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PubMed1996

MR evaluation of patients with congenital hyposmia or anosmia.

OBJECTIVE: The purpose of this study was to evaluate patients with reduced or no sense of smell since birth for sites of abnormality by MR imaging. MATERIALS AND METHODS: Twenty-five patients who reported no olfactory function since birth were evaluated by olfactory testing, sinonasal endoscopy, and MR imaging. Surface coil and head coil images of the olfactory bulbs, olfactory tracts, subfrontal cortex, and temporal lobes in contiguous 3-mm sections were obtained. Two reviewers determined unilateral olfactory bulb and tract volumes and temporal lobe volumes in two separate sessions. Qualitative grading for olfactory bulb, olfactory tract, olfactory sulcus, subfrontal region, hippocampus, and temporal lobe damage also was performed. RESULTS: The absence of olfactory bulbs and tracts (68-84%) or the presence of hypoplasia (16-32%) was noted in all cases. Eight individuals had Kallmann's syndrome (hypogonadotropic hypogonadism with anosmia). Temporal and/or frontal lobe volume loss was noted in five individuals and was mild in all but one individual. CONCLUSION: Congenital anosmia or hyposmia appears to be an olfactory bulb-olfactory tract phenomenon rather than a cerebral process.

Adult↗
PubMed2006

Learning-induced reversal of the effect of noradrenalin on the postburst AHP.

Pyramidal neurons in the piriform cortex from olfactory-discrimination-trained rats have reduced postburst afterhyperpolarization (AHP), for 3 days after learning, and are thus more excitable during this period. Such AHP reduction is caused by decreased conductance of one or more of the calcium-dependent potassium currents, I(AHP) and sI(AHP), that mediate the medium and slow AHPs. In this study, we examined which potassium current is reduced by learning and how the effect of noradrenalin (NE) on neuronal excitability is modified by such reduction. The small conductance (SK) channels inhibitor, apamin, that selectively blocks I(A)(HP), reduced the AHP in neurons from trained, naïve, and pseudotrained rats to a similar extent, thus maintaining the difference in AHP amplitude between neurons from trained rats and controls. In addition, the protein expression level of the SK1, SK2, and SK3 channels was also similar in all groups. NE, which was shown to enhance I(AHP) while suppressing (S)I(AHP), reduced the AHP in neurons from controls but enhanced the AHP in neurons from trained rats. Our data show that learning-induced enhancement of neuronal excitability is not the result of reduction in the I(AHP) current. Thus it is probably mediated by reduction in conductance of the other calcium-dependent potassium current, sI(AHP). Consequently, the effect of NE on neuronal excitability is reversed. We propose that the change in the effect of NE after learning may act to counterbalance learning-induced hyperexcitability and preserve the piriform cortex ability to subserve olfactory learning.

Animals↗
PubMed1996

IRK(1-3) and GIRK(1-4) inwardly rectifying K+ channel mRNAs are differentially expressed in the adult rat brain.

Molecular cloning together with functional characterization has shown that the newly identified family of inwardly rectifying K+ channels consists of several closely related members encoded by separate genes. In this report we demonstrate the differential mRNA expression and detailed cellular localization in the adult rat brain of seven members of the IRK and GIRK subfamilies. Using both radiolabeled cRNA riboprobes and specific oligonucleotide probes directed to nonconserved regions of both known and newly isolated rat brain cDNAs, in situ hybridization revealed wide distribution with partly overlapping expression of the mRNAs of IRK1-3 and GIRK1-4. Except for the low levels of GIRK4 transcripts observed, the overall distribution patterns of the other GIRK subunits were rather similar, with high levels of expression in the olfactory bulb, hippocampus, cortex, thalamus, and cerebellum. Marked differences in expression levels existed only in some thalamic, brainstem, and midbrain nuclei, e.g., the substantial nigra, superior colliculus, or inferior olive. In contrast, IRK subunits were expressed more differentially: all mRNAs were abundant in dentate gyrus, olfactory bulb, caudate putamen, and piriform cortex. IRK1 and IRK3 were restricted to these regions, but they were absent from most parts of the thalamus, cerebellum, and brainstem, where IRK2 was expressed predominantly. Because channel subunits may assemble as heteromultimers, additional functional characterization based on overlapping expression patterns may help to decipher the native K+ channels in neurons and glial cells.

Animals↗
PubMed1986

Olfactory evoked potentials in the rat.

