Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Piriform Cortex”

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 919 records · Page 51Linked to original sources
PubMed1996

MR spectroscopic imaging and diffusion-weighted MRI for early detection of kainate-induced status epilepticus in the rat.

Previous studies have shown that reduction of N-acetyl-aspartate (NAA) is correlated with the degree of neuronal loss at 3 days after kainate-induced status epilepticus in the rat. In this study, magnetic resonance spectroscopic imaging (MRSI), measurement of NAA and lactate, T2-weighted MRI, and diffusion-weighted MRI were used to study early alterations in rat piriform cortex at 12 and 26 h after kainate administration. The major findings are that decreased NAA signal, increased lactate signal, and decreased apparent diffusion coefficient (ADC) were observed at 12 h, with little evidence of histological and T2-weighted MRI changes. These results support the hypothesis that NAA, lactate signals, and ADC provide sensitive methods for detection of early and minimal brain damage in vivo.

Animals↗
PubMed1991

Development of paleocortical projections through the anterior commissure of hamsters adopts progressive, not regressive, strategies.

The perinatal development of anterior commissure projections was studied in hamsters by use of carbocyanine crystals implanted either into the commissure or into the ventrolateral prosencephalon. The earliest fascicles of growing commissural fibers had reached the midline on day 14 of gestation (E14). On E15, these fibers had entered the opposite hemisphere and reached the borders of their target regions. No waiting period was observed, since on E16 axons were already collateralizing into most targets. On P1, labelled cells were seen in all regions projecting through the anterior commissure in adults, namely, the anterior olfactory nucleus, olfactory tubercle, piriform cortex, nucleus of the lateral olfactory tract, bed nucleus of the stria terminalis, insular, perirhinal, entorhinal, and temporal cortices, as well as the amygdaloid complex. No evidence of topographical exuberance was detected. Counts of labelled neurons showed that the number of commissural cells increased gradually after birth. It is concluded that the development of paleocortical connections through the anterior commissure employs progressive strategies, lacking the regressive phenomena that are characteristic of the neocortical projections through the corpus callosum.

Aging↗
PubMed2004

Effects of 6-cyano-7-nitroquinoxaline-2,3-dione on nicotinic receptor subunit transcript expression in the rat brain.

The nicotinic cholinergic system exerts potent modulatory effects on glutamatergic neurotransmission, an effect mediated in part by increased glutamate release following activation of presynaptic nicotinic cholinergic receptors. Ionotropic glutamate receptor agonists also stimulate release of acetylcholine, suggesting that these neurotransmitter systems reciprocally regulate one another. We investigated an interface between the nicotinic cholinergic and glutamatergic systems by measuring nicotinic receptor subunit transcript expression following administration of 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX), an antagonist of the AMPA and kainate subtypes of glutamate receptors. Using [(35)S] in situ hybridization, we measured expression of alpha 2, alpha 3, alpha 4, alpha 5, alpha 7, beta 2, beta 3, and beta 4 nicotinic receptor subunit transcripts in the rat forebrain. Following 7 days of treatment with vehicle or CNQX (1 mg/kg/day or 10 mg/kg/day), changes in nicotinic receptor subunit transcript expression were restricted to subunits that form heteromeric receptors. We found increased levels of transcripts for alpha 2 and beta 2 nicotinic receptor subunits in the hippocampus, decreased alpha 4 subunit transcripts in the medial habenula and amygdala, and increased beta 2 subunit transcripts in the septum and piriform cortex. We did not detect changes in expression of transcripts for the alpha 7 subunit, which forms homomeric nicotinic receptors. Our findings indicate that expression of nicotinic cholinergic receptor subunit transcripts are regulated in a subunit- and region-specific fashion by CNQX, an antagonist of non-NMDA ionotropic glutamate receptors.

6-Cyano-7-nitroquinoxaline-2,3-dione↗
PubMed2006

GABA and opioid binding distribution in the brain of the seizure-resistant Proechimys guyannensis: an autoradiography study.

