Antidromic units in the prepyriform cortex driven by olfactory peduncular volleys.
Explore the source record for details and available documents.
Animals↗
SEARCH · Search PubMed
Results for “Olfactory 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.
Distribution of the serotonin 5-HT2 receptor family mRNAs: comparison between 5-HT2A and 5-HT2C receptors.
Because of their similarities, serotonin 5-HT2, 5-HT1C, and the recently described 5-HT2F receptors have been classified as members of the 5-HT2 receptor family, and they have been renamed 5-HT2A, 5-HT2C and 5-HT2B, respectively. The regional distribution and cellular localization of mRNA coding for the members of 5-HT2 receptor family were investigated in consecutive tissue sections from the rat brain by in situ hybridization histochemistry. No evidence for the expression of 5-HT2B receptor was found. High levels of 5-HT2A (formerly 5-HT2) receptor mRNA were observed only in few areas, as the frontal cortex, piriform cortex, ventro-caudal part of CA3, medial mammillary nucleus, the pontine nuclei and the motor cranial nerve nuclei in the brainstem, and the ventral horn of the spinal cord. The distribution of 5-HT2A receptor mRNA is generally in good agreement with that of the corresponding binding sites, although discrepancies were sometimes observed. 5-HT2C (formerly 5-HT1C) mRNA was present at very high levels in the choroid plexuses. However, very high levels were also seen in many other brain regions, as the retrosplenial, piriform and entorhinal cortex, anterior olfactory nucleus, lateral septal nucleus, subthalamic nucleus, amygdala, subiculum and ventral part of CA3, lateral habenula, substantia nigra pars compacta, several brainstem nuclei and the whole grey matter of the spinal cord. These results confirm and extend previous observations that 5-HT2C receptor mRNA is present in many brain areas in addition to those autoradiographically shown to have the corresponding binding sites and that 5-HT2C receptor subtype is a principal 5-HT receptor in the brain. From the comparison between their distributions, 5-HT2A and 5-HT2C receptor mRNAs appeared to be expressed in distinct but overlapping sets of brain regions. Both mRNAs coexisted at high levels in the anterior olfactory nucleus, piriform cortex, endopiriform nucleus, claustrum, pyramidal cell layer of the ventral part of CA3, taenia tecta, substantia nigra pars compacta, and several brainstem nuclei. In other regions both mRNAs were present but with different distributions, as the caudate-putamen. These results are also discussed in relation to the physiological meaning of the existence of two so similar receptor subtypes in the brain.
Animals↗
Determination of cell fate within the telencephalon.
The telencephalon (basal ganglia, septum, cerebral cortex and olfactory bulb) contains two general classes of neurons: those that project axons to distant targets and those that make only local connections. While projection neurons can be either excitatory (such as those in the olfactory bulb and cortex) or inhibitory (such as those in the striatum), local circuit neurons (interneurons) are usually inhibitory. Within these two general classes of neurons there are a myriad of cell subtypes based upon axonal and dendritic morphology, chemical markers, neurotransmitters, connectivity and physiology. A crucial issue regarding the development of the telencephalon is the molecular determination of neuronal subtypes. Since important aspects of neuronal fate determination occur within the proliferative zone, the consideration of determinants of a mature neuron's fate requires consideration of that cell's origin.
Animals↗
Characterization and topography of high-affinity 125I-neurotrophin-3 binding to mammalian brain.