Routine clinical assessment of the integrity of the olfactory pathway using olfactory evoked potentials remains an elusive goal. One important difficulty arises from the uncertainty of the exact origin of the potentials: are they produced by olfactory or trigeminal elements? To resolve this problem, an animal model using the rat was developed. Amylacetate was used as an odorant stimulus, and potentials were measured and computer averaged after elimination of trigeminal and vomeronasal activity. A positive-negative wave was recorded from the olfactory bulb surface, and a negative wave often followed by a positive wave was recorded from the surface of the cerebral cortex. Measurements from the scalp surface gave comparable results. Lesioning experiments of the olfactory pathway indicate that the evoked potentials recorded at the vertex originate in the ventral forebrain, specifically in the prepyriform cortex, olfactory tubercle, and anterior olfactory nucleus.

Animals↗
PubMedDate not supplied

[Functional organization of the rabbit hypothalamo-paleocortical system].

Investigation of the ascending hypothalamic connections with principal paleocortical centers (the olfactory tubercule, prepiryform cortex) indicates that the most short latent, poorly exhausted by rhythmic stimulation or by neuronal reactions EPs in these olfactory centers are elicited by stimulation of phylogenetically ancient hypothalamic areas of the anterior LPO and lateral LHA. It was also shown that the third deep layer of the prepiryform cortex is the main center for total ascending afferentation from these ancient parts of the hypothalamus. EPs and cellular responses to stimulation of phylogenetically new hypothalamic regions could be revealed with difficulties and were characterized by long latent periods or high degree of exhaustion by rhythmic stimulation. Paleo-hypothalamic system in the rabbit exhibits strict organization of functional connections. It was demonstrated that during stimulation of the main olfactory centers of the forebrain, EPs and neuronal responses originate chiefly in the anterior (LPO) and in the narrow zone of the lateral hypothalamus. Under the conditions used, cellular responses in VMH and SMA were not revealed.

Afferent Pathways↗
PubMed1990

125I-insulin binding is decreased in olfactory bulbs of aged rats.

125I-insulin binding was studied in membrane preparations of olfactory bulb, frontal cortex, hippocampus and hypothalamus from mature (5-month-old) and aged (22-month-old) rats. In the young animals the highest level of specific insulin binding was found in the olfactory bulb, with lower values of specific insulin binding in the frontal cortex, hippocampus and hypothalamus. In the aged rats the specific insulin binding was not changed in the frontal cortex, hippocampus and hypothalamus as compared to the young ones. A significant decrease of total insulin binding was observed only in the olfactory bulbs of aged rats (0.67 +/- 0.04 pmol insulin/mg protein) as compared to the mature animals (1.3 +/- 0.08 pmol insulin/mg protein). Scatchard analysis of insulin binding data revealed that this decrease was due to changes in the number of binding sites rather than to changes in the affinity of insulin receptors. It was suggested that the decrease observed in insulin receptor number in olfactory bulbs of aged rats might be due to the atrophic changes in the structure of olfactory bulbs previously shown by electron microscopy for aged rats.

Aging↗
PubMed1996

Dopamine D3 receptors are not involved in the induction of c-fos mRNA by neuroleptic drugs: comparison of the dopamine D3 receptor antagonist GR103691 with typical and atypical neuroleptics.

The effect of acute and chronic administration of dopamine receptor antagonists on the expression of mRNA encoding the cellular immediate-early gene c-fos was investigated in rat brain by in situ hybridization using 35S-labelled oligonucleotide probes. The selective dopamine D3 receptor antagonist GR103691 had no effect on the level of c-fos mRNA after acute or chronic treatment. Acute treatment with haloperidol increased the level of c-fos mRNA in the caudate-putamen, nucleus accumbens shell and core, olfactory tubercle and parietal cortex. After chronic treatment with haloperidol increases in the level of c-fos mRNA in the caudate-putamen and nucleus accumbens core were no longer observed. The increase in the level of c-fos mRNA in the nucleus accumbens shell was attenuated but still significantly elevated above the level measured in vehicle-treated animals. In the olfactory tubercle, parietal cortex, frontal cortex and cingulate cortex the level of c-fos mRNA was decreased after chronic haloperidol treatment. Acute sulpiride treatment reduced the level of c-fos mRNA in the olfactory tubercle, parietal cortex and cingulate cortex. After chronic treatment with sulpiride the level of c-fos mRNA was reduced in the dorsal caudate-putamen only. Acute clozapine treatment increased the level of c-fos mRNA in the nucleus accumbens shell and islands of Calleja. After chronic treatment with clozapine the level of c-fos mRNA remained elevated in the islands of Calleja but not in the nucleus accumbens shell. These results indicate that acute and chronic blockade of dopamine D3 receptors does not cause induction of c-fos transcription in limbic, striatal or cortical regions of rat brain. This study also demonstrated that acute blockade of dopamine receptors with haloperidol, sulpiride and clozapine induced different regionally specific patterns of c-fos expression which were altered after chronic blockade.