Proechimys guyannensis rodents present resistance to epilepsy. Autoradiography was used to map GABA(A) ((3)H-Muscimol), benzodiazepine ((3)H-Flunitrazepam), mu ((3)H-DAMGO), and delta ((3)H-DPDPE) opioid receptor binding in adult Proechimys guyannensis brain under normal conditions. Results were compared with values obtained from adult Wistar rats. Proechimys presented reduced (3)H-Muscimol binding in several cortices, thalamus, medial amygdala nucleus, and dorsal dentate gyrus. (3)H-Flunitrazepam binding was reduced in periaqueductal gray, frontal and entorhinal cortices, and enhanced in piriform cortex and ventral CA2 field of Ammons horn. Concerning (3)H-DAMGO binding, high values were found in several cortices, medial amygdala nucleus, dorsal dentate gyrus, and periaqueductal gray, whereas reduced binding was detected in anterior olfactory tubercle, cingulated cortex, thalamus, basolateral amygdala, substantia nigra, and dorsal and ventral CA fields. High (3)H-DPDPE binding was noticed in CA1 field from dorsal hippocampus, while reduced values were found in cingulate cortex, olfactory tubercle, thalamus, and substantia nigra. These findings provide the first description of receptor binding distribution of the Proechimys brain and suggest natural endogenous anticonvulsant mechanisms of theses rodents under normal conditions.

Animals↗
PubMed1993

Expression of c-fos protein in the experimental epilepsy induced by pilocarpine.

The expression of the c-fos proto-oncogene, as estimated by immunohistochemistry of the FOS nuclear protein, was studied in both focal and generalized seizures induced in rats by systemic administration of pilocarpine. Focal seizures, as indicated by the occurrence of stereotyped oral movements, chewing and sniffing, were evoked by either a subconvulsant dose of pilocarpine (200 mg/kg) or the association of a convulsant dose of pilocarpine (400 mg/kg) with SCH 23390, a selective D-1 dopamine receptor antagonist. This seizure pattern resulted in FOS accumulation in certain limbic areas, namely, the piriform cortex, amygdala, and olfactory tubercle. On the other hand, in rats developing generalized seizures, accumulation of FOS was also found in hippocampus, cingulate cortex, frontal cortex, striatum, accumbens, as well as in certain thalamic nuclei. Generalized seizures, including motor limbic seizures and status epilepticus, were induced by either a convulsant dose of pilocarpine (400 mg/kg) or a low dose of pilocarpine (15-200 mg/kg) combined with either lithium or the D-1 selective agonist SKF 38393. These findings indicate a close correlation between the sequence of behavioural alterations induced by pilocarpine and the proto-oncogene activation. The results provide the basis for mapping the areas of origin and the pathways of generalization of seizure activity. As shown by the effects of dopamine receptor agonists and antagonists, the process of generalization appears to be controlled by the dopamine system.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗
PubMed1993

Levodopa induction of Fos immunoreactivity in rat brain following partial and complete lesions of the substantia nigra.

It is controversial whether levodopa (L-DOPA) therapy in the early stages of Parkinson's disease (PD) predisposes to later complications. Partial lesions of the substantia nigra (SN) in rat provide a model of the early stages of PD. We have investigated the potential effects of L-DOPA in early PD by analyzing its influence on the activity of the immediate early gene Fos in the partially lesioned rat. Fos has been used to examine neuronal response to a variety of stimuli in vivo, and L-DOPA is known to increase Fos-like immunoreactivity (FosLI) in striatal neurons after complete lesions of the SN. To determine its effects following partial lesions, we analyzed FosLI in rats given L-DOPA after partial (50-90%) and complete (> 90%) unilateral 6-hydroxydopamine lesions of the SN. Behavioral responses to intraperitoneal injections of apomorphine and amphetamine during life and cell counts of neurons in the SN with tyrosine hydroxylase-like immunoreactivity established the extent of nigral cell loss. FosLI was present in the striatum on the lesioned side predominantly laterally in rats with partial lesions and throughout in rats with complete lesions. Sections counterstained with toluidine blue revealed that only medium-sized striatal neurons displayed FosLI. Prominent FosLI was also found in the ipsilateral piriform cortex and amygdala in both groups and additionally in the ipsilateral zona incerta in the complete group. Therefore L-DOPA induces Fos in the striatum after partial as well as complete SN lesions. This result suggests that L-DOPA-induced Fos expression may occur in the early stages of PD and may not require dopamine receptor upregulation, which is believed to develop only in completely lesioned rats and in later stages of PD. The unexpected induction of Fos activity in brain regions besides the striatum suggests that L-DOPA therapy in patients with PD may have more widespread effects than previously anticipated. Since Fos is known to regulate gene transcription, potential alterations in its activity may contribute to the complications associated with L-DOPA therapy in PD.