The binding of biologically active and 125I-labeled neurotrophin-3 (NT-3) was studied with both dry film and emulsion autoradiography to compare with NGF binding and discover areas where NT-3 may function in vivo. The equilibrium binding of 300 pM 125I-NT-3 to rat brain sections was reversible and inhibited by unlabeled NT-3 (IC50, 420 pM). 125I-NT-3 bound in a saturable manner, with high affinity (Kd, 227-269 pM), and with a capacity (Bmax, 26 fmol/mg protein) that exceeded that of NGF by threefold. As with NGF, 125I-NT-3 also bound to a second population of sites with lower affinity (Kd, 2.8 nM) and higher capacity (Bmax, 170 fmol/mg protein). 125I-NT-3 binding was not blocked by NGF, or serum proteins, and brain-derived neurotrophic factor (BDNF) competed for it in a distinctly biphasic manner (IC50 values of 230 pM and 37 nM). Microdensitometry confirmed graphically and by Hill analysis the monophasic displacement of 125I-NT-3 and the biphasic displacement of 125I-NT-3 binding by BDNF in hippocampus, caudate-putamen, neocortex, and olfactory tubercle. In rat or cat, the topography of 125I-NT-3 binding differed from that reported for 125I-NGF binding or for the low-affinity NGF receptor. The highest binding densities were found in neocortical layers 1 and 2, the stratum oriens and radiatum of hippocampus, molecular layer of the dentate gyrus, nucleus of the lateral olfactory tract, entorhinal cortex, anterior olfactory nucleus, anteromedial thalamic nucleus, and amygdala. Moderate densities were found in neocortical layers 4-6, the neostriatum, amygdala, the dorsal root ganglia, and the central gray of spinal cord. Emulsion autoradiography also revealed binding in nerve terminal-rich regions of superficial neocortex and hippocampus but not on neural cell bodies. Binding was absent in many other brain regions, including cholinergic nuclei, and in all peripheral organs studied including liver, kidney, pancreas, heart, and skeletal muscle. 125I-NT-3 binding to sections of human basal ganglia resembled that seen in rat or cat, including high densities in the caudate, putamen, and superficial neocortex. The unique distribution and pharmacology of 125I-NT-3 binding to BDNF-sensitive and -insensitive sites in brain predict predominantly neuronal actions for these factors that are likely to be more widespread and distinct from those of NGF.
Animals↗
Immunocytochemical localization of angiotensinogen in the rat brain.
The distribution of angiotensinogen-like immunoreactivity in the rat brain was investigated using specific antisera against pure rat plasma angiotensinogen in conjunction with the sensitive streptavidin-biotin peroxidase method. Angiotensinogen antisera were shown by radioimmunoassay and Western blotting to recognize angiotensinogen from both rat plasma and cerebrospinal fluid, and to cross-react with des-AI-angiotensinogen (100%) but not with angiotensin I and II, tetradecapeptide, luteinizing hormone-releasing hormone, rat albumin and angiotensinogen from eight other species. Angiotensinogen-like immunoreactivity was detected throughout the rat brain in both neuroglia and neurons. The highest concentration of neuroglial angiotensinogen-like immunoreactivity was in the hypothalamus and preoptic areas, with moderate to heavy concentrations in the mesencephalon and myelencephalon. The cerebellum demonstrated neuroglial staining in the granular layer and fibre tracts. Very little neuroglial staining was noted in the cerebral cortex or olfactory bulbs. Neuronal immunostaining was observed throughout the globus pallidus and the caudate putamen, in various parts of the thalamus and the supraoptic nucleus of the hypothalamus. In the midbrain moderate immunostaining was observed in periaquaductal central gray, the deep mesencephalic nucleus, the inferior colliculus and in scattered cells in the anterior mesencephalon. In the medulla, neuronal staining was localized to the vestibular nuclei and to other cell bodies mainly in the dorsolateral regions. In the cerebellum, staining was noted mainly in the deeper cerebellar nuclei and in the Purkinje cells. Immunostaining in the cerebral cortex was localized to the cingulate cortex and the primary olfactory cortex. Light staining was present in the endopiriform cortex and in scattered neurons adjacent to the external capsule. In the olfactory bulbs light neuronal staining was mainly associated with the mitral cell layer. The widespread distribution of angiotensinogen-like immunoreactivity supports the view that it is synthesized in the central nervous system and forms part of a brain renin-angiotensin system. In addition, its presence at sites other than those normally associated with the control of blood pressure and fluid and electrolyte homeostasis suggests that its involvement may not be limited to these regulatory functions.
Angiotensinogen↗
The anterior olfactory nucleus and piriform cortex of the echidna and platypus.
