemoreceptor neurons: carnosine, carnosine synthetase activity and the olfactory marker protein, were measured in the olfactory bulb and epithelium. Parallel observations were made by light microscopy as well as at the ultrastructural level. The specific biochemical markers decrease rapidly in both bulb and epithelium and reach a minimum by the end of the first week after surgery. They then slowly return to 80% of control values by one month. Carnosinase activity in epithelium was essentially unaffected. These biochemical observations coincide temporally with the onset of degenerative changes seen morphologically, in both the bulb and epithelium. The degenerative changes persist for up to two weeks in the bulb and for about one week in the epithelium. At this time basal cell division and differentiation begins in the epithelium with subsequent regrowth of olfactory axons into the glomerular layer of the olfactory bulb with ther reappearance of olfactory axon terminals. The temporal coincidence of these biochemical and morphological observations suggests they are manifestations of the same process, and is consistent with the idea that the olfactory chemoreceptor neurons are perhaps unique in being able to be replaced from undifferentiated stem cells.

Animals↗
PubMed1977

Clinical testing of olfaction reassessed.

Odours in current use for testing olfaction (e.g., peppermint, camphor) cause considerable trigeminal nerve stimulation; this would render them relatively inefficacious in the detection of lesions of the main olfactory pathway. Musks and floral odours are considered to be relatively 'pure' olfactory stimulants, acting virtually exclusively via the first cranial nerve. These odours have been compared with standard odours in a group of patients whose olfactory pathways had been damaged by frontal tumours, surgical operation, head injury, multiple sclerosis and miscellaneous causes. Hyposmia or anosmia was detected more frequently and more reliably by musks and floral odours in all groups of patients; a number of patients had gross deficits of odour description without hyposmia or anosmia. Two-thirds of an unselected group of patients with multiple sclerosis had olfactory abnormalities. A substantial improvement in the rate of detection of organic lesions affecting the olfactory pathway can be achieved by substituting odours such as musk ketone, exaltolide, linalyl acetate and coumarin for those in current use.

Humans↗
PubMed1975

An olfactory projection area in orbitofrontal cortex of the monkey.

An olfactory projection area was studied in monkeys anesthetized with Nembutal. 1. Evoked potentials were recorded when the olfactory bulb (OB) was electrically stimulated in the lateroposterior portion of the orbitofrontal cortex (LPOF). However, those potentials disappeared when the anterior pyriform cortex (AP) (probably together with the medial portion of the amygdala (MA)) was aspirated or electrically destroyed. 2. In nearly the entire hypothalamic region, evoked potentials were recorded by the same stimulation of the OB. When the hypothalamic region was stimulated, evoked potentials were recorded in the LPOF. 3. The evoked potentials in the LPOF due to the OB stimulation never disappeared even when the thalamus was extensively aspirated or destroyed electrically, but they did disappear when the anterolateral and dorsoposterior portions of the hypothalamus were absorbed or electrocoagulated. 4. Evoked potentials in the mediodorsal nucleus (MD) of the thalamus were recorded when the OB was stimulated. When this nucleus was stimulated, evoked potentials were observed in the broad extent of the orbitofrontal cortex anterior to the LPOF, but never in the LPOF itself. 5. Monkeys were conditioned to discriminate two odors. When the LPOF was removed, such ability strikingly decreased; but when other areas in the prefrontal cortex were removed, the ability decreased only slightly. 6. It was concluded that there exists an olfactory pathway from the OB to the LPOF through the AP (and probably the MA) and the hypothalamus, but none through the thalamus, and that the LPOF plays an important role in the discrimination of odors. 7. It was proved that the entorhinal cortex (ER) is neither located as an intermediate olfactory area nor is it situated as a higher area than the LPOF in the newly found olfactory pathway stated above. It may be a link between the high olfactory area and the limbic system.

Animals↗
PubMed1979

Failure of deodorized males to induce oestrus in the wild mouse.

The ability of female mice to return to oestrus following exposure to males perfumed either with oil of wintergreen or with the commercial perfume, "Kanta" was evaluated. Unisexual grouping of female mice induced anoestrus in all individuals. Oestrus was, however, promptly induced in the majority of unisexually grouped females by exposure to normal males. By contrast, exposure to perfumed males failed to induce oestrus in unisexually grouped females. The results suggest that male urine which is the source of the primer pheromone involved in the induction of oestrus was ineffective because of the masking effect of artificial scents. Hence the unisexually grouped females were unable to perceive the pheromone from males and continued to remain in anoestrus following exposure to perfumed males. The results provide additional evidence in support of the view that the urinary pheromone produced by males induces oestrus in females by acting through olfactory pathways.

Animals↗
PubMed1975

[Evaluating function and disorders of smell].

Firstly the review deals with the olfactometry after discussing the olfactory and trigeminal sensitivity of the sense of smell. The term olfactometry will be newly fixed concerning the present problems of odor analysis. Under clinical aspects the methods of subjective olfactometry are discussed and valued. Olfactory tests basing on registering several psychosomatic reflexes (e.g. cardial and/or respiratory frequencies) cannot be described as "objective". Rather methods are objective which record poststimulatory electrophysiological events at different steps of olfactory pathways. The electric response olfactometry representing a cortical evoked so-called twin-potential containing equivalents for trigeminal and olfactory sense activity starts to demonstrate its efficiency. At least a complete test of olfactory function today includes the rhinomanometry for recording ability in nasal odor transport capacity. In the second part are discussed the olfactory disorders with clinical importance. Air borne disorders are confronted with sensorineural, which again are divided in prebulbar, bulbar, and postbulbar ones so far as possible. Respiratory smell disorders depend on nasal ventilation and occur in nasal deformations, in abnormalities of respiratory pathways, in cases of foreign bodies, mucosal inflammations, tumors, intoxications and allergy. Sensorineural olfactory disorders can be attached to age, to malformations or idiopathic defects, inflammations of the olfactory-neural apparatus, head injuries, brain tumors, metabolic or endocrinological diseases. Furthermore often they are accompanied with neurological and psychiatric diseases or professional and chemical intoxications and/or iatrogenic influences. The poor therapeutical possibilities are demonstrated as far as possible. Finally the experting problems in olfactory disorders are delineated, at which the evidence of objective olfactometry can be distincted.