Animals↗
PubMed1997

Differential spatial patterns of Fos induction following generalized clonic and generalized tonic seizures.

The expression of generalized clonic and generalized tonic seizures has been suggested to result from the activation of different and independent neuronal circuits. Using the induction of the c-fos protein (Fos) as a marker of neuronal activity, we identified brain structures that are differentially associated with the expression of electroconvulsive shock-induced generalized clonic and generalized tonic seizures. Expression of either seizure phenotype resulted in a similar bilaterally symmetrical increase in Fos immunoreactivity in many forebrain structures, including the bed nucleus of the stria terminalis, hippocampal dentate gyrus, amygdala, and piriform cortex, compared to controls. However, following tonic hindlimb extension (THE), the degree of labeling in specific thalamic, hypothalamic, and brain stem areas was significantly greater than that of either controls or animals exhibiting clonic seizures. While a greater number of neurons in the hypothalamus (e.g., ventromedial nucleus), subparafascicular thalamic nucleus, peripeduncular area, deep medial superior colliculus, dorsal and lateral central gray, and paralemniscal nuclei were robustly labeled following THE, noticeably fewer cells were immunoreactive following face and forelimb clonic seizure behaviors. These differences were also found to be independent of the stimulus magnitude. In animals stimulated with the same current intensity but expressing either of the two seizure phenotypes, the pattern of Fos induction was consistent with the seizure phenotype expressed. These results demonstrate that specific subsets of neurons are differentially activated following the expression of different generalized seizure behaviors and that activity in discrete mesencephalic and diencephalic structures is more frequently associated with the expression of generalized tonic seizures than with the expression of generalized clonic seizures.

Animals↗
PubMed1997

Regeneration of the olfactory tract following neonatal lesion in rats.

Neuronal regeneration following early postnatal olfactory tract transection (OTS) was investigated in newborn Wistar rats. Olfactory tract lesioned rats were sacrificed at different time periods and the brains processed for Nissl staining. This was used to study the neural cell architecture; fiber tracts (myelinated fibers) were examined with Luxol Fast Blue staining. In addition, a neuronal tracing technique (i.e., retrograde labeling) was employed to study the reestablishment of connections with the target sites following transection of the tract. Degeneration of the olfactory tract was evident at the 7th day following lesion. Regeneration of the tract was not apparent even up to 60 days following transection. However, by 240 days, the olfactory tract had regenerated and the tract fibers had reestablished connection. This was confirmed by retrograde labeling of mitral cells of the olfactory bulb with Fast Blue (FB) injected into the piriform cortex, the target site of these neurons. In this study, we show that mammalian olfactory tract can regenerate spontaneously if the olfactory tract is lesioned neonatally. The results suggest that the olfactory tract is an excellent model to investigate some issues related to central nervous system regeneration.

Amidines↗
PubMed1997

Increased axon number in the anterior commissure of mice lacking a corpus callosum.

Relatively few behavioral deficits are apparent in subjects with hereditary absence of the corpus callosum (CC). The anterior commissure (AC) has been suggested to provide an extracallosal route for the transfer of interhemispheric information in subjects with this congenital defect. Anterior commissure size, axon number, axon diameter, and neuronal distribution were compared between normal mice and those with complete CC absence. No difference in midsagittal AC area was found between normals and acallosals, nor were differences found in the numbers or diameters of myelinated axons. However, axon counts indicated an 17% increase or about 70,000 more unmyelinated axons in the AC of acallosal mice, and the mean diameter of unmyelinated axons was slightly less than in normal mice (0.24 vs 0.26 microm). This decrease in axon diameter enabled more axons to pass through the AC without increasing its midsagittal area. The topographical distribution of neurons sending axons through the AC, assessed with lipophilic dyes, was qualitatively similar for almost all the known regions of origin of the anterior commissure in normal and acallosal mice. There was a pronounced deficit of AC cells in the anterior piriform cortex of BALB/c mice, but this occurred whether or not the mouse suffered absent CC. Although the increase in AC axon number is far smaller than the number of CC axons that fail to reach the opposite hemisphere, the higher number of axons present in the AC of acallosal mice may contribute to the functional compensation for the loss of the CC.

Agenesis of Corpus Callosum↗
PubMed2001

NOGO mRNA expression in adult and fetal human and rat nervous tissue and in weight drop injury.