The cyto- and chemoarchitecture of the anterior olfactory nucleus and piriform cortex of the short-beaked echidna and platypus were studied to determine: (1) if these areas contain chemically distinct subdivisions, and (2) if the chemoarchitecture of those cortical olfactory regions differs from therians. Nissl and myelin staining were applied in conjunction with enzyme reactivity for NADPH diaphorase and acetylcholinesterase, and immunoreactivity for calcium-binding proteins (parvalbumin, calbindin and calretinin) and tyrosine hydroxylase. Golgi impregnations were also available for the echidna. In the echidna, the anterior olfactory nucleus is negligible in extent and merges at very rostral levels with a four-layered piriform cortex. Several rostrocaudally running subregions of the echidna piriform lobe could be identified on the basis of Nissl staining and calcium-binding protein immunoreactivity. Laminar-specific differences in calcium-binding protein immunoreactivity and NADPH-d-reactive neuron distribution were also noted. Neuron types identified in echidna piriform cortex included pyramidal neurons predominating in layers II and III and non-pyramidal neurons (e.g., multipolar profusely spiny and neurogliaform cells) in deeper layers. Horizontal cells were identified in both superficial and deep layers. By contrast, the platypus had a distinct anterior olfactory nucleus and a three-layered piriform cortex with no evidence of chemically distinct subregions within the piriform cortex. Volume of the paleocortex of the echidna was comparable to prosimians of similar body weight and, in absolute volume, exceeded that for eutherian insectivores such as T. ecaudatus and E. europaeus. The piriform cortex of the echidna shows evidence of regional differentiation, which in turn suggests highly specialized olfactory function.
Animals↗
Facilitation of olfactory recognition by lateral entorhinal cortex lesion in rats.
An original olfactory recognition task was developed in order to examine the effect of lateral entorhinal cortex (LEC) lesion on olfactory mnesic processes. The task was based on the spontaneous exploratory behavior of rats toward odor sources. It consisted of a learning phase during which an odor was presented twice and in a recognition test, during which the same odor plus a new one was presented. The time rats spent sniffing the odor sources was measured. Olfactory recognition was identified by a short investigatory duration for the familiar odor as compared to a normal investigatory duration for the new odor during the test. The first three experiments aimed to validate the procedure. Experiment 1 was designed to show the decay of investigatory behavior caused by repeated exposure of the rats to one odor. Experiment 2 showed that normal rats display recognition when a short (5 or 40 min) pre-test delay was used, but not when a long pre-test delay (120 min) was used. Experiment 3 showed that FG7142, a well-known promnesic drug, enhanced the performance of the rats in this test as it allowed recognition at longer pre-test delays. The last experiment aimed at testing the effects of aspirative lesion of the LEC. Therefore, LEC-lesioned and sham-lesioned rats were submitted to variable pre-test delays. The experiment showed that an entorhinal lesion did not produce an impairment, but on the contrary facilitated olfactory recognition, as lesioned rats displayed recognition for delays at which sham-operated rats did not. These results show that LEC lesion apparently prolongs the duration of the olfactory mnesic trace. This effect might result from a modification of the functioning of structures innervated by the LEC. In this regard, it is noteworthy that LEC lesion produced a sprouting of septo-hippocampal fibers in the dentate gyrus of the hippocampus as assessed by acetylcholinesterase staining. Although the functional significance of this regrowth is not fully understood, the possible role of this sprouting should be considered.
Animals↗
Polysynaptic activation of the dentate gyrus of the hippocampal formation: an olfactory input via the lateral entorhinal cortex.
The possibility that olfactory input is transmitted to specific subregions of the hippocampal formation via the entorhinal cortex was investigated electrophysiologically by analyzing the laminar profiles of potentials evoked in the hippocampal formation by stimulation of the lateral olfactory tract (LOT). LOT stimulation resulted in long latency (14--20 ms) evoked responses in the dentate gyrus of the hippocampal formation ipsilateral to the stimulation. The variable long latency of these responses and their inability to follow stimulus rates of 40/s suggested that these potentials reflected polysynaptic activation. Analysis of the laminar profiles of the evoked potentials indicated that the responses originated from a synaptic field localized in the outer portion of the stratum moleculare of the dentate gyrus, a terminal distribution which overlaps that of the lateral entorhinal cortical (LEC) projection to the dentate gyrus. Lesions of the LEC eliminated the long latency responses in the dentate gyrus evoked by LOT stimulation. In addition, a conditioning pulse delivered either to the LOT or to the LEC produced paired pulse potentiation of the response elicited by subsequent stimulation of the other structure. No evidence was found to indicate that responses were generated in regio superior of the hippocampus proper following LOT stimulation. Taken together, these results suggest that stimulation of the LOT activates the dentate gyrus of the hippocampal formation by multisynaptic pathways which relay through the lateral portion of the entorhinal area. This finding is discussed with regard to entorhinal cortical organization and the known olfactory projections to the LEC.
Animals↗
Projections from orbitofrontal cortex to anterior piriform cortex in the rat suggest a role in olfactory information processing.