Animals↗
PubMed1977

The development of olfactory and hippocampal pathways in the brain of the rat.

The temporal order of development of olfactory, hippocampal and thalamocortical connections has been determined by light microscopy. Scalpel lesions were made to interrupt these connections and the resulting terminal degeneration was stained by Eager's method (1970). A post-operative survival time of one to four days was used. Evidence of the development of these connections was first obtained at the following ages: Olfactory mucosa to olfactory bulb: axon fascicles by 16 days of gestation and terminals in glomeruli at birth; Olfactory bulb to prepyriform cortex at birth; Prepyriform to entorhinal cortex at 13 days after birth; Entorhinal cortex to hippocampus (the perforant path) at 9 days; Hippocampal dentate-Ammonic mossy fibres at 9 days; Hippocampal efferent projection to the septum at birth; Subicular projections to the anterior thalamus at birth and to the mammillary body at 6 days; Hippocampal commissural connections at birth; Corticothalamic and thalamocortical connections by 2 days. These results are discussed in relation to the question of how the development of brain connections is programmed.

Animals↗
PubMed1975

[Comparison of the effects of anosmia induced by either peripheral lesion or bulbectomy upon the feeding pattern of the rat (author's transl)].

In order to support the contention that the feeding pattern seen after olfactory bulb removal is due to a sensory loss, the feeding pattern of rats was studied after a peripheral chemical lesion of the olfactory mucosa. A conditioned smell aversion procedure was used to assess the occurence and duration of anosmia after the topical application of zinc sulfate to the olfactory mucosa. It was found that the sensory deficit induced by the peripheral lesion lasted from four to six days. The occurrence of the disrupted feeding pattern in the peripherally lesioned rats coincided in time with the short period of anosmia. Thus, the disruption of the feeding pattern after bulbectomy and after lesions of the central olfactory pathways is clearly the result of anosmia and not of the loss of other non-sensory functions of the olfactory bulbs.

Animals↗
PubMed1979

Responses of olfactory bulb neurones to the dipeptide carnosine.

Carnosine has been applied by microiontophoresis ot identified neurones in the olfactory bulb of the rat from solutions of different pH. Although mainly without effect when compared with conventional excitatory and inhibitory amino acids, the dipeptide tended to be depressive when ejected as a cation and excitant when ejected as an anion. The results obtained are not in favour of this substance being an excitatory transmitter in the primary olfactory pathway.

Amino Acids↗
PubMed1975

A degeneration study of some habenular efferents to the midbrain in a wallaby.

In this study, specimens of both sexes of a Western Australian wallaby (Steonix brachyurus) had surgical or electrolytic lesions made in the habenular complex unilaterally. Thirty-five-micron sections, cut coronally and parasagittally, were stained by the Nauta-Gygax ('54) or the Fink-Heimer ('67) technique to demonstrate degenerating fibers. Degeneration was seen in the habenular commissure and bilaterally in the habenula and fasciculus retroflexus, but was most extensive ipsilaterally. Habenular fibers destined for the tegmentum and central gray passed caudally into the midbrain in a continuous fan-like array which extended from the central gray dorsally to the interpeduncular nucleus ventrally. In their posterior course some fibers crossed the midline with the decussating cerebellar fibers. The majority of fibers, with those in the fasciculus retroflexus which passed ventral to the decussation of the superior cerebellar peduncle, turned dorsally. They passed mostly just lateral to the midline nuclei and into the central gray where degeneration was seen throughout the entire extent. Terminal degeneration was seen in the interpeduncular nucleus primarily in the dorsal and posterior parts, in the ventral tegmental nucleus and throughout the central gray, but was more densely clustered in the region of the dorsal tegmental nucleus.

Animals↗
PubMed1979

The organization of feline entopenduncular nucleus projections: anatomical studies.

The organization of entopeduncular nucleus (EPN) projections was studied in cats using autoradiographic and horseradish peroxidase (HRP) techniques. In autoradiographic studies, EPN axons were found to terminate in a J-shpaed region in the dorsal and medial part of the ventral anterior nucleus (VA) and the rostral portion of the adjacent ventral lateral nucleus (VL). EPN axons also terminated in the rostral portion of the centrum medianum (CM), the ventrolateral portion of the lateral habenular nucleus (LHB), and the pedunculopontine nucleus (PP). The VA included the largest terminal field although the LHB had the greatest density of terminals. Regardless of the region of EPN into which amino acids were injected, the terminal fields were the same: there was no localization within the EPN of the cells projecting to one region. HRP-containing cells were distributed throughout the EPN following injections into the VA, LHB, or PP, although many more cells were labeled following injections into either VA or LHB than PP. EPN cells containing HRP following injections into either VA or LHB were not morphologically different from those not containing HRP in the same respective animals. Following HRP injections into stria medullaris, only cells in the rostral part of the EPN were labeled, providing evidence that rostrally and caudally located EPN neurons have different paths to LHB. Although there may be a rostrocaudal organization of pathways to LHB, individual regions of the nucleus project to the same areas.

Animals↗