Nogo is a myelin-associated protein known to inhibit growth of neurites. In order to understand possible physiological roles of Nogo, we performed in situ hybridization using rat and human probes complementary to a Nogo-A-specific sequence and a sequence shared by all known Nogo transcripts recognizing nogo-A, -B, and -C. We studied the cellular distribution of nogo-mRNA in fetal and adult human and rat tissues, with a focus on the spinal cord and ganglia. Rat mRNA expression was also studied in a spinal cord weight-drop model and in animals exposed to kainic acid. In human fetal tissue, nogo-A was strongly expressed in the ventral two-thirds of the spinal cord, the dorsal root ganglia, and autonomic ganglia. Similarly, nogo-A mRNA expression was observed in the adult human spinal cord and ganglia. High levels of nogo-A message were observed in neurons, such as motor neurons and sensory ganglia neurons. The distribution of nogo message in rats resembled that seen in human tissues. Thus, nogo mRNA was expressed in neurons and oligodendrocytes, but not astrocytes or Schwann cells. In addition, expression of nogo-A mRNA was observed in human and rat developing muscle tissue. High level of nogo-mRNA were also expressed in the rat trigeminal ganglion and trigeminal pontine nucleus. In fetal rats the adrenal gland and cell clusters in the liver were positive for the nogo-ABC pan-probe, but negative for the nogo-A probe. While neurons in the adult rat brain were generally positive, very prominent nogo-A mRNA and nogo-ABC mRNA signals were obtained from neurons of the hippocampus, piriform cortex, the red nucleus, and the oculomotor nucleus. Nogo-A mRNA expression was markedly reduced in the epicenter of a lesion in the spinal cord of adult rats 6 and 24 h after a weight-drop injury, while no perifocal upregulation of nogo mRNA was seen. No obvious change of nogo expression was detected in kainic acid exposed animals. In conclusion our in situ hybridization study has demonstrated widespread expression of nogo mRNA in the fetal, developing and adult nervous system of rat and man. In addition to oligodendroglial cells, high levels of nogo-A mRNA expression were found in neurons, raising important questions about the function of neuronal nogo mRNA. No obvious regulation of nogo was detected following injury.

Adult↗
PubMed2002

L-4-chlorokynurenine attenuates kainate-induced seizures and lesions in the rat.

Blockade of the strychnine-insensitive glycine site of the NMDA receptor is considered an attractive strategy for the development of novel neuroprotective and anticonvulsive agents. 7-Cl-kynurenic acid (7-Cl-KYNA) is a potent, selective antagonist of the NMDA/glycine receptor but penetrates poorly through the blood-brain barrier. Its prodrug, L-4-Cl-kynurenine (4-Cl-KYN), readily enters the brain from the circulation and provides antiexcitotoxic neuroprotection after systemic application. We now examined the effect of 4-Cl-KYN on seizures and neuronal loss caused by the systemic administration of the chemoconvulsant kainate (KA). 4-Cl-KYN (50 mg/kg, ip) was given 10 min before and 30, 120, and 360 min after KA (10 mg/kg, sc). Microdialysis and tissue level measurements in 4-Cl-KYN-treated rats showed increases in the concentration of 7-Cl-KYNA in several limbic brain regions of KA-injected animals. Continuous EEG recording for 24 h revealed that 4-Cl-KYN significantly delayed seizure onset and reduced the total time spent in seizures. Repeated 4-Cl-KYN administration also prevented KA-induced lesions in the piriform cortex and provided protection of hippocampal pyramidal cells in area CA1. In contrast, neurons in the hilus and in layer III of the entorhinal cortex were not protected. Consistent with the in vivo results, in vitro application of 7-Cl-KYNA to brain slices containing hippocampus and entorhinal cortex preferentially blocked low Mg(2+)-induced seizure activity in hippocampal pyramidal cells. Taken together, these data suggest that a prodrug approach using 4-Cl-KYN might offer advantages in the treatment of temporal lobe epilepsy.

Animals↗
PubMed1994

Desensitization of c-fos mRNA expression in rat brain following cortical lesions.