The orbitofrontal cortex (OFC) has been characterized as a higher-order, multimodal sensory cortex. Evidence from electrophysiological and behavioral studies in the rat has suggested that OFC plays a role in modulating olfactory guided behavior, and a significant projection to OFC arises from piriform cortex, the traditional primary olfactory cortex. To discern how OFC interacts with primary olfactory structures, the anterograde tracer Phaseolus vulgaris leucoagglutinin was injected into orbitofrontal cortical areas in adult male rats. Labeled fibers were found in the piriform cortex and olfactory bulb on the side ipsilateral to the injection. Notably, the projection to piriform cortex was predominantly from ventrolateral orbital cortex, and was not uniform; rostrally, the projection to the ventral portion of the anterior piriform cortex (APC) was substantial, while the dorsal APC was virtually free of labeled fibers. Labeled fibers were found in both the dorsal and ventral portions in more caudal regions of APC. Most labeled fibers were found in layer III, although a substantial number of fibers were observed in layers Ib and II. Labeled fibers in posterior piriform cortex also were seen after injection into orbitofrontal areas. Taken together with previous reports, these findings suggest that piriform cortex includes multiple subdivisions, which may perform separate, parallel functions in olfactory information processing. Further, these results suggest that the OFC, in addition to its putative role in encoding information about the significance of olfactory stimuli, may play a role in modulating odor response properties of neurons in piriform cortex.
Animals↗
Odorant deprivation reversibly modulates transsynaptic changes in the NR2B-mediated CREB pathway in mouse piriform cortex.
The olfactory system is an outstanding model for understanding activity-dependent neuronal plasticity in mammals. Olfactory sensory neurons (OSNs) in the periphery project onto mitral/tufted cells in the olfactory bulb (OB) and these mitral/tufted cells in turn project to piriform cortex (PC). Numerous studies have examined changes in OB after a permanent OSN ablation, but little is known about "trans-transsynaptic" changes taking place in the PC. Permanent zinc sulfate lesion of the olfactory epithelium resulted in a selective loss of the NMDA receptor NR2B protein and mRNA expression in pyramidal cells in layer IIb of PC after 2-7 d. Regulatory elements affected by NR2B signaling, namely the phosphorylation of CREB, were also downregulated only in layer IIb neurons. These changes could be caused by OSN axon loss in the zinc sulfate lesion, or to a reduced activity. To test this hypothesis, we performed both permanent and reversible naris occlusion, which blocks odorant access to the nasal cavities and OSN activity. The expression of NR2B and phospho-CREB were downregulated 5 d after occlusion and this reduction was fully restored 10 d after reopening of the naris. Subsequently, we identified the subset of pyramidal cells in layer IIb that are especially sensitive to the loss of odor-evoked activity using double retrograde tracers. In summary, the present study provides an initial characterization of the molecular mechanisms associated with odor stimulation on second order neuronal plasticity and phenotype in the olfactory system.
Animals↗
Glyoxylate oxidoreductase activity and glyoxylate-like molecules in the motor, somatosensory, cyngulate and olfactory areas of the rat frontoparietal cortex. Histoenzymological and immunohistochemical study.
In the present paper the presence of glyoxylate-oxidoreductase (GOR, GLYO-DH) activity and glyoxylate-like molecules has been investigated in several areas of the rat frontoparietal cortex-motor, somatosensory, cyngulate and olfactory areas-, using the histoenzymological and immunocytochemical methods. Antibodies against glyoxylate-like molecules have been obtained using a glyoxylate-BSA conjugate as immunogen. GOR activity as well as immunostaining for glyoxylate-like molecules were observed in the periphery of the perikaryon and neuronal processes of scattered neurons in the above mentioned cortical areas. At the electron microscopic level positive immunoreaction was found associated to synaptic vesicles in axon terminals, and also within glial cells. These findings reveal both the presence of glyoxylate-like molecules and glyoxylate metabolism in neurons of the motor, somatosensory, cyngulate and olfactory areas of the rat frontoparietal cortex. The presence of such molecules associated to synaptic vesicles within the axon terminals suggest the possible involvement of these molecules in some type of neurotransmission.
Alcohol Oxidoreductases↗
Spread of bovine herpesvirus type 5 (BHV-5) in the rabbit brain after intranasal inoculation.