Animals↗
PubMed2000

Olfactory bulbectomy increases met-enkephalin- and neuropeptide-Y-like immunoreactivity in rat limbic structures.

Bilateral olfactory bulbectomy (OBX) in rats produces a well-characterized syndrome of behavioral, physiological, and neurochemical changes identical to those seen in depression. Previous experiments using in situ hybridization histochemistry have demonstrated that OBX increases prepro-neuropeptide-Y (NPY) and prepro-enkephalin (ENK) mRNA levels in limbic structures. The present experiments determined whether increases in peptide immunoreactivity occur in conjunction with increases in mRNA levels following OBX. In situ hybridization analyses in olfactory bulbectomized and sham-operated rats revealed increased prepro-ENK mRNA in the piriform cortex (PIR) and olfactory tubercles (OTs) of bulbectomized rats. Prepro-NPY mRNA levels were significantly increased in the PIR of bulbectomized rats as comapred to controls. Radioimmunoassays (RIAs) revealed significant elevations in ENK-like immunoreactivity in the OTs following OBX. NPY-like immunoreactivity was significantly elevated in the PIR following OBX. These data reveal that OBX-induced increases in ENK-like immunoreactivity occur concomitantly with increases in prepro-ENK mRNA, and NPY-like immunoreactivity occur concomitantly with increases in prepro-NPY mRNA.

Animals↗
PubMed2001

Selective loss of cholinergic neurons projecting to the olfactory system increases perceptual generalization between similar, but not dissimilar, odorants.

The neuromodulator acetylcholine is thought to modulate information processing in the olfactory system. The authors used 192 IgG-saporin, a lesioning agent selective for basal forebrain cholinergic neurons, to determine whether selective lesions of cholinergic neurons projecting to the olfactory bulb and cortex affect odor perception in rats. Lesioned and sham-operated rats were tested in an olfactory generalization paradigm with sets of chemically related odorants (n-aliphatic aldehydes, acids, and alcohols). Lesioned rats generalized more between chemically similar odorants but did not differ from controls in their response to chemically unrelated odorants or in acquisition of the conditioned odor. Results show that cholinergic inputs to the olfactory system influence perceptual qualities of odorants and confirm predictions made by computational models of this system.

Acetylcholine↗
PubMed1992

Distribution and cellular localization of mRNA coding for 5-HT1A receptor in the rat brain: correlation with receptor binding.

In order to localize the cells expressing 5-HT1A receptors in the rat brain, we used in situ hybridization histochemistry to visualize the distribution of the mRNA coding for 5-HT1A receptors. Oligonucleotides derived from different parts of the coding region of the rat 5-HT1A receptor gene were used as hybridization probes. 5-HT1A binding sites were visualized on consecutive sections by receptor autoradiography using 3H-8-hydroxy-2-(di-n-propylamino)tetralin as ligand. The highest levels of hybridization were observed in the dorsal raphe nucleus, septum, hippocampus, entorhinal cortex, and interpeduncular nucleus. Positive hybridization signals were also present in other areas, such as the olfactory bulb; cerebral cortex; some thalamic and hypothalamic nuclei; several nuclei of the brainstem, including all the remaining raphe nuclei, nucleus of the solitary tract, and nucleus of the spinal tract of the trigeminus; and the dorsal horn of the spinal cord. The distribution and abundance of 5-HT1A receptor mRNA in different rat brain areas generally correlate with those of the binding sites, suggesting that 5-HT1A receptors are predominantly somatodendritic receptors.

8-Hydroxy-2-(di-n-propylamino)tetralin↗
PubMed1992

Basic fibroblast growth factor mRNA increases in specific brain regions following convulsive seizures.

Basic fibroblast growth factor (bFGF) is a trophic factor synthesized in the central nervous system (CNS), where it is believed to play a role in neuronal maintenance and repair. Little is known about the regulation of this growth factor in the CNS. To determine whether the expression of the bFGF gene in the brain of adult animals changes in response to alterations of neuronal activity, we examined bFGF mRNA levels in several brain regions of rats experiencing focally-evoked convulsive seizures. Seizures were induced by microinjecting bicuculline unilaterally into an epileptogenic site within the deep prepiriform cortex, area tempestas (AT). By 5 h after initiation of brief limbic motor seizures from AT, there was a four fold increase in the levels of bFGF mRNA in the entorhinal cortex, hippocampus and olfactory bulb, but not in the caudate-putamen. The maximal expression of bFGF mRNA was reached by 10 h after seizure onset. In the same animals, the mRNA encoding nerve growth factor (NGF) was increased in entorhinal cortex and hippocampus, but not in the olfactory bulb. Our results demonstrate that neuronal activity can influence bFGF expression in an anatomically selective fashion and that acute changes in bFGF can occur in the uninjured mature brain. The increase in bFGF expression in response to excessive activation of specific neuronal circuitry may represent an adaptive response to protect against potential injury in those circuits.