The effect of cortical lesions on the c-fos mRNA expression in adult rat brain was studied using in situ hybridization and Northern blot analysis. It was observed that the single cortical lesion evoked a rapid increase in the content of c-fos mRNA in whole brain. However, when rats received a second and third cortical injury 4 and 8 h after the first one, there was reduced elevation of c-fos mRNA after the second (60%) and third (75%) injuries in comparison with those seen after a single cortical lesion. These results represent the desensitization period during which the induction of c-fos mRNA by repeated cortical lesions was decreased. On the contrary, when animals were treated with a fourth cortical lesion 24 h after the first injury, with recovery for 16 h after the third one, the levels of c-fos mRNA were again elevated to a degree almost comparable to that seen after the single injury alone. The anatomical distribution of c-fos mRNA-expressing cells after cortical lesions revealed a large increase of hybridization to a heterogeneous population of hippocampal neurons including small cells of stratum granulosum in the dentate gyrus and larger cells within hippocampal stratum pyramidale. A dramatic labeling of neurons with c-fos riboprobe in frontoparietal and piriform cortex was also observed but with predominantly localized hybridization to c-fos mRNA on the damaged side of the cortex following the first and second cortical injury. However, hippocampal distribution of c-fos mRNA-containing cells was bilateral as a result of polysynaptic potentials evoked by cortical lesions.

Animals↗
PubMed1994

Glucocorticoid receptor mRNA ontogeny in the fetal and postnatal rat forebrain.

Glucocorticoid receptor (GR) ontogeny and distribution in postnatal rat brain have been demonstrated, but onset and distribution of GR gene expression during fetal life has not been reported. This study focuses on the distribution of GR-mRNA in the fetal and postnatal rat forebrain, with emphasis on hypothalamic and limbic structures. Time pregnant rats were decapitated at 8:30-9:30 AM on Gestational Days 14 (F14), F16, F17, F18, and F19. Postnatally, rats were sacrificed on Days 1, 4, 6, 10, and 16. Cryostat sections were subjected to in situ hybridization, using a cRNA probe directed to the GR-mRNA. GR-mRNA was detectible in the hippocamposeptal formation as early as F14. By F16, GR gene expression was evident in the hypothalamic paraventricular nucleus (PVN) as well. During late gestation (F17-F19), GR-mRNA was localized also in the thalamus, hippocampus, amygdala, and discrete cortical regions. Postnatally, GR-mRNA abundance was high in the PVN, CA1/CA2 hippocampal field, piriform cortex and dorsal endopiriform nucleus, specific amygdaloid nuclei, and the suprachiasmatic nucleus. In PVN, GR-mRNA was present prior to the onset of CRH gene expression (F17), which may suggest a role for GR in neuronal differentiation.

Aging↗
PubMed1999

A novel neuron-specific DNA end-binding factor in the murine brain.

To characterize the distribution of transcription factor AP-1 and YY1 DNA-binding activities in the rat brain, the labeled target oligonucleotides were loaded on brain sections and after incubation and washing, the residual signal was registered by autoradiography. The binding was predominantly associated with neurons and was regionally specific with highest levels in the cerebellum, hippocampus, and piriform cortex. The identified binding factor was not, however, sequence-specific, but apparently recognized DNA ends and was activated by long double-stranded DNA. UV cross-linking identified the molecular mass of the factor to be about 80 kDa. The factor was not found in soluble brain extracts, suggesting its association with membranes or the nuclear matrix. Despite apparent similarities with Ku protein, which targets DNA-ends, the DNA end-binding activity was present in brains of Ku86- and Ku70-deficient mice. Since DNA end-binding factors are generally involved in DNA repair, the same function may be suggested for the novel factor identified in the present study.

Animals↗
PubMed1995

Activation of astrocytes during epileptogenesis in the absence of neuronal degeneration.

The issue of whether neuronal degeneration is a primary factor in activation of astrocytes during epileptogenesis was addressed using the kindling model of epilepsy. No degenerative changes specific to the kindling process were observed in brain sections from kindled animals, sampled from the olfactory bulbs through to cerebellum and processed with the degeneration-sensitive cupric silver stain. Also, examination of lectin-stained sections did not reveal any reactive microglia. At the same time, reactive astrocytes, as judged by an increase in glial fibrillary acidic protein immunoreactivity and a de novo vimentin immunoreactivity, were prominent in amygdala, piriform cortex, entorhinal cortex and hippocampus. These results suggest that loss of neurones is not a prerequisite for establishment of epilepsy-prone state, that seizures of short duration do not necessarily result in neuronal death, and that in kindling, astrocytes are activated by factors that are not related to neuronal degeneration, but which are likely associated with abnormal neuronal activity.

Animals↗
PubMed1996

Changes in the expression of synapsin I and II messenger RNA during postnatal rat brain development.