Following intranasal inoculation of wild-type BHV-5 in rabbits, we studied the sequential transneuronal passage of the virus in the CNS by immunocytochemistry, histopathology, and virus isolation. At 4 and 6 days postinfection (d.p.i.), rabbits had no or mild neurological signs, and virus was isolated only from the olfactory bulbs. At 8 and 9 d.p.i., infected rabbits had severe neurological signs, and virus could be isolated from multiple regions of the brain segments. In these rabbits, high titers of virus were consistently present in the anterior and posterior cortices, including frontal, piriform/entorhinal, temporal, parietal, and occipital cortices, the hippocampus and the amygdala. Virus was isolated occasionally from the midbrain/diencephalon and pons/medulla. Virus was not isolated from the cerebellum and trigeminal ganglion of rabbits examined from 2-12 d.p.i. Immunocytochemistry revealed virus-specific antigens at 4 d.p.i. within the glomerular layer, external plexiform layer, and mitral cell layer of the main olfactory bulb. At 6 d.p.i., virus-specific antigens were also present within the inner granular layer of the main olfactory bulb. At 8 and 9 d.p.i., widespread BHV-5-specific staining occurred in the areas of the brain connected to the main olfactory bulb, including the frontal/cingulate cortex, anterior olfactory nucleus, lateral olfactory tubercle, piriform/entorhinal cortex, hippocampus, amygdala, dorsal raphe, and locus coeruleus. In the trigeminal ganglion, specific staining was detected within a few neurons at 2,4, 6, 8 d.p.i. However, further spread of the virus along the trigeminal pathway was not evident. These data indicate that BHV-5 replicates and spreads preferentially in the olfactory pathway following intranasal instillation and that this viral spread correlated with the severity of neurological symptoms and histopathological lesions.
Alphaherpesvirinae↗
Electrophysiological connections of neurons in ventral pallidal regions of the olfactory tubercle with the main olfactory bulb and piriform cortex.
Field potential and single unit recordings were used to assess the connections of the olfactory tubercle (OT) with the main olfactory bulb (MOB) and the piriform cortex (PC) in urethane-anesthetized rats. Current generators of depth profiles evoked in OT following MOB stimulation were localized 300 microns superficial to those elicited by PC shocks, suggesting that afferents from the MOB and PC end in different regions of the OT. Following MOB and PC stimulation antidromically invaded neurons were recorded in the ventral pallidal regions of the OT and in the vicinity of the islands of Calleja, respectively. These results demonstrate that the OT, which receives a monosynaptic input from the MOB, projects back to the bulb and that the PC seems to be also reciprocally linked with differentiated structures in the OT.
Animals↗
Memory of early maltreatment: neonatal behavioral and neural correlates of maternal maltreatment within the context of classical conditioning.
BACKGROUND: While children form an attachment to their abusive caregiver, they are susceptible to mental illness and brain abnormalities. To understand this important clinical issue, we have developed a rat animal model of abusive attachment where odor paired with shock paradoxically produces an odor preference. Here, we extend this model to a seminaturalistic paradigm using a stressed, "abusive" mother during an odor presentation and assess the underlying learning neural circuit. METHODS: We used a classical conditioning paradigm pairing a novel odor with a stressed mother that predominantly abused pups to assess olfactory learning in a seminaturalistic environment. Additionally, we used Fos protein immunohistochemistry to assess brain areas involved in learning this pain-induced odor preference within a more controlled maltreatment environment (odor-shock conditioning). RESULTS: Odor-maternal maltreatment pairings within a seminatural setting and odor-shock pairings both resulted in paradoxical odor preferences. Learning-induced gene expression was altered in the olfactory bulb and anterior piriform cortex (part of olfactory cortex) but not the amygdala. CONCLUSIONS: Infants appear to use a unique brain circuit that optimizes learned odor preferences necessary for attachment. A fuller understanding of infant brain function may provide insight into why early maltreatment affects psychiatric well-being.
Animals↗
Administration of 3,3'-iminodipropionitrile to the rat results in region-dependent damage to the central nervous system at levels above the brain stem.