Animals↗
PubMed2003

Olfactory learning and memory impairments following lesions to the hippocampus and perirhinal-entorhinal cortex.

The role of the hippocampus and perirhinal-entorhinal cortex was examined in an olfactory discrimination paradigm. Small neurotoxic lesions of the hippocampus (21% tissue damage) yielded relatively unimpaired olfactory retention across brief (30 s), intermediate (approximately 5 min), and 24-hr delays, whereas impairments were noted at 5-day retention intervals. Larger hippocampal lesions (63% tissue damage) spared memory at intermediate delays, with no impact at 8-day retention intervals. Aspiration lesions directed at the perirhinal-entorhinal cortex produced a variable performance pattern, with impairments noted at intermediate, 24-hr, and 5-day delays. Results suggest the hippocampus is not specifically involved in retaining olfactory information, with additional consideration given to the relationship between lesion size and memory impairment.

Animals↗
PubMed2002

Learning and memory of cue-reward association meaning by modifications of synaptic efficacy in dentate gyrus and piriform cortex.

This article begins with a review of recent experiments investigating the synaptic efficacy changes occurring in rat dentate gyrus and piriform cortex during an associative olfactory task. In all these experiments, animals were trained to discriminate among an artificial cue, a patterned electrical stimulation distributed to the lateral olfactory tract associated with a water reward, and a natural odor associated with a flash of light. Monosynaptic field potential responses evoked by single electrical stimuli to the lateral olfactory tract were recorded in the ipsilateral piriform cortex before and just after each training session. Monosynaptic field and polysynaptic field potentials evoked by single electrical stimuli applied respectively to the lateral perforant pathway and lateral olfactory tract were also recorded in ipsilateral dentate gyrus. The results showed an increase in synaptic efficacy subsequent to the first training session in the dentate gyrus network when compared with piriform cortex at the later stage of the learning. The early increase of monosynaptic response in the dentate gyrus was observed immediately after the first learning session but disappeared 24 h later. Inversely, a synaptic depression developed across sessions, becoming significant at the onset of the last (fifth) session. The polysynaptic potential recorded in this structure increased substantially when rats began to discriminate the leaming cues, usually after the second or third learning session. Then, from the third to the fifth session, an LTP like-phenomenon appeared in piriform cortex when rats perfectly mastered the associations. Experiments using high-frequency stimulation to prevent changes in gyrus dentatus indicated that the onset of the observed depression was necessary for the learning of the olfactory associations. The fact that hippocampal and cortical neuronal networks exhibited different timing in synaptic efficacy changes could physiologically explain learning and memory processes.

Animals↗
PubMed2004

Olfactory system activation from sniffing: effects in piriform and orbitofrontal cortex.

Neuroimaging studies suggest that piriform cortex is activated at least in part by sniffing. We used H(2)(15)O positron emission tomography (PET) to study 15 healthy volunteers while they participated in four conditions, two of which were sniffing odorants and odorless air. The remaining two conditions involved a constant, very low flow of either odorized or odorless air during velopharyngeal closure (VPC), a technique that prevents subject-induced airflow through the nasal passages. Contrary to expectation, sniffing under odorless conditions did not induce significant piriform and surrounding cortical (PC+) activity when compared to odorless VPC, even at a liberal statistical threshold. However, a small correlation emerged in PC+ between the difference signal of [odorless sniffing - odorless VPC] and peak rate of nasal pressure change. PC+ activity was, however, strongly evoked by odorant exposure during sniffing and VPC, with neither technique showing greater activation. Activity in orbitofrontal (olfactory association) cortex was absent during odorant stimulation (OS) with VPC, but present during odorant sniffing. Sniffing may therefore play an important role in facilitating the higher-order analysis of odors. A right orbitofrontal region was also activated with odorless sniffing, which suggests a possible orbitofrontal role in guided olfactory exploration.

Adult↗
PubMedDate not supplied

Changes in GABA-benzodiazepine receptor complex and in peripheral benzodiazepine receptors in male mice after copulation.