Synapsin Ia, Ib, IIa, and IIb are neuronal phosphoproteins, which are supposed to play a role in the short-term regulation of neurotransmitter release. Besides a high degree of homology among the four synapsin subtypes, there are structural differences in the 3'end of their coding region. Here we present the first extensive study of the expression of their gene transcripts by using in situ hybridization and northern blot analysis. Our results show regionally and temporally distinct expression patterns of synapsin Ia, Ib, IIa, and IIb, which suggests different functional properties of the four synapsin subtypes. There was no specific messenger RNA (mRNA) expression of synapsin IIb in most brain regions apart from the cerebellum, suggesting a minor functional role of this synapsin subtype. Synapsin Ia, Ib, and IIa mRNA were expressed earlier in ontogenetically older brain regions such as the piriform cortex, the thalamus, and the hippocampus and later in ontogenetically younger areas such as the neocortex and the cerebellum. Owing to the distinct expression pattern of the synapsin subtypes, we suppose that the synapsins might be essential for the underlying molecular mechanism of pattern formation and plasticity in distinct brain regions during different states of rat brain development.

Animals↗
PubMed1996

Cellular hybridization for BDNF, trkB, and NGF mRNAs and BDNF-immunoreactivity in rat forebrain after pilocarpine-induced status epilepticus.

The messenger RNAs (mRNAs) for the neurotrophins, brain-derived neurotrophic factor (BDNF), and nerve growth factor (NGF), are upregulated during epileptic seizure activity, as visualized by in situ hybridization techniques. Neurotrophins might be protective against excitotoxic cell stress, and the upregulation during seizures might provide such cell protection. In this study, a high dose of pilocarpine (300 mg/kg) was used to induce long-lasting, limbic motor status epilepticus and a selective pattern of brain damage. The regulation of BDNF, trkB, and NGF mRNA was studied by in situ hybridization at 1, 3, 6, and 24 h after induction of limbic motor status epilepticus. BDNF immunoreactivity was examined with an anti-peptide antibody and the neuropathological process studied in parallel. BDNF mRNA increased in hippocampus, neocortex, piriform cortex, striatum, and thalamus with a maximum at 3-6 h. Hybridization levels increased earlier in the resistant granule and CA1 cells as compared to the vulnerable CA3 neurons. BDNF immunoreactivity was elevated in dentate gyrus at 3-6 h. trkB mRNA increased in the entire hippocampus. NGF mRNA in hippocampus appeared in dentate gyrus at 3-6 h and declined in hilar neurons at 6-24 h. Cell damage was found in the CA3 area, entire basal cortex, and layers II/III of neocortex. Endogenous neurotrophins are upregulated during status epilepticus caused by pilocarpine, which is related to the coupling between neuronal excitation and trophic factor expression. This upregulation of neurotrophic factors may serve endogenous protective effects; however, the excessive levels of neuronal hyperexcitation resulting from pilocarpine seizures lead to cell damage which cannot be prevented by endogenous neurotrophins.

Animals↗
PubMed1986

Transneuronal transport of peroxidase-conjugated wheat germ agglutinin (WGA-HRP) from the olfactory epithelium to the brain of the adult rat.

The sensory neurons of the olfactory epithelium, as a consequence of their odor detection function, contact both the external environment and the central nervous system. The possibility that substances applied to the epithelium might reach the central nervous system was investigated by the intranasal application of peroxidase-conjugated wheat germ agglutinin (WGA-HRP). WGA-HRP was transported through olfactory receptor axons to the glomerulus of the olfactory bulb. Reaction product was localized electron microscopically to tubulovesicular profiles and dense bodies in sensory axons. Evidence of transneuronal transport was indicated by reaction product localized in dense bodies in dendrites postsynaptic to receptor cell axons. Periglomerular, tufted and mitral cells in the olfactory bulb also were transneuronally labeled. Anterograde transneuronal labeling occurred in the olfactory tubercle, piriform cortex and surrounding the lateral olfactory tract. Retrograde transneuronal label was found in neurons of the basal forebrain with the largest number of perikarya in the lateral nucleus of the horizontal limb of the diagonal band, a major source of cholinergic afferents to the olfactory bulb. These data suggest that substances, specifically those which bind to receptors, are transported from the olfactory receptor neurons in the nasal epithelium to the brain. Thus, the olfactory system may provide a route of entry for exogenous substances to the basal forebrain.

Animals↗