Axonal swellings and neurofilamentous accumulations in the brain stem, spinal cord and peripheral nervous system are the most widely documented effects of exposure to 3,3'-iminodipropionitrile (IDPN). Evidence from morphological and functional studies, however, suggests that IDPN also may damage areas of the central nervous system above the level of the brain stem. To examine this possibility, we evaluated the astrocyte reaction to injury as an indirect means of detecting potential sites of IDPN-induced damage to the central nervous system. An immunoassay for the astrocyte intermediate filament protein, glial fibrillary acidic protein (GFAP), was used to quantify gliosis. Rats were given IDPN (0-600 mg/kg/day i.p.) for 3 days. The concentration of GFAP in discrete brain regions was examined at postdosing times ranging from 3 days to 3 weeks. IDPN caused time-, dose- and region-dependent increases in GFAP; elevations were observed in the pons-medulla, midbrain, cerebral cortex and olfactory bulbs, but not in cerebellum, hypothalamus, hippocampus and striatum. Of these areas, cortex and olfactory bulbs showed the largest increases. Dissection of cortex into four subregions showed that the IDPN-induced increase in cortical GFAP was relatively uniform across this brain region. Application of the de Olmos cupric-silver degeneration stain to IDPN-treated tissue revealed intense argyrophilia in the glomerular layer of the olfactory bulbs and diffuse staining of axons in several regions of the cortex. The data indicate that IDPN is neurotoxic to the olfactory bulbs and cortex of the rat.
Animals↗
Reciprocal connections between olfactory structures and the cortex of the rostral superior temporal sulcus in the Macaca fascicularis monkey.
Convergence of sensory modalities in the nonhuman primate cerebral cortex is still poorly understood. We present an anatomical tracing study in which polysensory association cortex located at the fundus and upper bank of the rostral superior temporal sulcus presents reciprocal connections with primary olfactory structures. At the same time, projections from this polysensory area reach multiple primary olfactory centres. Retrograde (Fast Blue) and anterograde (biotinylated dextran-amine and 3H-amino acids) tracers were injected into primary olfactory structures and rostral superior temporal sulcus. Retrograde tracers restricted to the anterior olfactory nucleus resulted in labelled neurons in the rostral portion of the upper bank and fundus of superior temporal sulcus. Injections of biotinylated dextran-amine at the fundus and upper bank of the superior temporal sulcus confirmed this projection by labelling axons in the dorsal and lateral portions of the anterior olfactory nucleus, as well as piriform, periamygdaloid and entorhinal cortices. Retrograde tracer injections at the rostral superior temporal sulcus resulted in neuronal labelling in the anterior olfactory nucleus, piriform, periamygdaloid and entorhinal cortices, thus providing confirmation of the reciprocity between primary olfactory structures and the cortex at the rostral superior temporal sulcus. The reciprocal connections between the rostral part of superior temporal sulcus and primary olfactory structures represent a convergence for olfactory and other sensory modalities at the cortex of the rostral temporal lobe.
Amino Acids↗
Olfactory learning: convergent findings from lesion and brain imaging studies in humans.
The role of temporal lobe structures in olfactory memory was investigated by (i) the examination of odour learning and memory in patients who had undergone resection from a temporal lobe (including primary olfactory regions) for the treatment of intractable epilepsy; and (ii) the examination of brain function during odour memory tasks as assessed via PET imaging of healthy individuals. In order to study different stages of odour memory, recognition of a 'list' of odours was tested after a first exposure, again after four exposures and once more after a 24 h delay interval. Patients with resection from a temporal lobe performed significantly less well than control subjects on all trials, and no significant differences were noted as a function of side of resection, indicating that there is not a strong hemispheric superiority for this task. The PET data yielded different levels of activity in piriform cortex (primary olfactory cortex), in relation to the 'no-odour' baseline scan, depending on the type of processing: no increase in activity noted during odour encoding, a small increase bilaterally during short-term recognition and a larger increase bilaterally during long-term recognition. These findings, together with findings in animal studies, suggest that piriform cortex may have an active role in odour memory processing, not simply in odour perception. Taken together, the findings from the lesion study and functional brain imaging of healthy subjects suggest that olfactory memory requires input from left and right temporal lobe regions for optimal odour recognition, and that, unlike with verbal or non-verbal visual material, there is not a strong functional lateralization for olfactory memory.
Adult↗
The piriform cortex is not a direct olfactory relay to the mediodorsal thalamic nucleus in cats and rabbits.
Following injections of horseradish peroxidase into the mediodorsal thalamic nucleus (MD), retrogradely labeled cells were found in various areas in the cat and rabbit. Among these, olfactory-related areas to which the olfactory bulb projects directly or indirectly via the piriform cortex were the olfactory tubercle, amygdala and insular cortex, while no labeled cells were detected in the piriform cortex and endopiriform nucleus in both species. These results indicate that the piriform cortex and endopiriform nucleus do not send their axons directly to the MD.
Amygdala↗