We studied the effect of copulation on GABA and benzodiazepine (BZD) receptors in the male mouse. After copulation, there was an 18% increase in the in vitro number of [3H]muscimol binding sites in frontal cortex. No changes were observed in central BZD binding sites labelled either in vivo by [3H]flunitrazepam or in vitro (in olfactory bulbs and in frontal cortex) by [3H]flumazenil, but further in vitro studies demonstrated that the GABA-stimulated [3H]flunitrazepam binding was reduced in both frontal cortex and olfactory bulbs. Copulation increased the number of peripheral BZD binding sites labelled by 3H-Ro 5-4864 in olfactory bulbs by 22% and in heart by 36%, but not in frontal cortex or in testes. The changes of GABA/BZD and peripheral BZD receptors in mouse suggest that the GABAergic system may be affected by copulation.

Animals↗
PubMed1995

The angiotensin receptor subtype AT1A predominates in rat forebrain areas involved in blood pressure, body fluid homeostasis and neuroendocrine control.

Subtypes of the angiotensin II (Ang II) type-1 (AT1) receptor are probably involved in distinct actions of the peptide, since their distribution in peripheral organs and regulation of their gene expression are different. We investigated the distribution of AT1A and AT1B receptor subtype mRNAs in the rat forebrain and pituitary using sensitive cRNA probes for in situ hybridization. High level of AT1A receptor mRNA expression is observed in the subfornical organ (SFO) and in the anterior hypothalamus, particularly the periventricular tissue surrounding the anterior portion of the 3rd ventricle (AV3V), which contains the organum vasculosum of the lamina terminalis (OVLT), the median preoptic nucleus and the preoptic periventricular nucleus as well as in the hypothalamic periventricular nucleus and in the parvocellular part of the paraventricular nucleus (PVN). Moderate to strong AT1A labeling was found in the anterior olfactory nucleus, the piriform cortex and the nucleus of the lateral olfactory tract. Very low AT1B receptor mRNA expression was found in the SFO and the PVN. In contrast, strong AT1B receptor mRNA expression coincided with low AT1A receptor mRNA expression in the anterior pituitary. Labeling was cytoplasmic at the light microscopic level. We thus suggest that the AT1A receptor is responsible for the central actions of Ang II in the rat forebrain whereas direct actions of Ang II on the anterior pituitary are mediated by the AT1B receptor subtype.

Animals↗
PubMed2003

Olfactory function after mild traumatic brain injury.

OBJECTIVE: The aim of this study was to determine the incidence of olfactory dysfunction after mild traumatic brain injury (MTBI). Damage to the olfactory bulbs or frontal cortex has been reported in MTBI, but olfactory dysfunction after MTBI has not been studied in a prospective way before. DESIGN: Patients with first-time MTBI were included. Patients' olfactory threshold values (Hyposmia Utility Kit by Olfacto-Labs) were measured 2 weeks after the trauma. Associations between olfactory threshold values and individual symptoms and S-100B and NSE concentrations were examined, using multiple linear regression analysis, adjusting for the influence of age. RESULTS: Twenty-two per cent of 111 included patients had hyposmia and 4% had anosmia. Thresholds at 2 weeks showed no significant associations with the presence of symptoms at the ER, nor with early concentrations of S-100B or NSE. CONCLUSIONS: Although a high prevalence of olfactory dysfunction was found, no correlation was found between olfactory dysfunction and acute parameters of MTBI.

Adolescent↗
PubMed1993

Viral infection and dissemination through the olfactory pathway and the limbic system by Theiler's virus.

Theiler's murine encephalomyelitis virus (TMEV) infection of mice can produce a biphasic disease of the central nervous system (CNS). Most susceptible strains of mice survive the acute infection and develop a chronic demyelinating disease. In this report, we analyzed the routes of spread of TMEV within the CNS of nude mice and target sites eventually infected in the CNS. Compared to the immunocompetent mouse, in which an antiviral immune response is mounted but virus persists, the nude mouse develops a severe encephalomyelitis due to the lack of functional T lymphocytes and provides a useful model for the study of viral dissemination. We demonstrated, by immunohistochemistry, the presence of viral antigen in defined regions of the CNS, corresponding to various structures of the limbic system. In addition, we found a different time course for viral spread using two different sites of intracerebral inoculation, ie, via the olfactory bulb or the cortex. Limbic structures were rapidly infected following olfactory bulb infection and then showed a decrease in viral load, presumably due to loss of target neurons. Using either route of infection, the virus was able to disseminate to similar regions. These results indicate that limbic structures and their connections are very important for the spread of TMEV in the brain. In the spinal cord, not only neuronal but hematogenous pathways were suspected to be involved in the dissemination of Theiler's virus.

Animals↗