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PubMed1981

Mesocortical dopamine neurons: rapid transmitter turnover compared to other brain catecholamine systems.

The decline of dopamine and norepinephrine after intravenous alpha-methyltyrosine was used to determine the rate constants for catecholamine turnover in the rat prefrontal cortex, olfactory tubercle and striatum. Dopamine turnover varied more between brain regions and was generally faster than the corresponding norepinephrine turnover. Prefrontal cortical dopamine was unaffected by dorsal noradrenergic bundle lesions. The turnover of prefrontal cortical dopamine was found to be 2-4 times faster than dopamine turnover in the olfactory tubercle and striatum.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1989

Effects of chronic antidepressant and benzodiazepine treatment on corticotropin-releasing-factor receptors in rat brain and pituitary.

We examined the effects of chronic treatment with antidepressants (imipramine or desipramine) or benzodiazepines (diazepam, alprazolam, or adinazolam) on modulation of corticotropin-releasing-factor (CRF) receptors in discrete areas of rat brain and in anterior pituitary. As previously reported, we found that chronic antidepressant treatment downregulated 5-HT2 serotonin and beta-adrenergic receptors in cerebral cortex. Although there was a trend toward increased CRF binding in brain stem, striatum, cerebellum, hypothalamus, and frontal cerebral cortex following antidepressant treatment, the changes were only statistically significant in brain stem in imipramine-treated rats. In addition, no significant changes were seen in CRF binding in other brain regions including parietal/temporal cerebral cortex, olfactory bulb, hippocampus, and anterior pituitary. Following chronic benzodiazepine treatment CRF receptor binding was significantly decreased in the frontal cerebral cortex and hippocampus; although there was a trend for CRF receptors to be decreased in other brain areas and increased in anterior pituitary, the changes were not statistically significant.

Alprazolam↗
PubMed1999

Molecular cloning of a cDNA encoding mouse A15, a member of the transmembrane 4 superfamily, and its preferential expression in brain neurons.

A15, a member of the transmembrane 4 superfamily (TM4SF), was isolated by differential screening of the cDNAs that are preferentially expressed on immature T cells. As a first step in the study of the biological function of the A15 molecule, we isolated cDNAs encoding the entire coding region of mouse A15. Nucleotide sequence analysis of the cDNAs revealed that mouse A15 shares 97% amino acid sequence identity with its human counterpart. The mouse A15 protein product has not yet been characterized, but is predicted to be 244 amino acids with four hydrophobic domains. Northern blot analysis of the RNA samples from various mouse tissues disclosed that the A15 transcripts are expressed most strongly in the brains, and are detectable in the colon, muscle, heart, kidney, and spleen. In situ hybridization of the mouse brain with ribo-probe established that the A15 transcripts are expressed primarily in neurons of the frontal cortex, olfactory bulb, dentate gyrus, caudoputamen, and CA3 region of the hypothalamus as well as in Purkinje cells in the cerebellar cortex, which strongly suggests that A15 may have a special function in the fundamental neuronal functioning of the higher nervous system.

Amino Acid Sequence↗
PubMed1997

Noradrenergic suppression of synaptic transmission may influence cortical signal-to-noise ratio.

Norepinephrine has been proposed to influence signal-to-noise ratio within cortical structures, but the exact cellular mechanisms underlying this influence have not been described in detail. Here we present data on a cellular effect of norepinephrine that could contribute to the influence on signal-to-noise ratio. In brain slice preparations of the rat piriform (olfactory) cortex, perfusion of norepinephrine causes a dose-dependent suppression of excitatory synaptic potentials in the layer containing synapses among pyramidal cells in the cortex (layer Ib), while having a weaker effect on synaptic potentials in the afferent fiber layer (layer Ia). Effects of norepinephrine were similar in dose-response characteristics and laminar selectivity to the effects of the cholinergic agonist carbachol, and combined perfusion of both agonists caused effects similar to an equivalent concentration of a single agonist. In a computational model of the piriform cortex, we have analyzed the effect of noradrenergic suppression of synaptic transmission on signal-to-noise ratio. The selective suppression of excitatory intrinsic connectivity decreases the background activity of modeled neurons relative to the activity of neurons receiving direct afferent input. This can be interpreted as an increase in signal-to-noise ratio, but the term noise does not accurately characterize activity dependent on the intrinsic spread of excitation, which would more accurately be described as interpretation or retrieval. Increases in levels of norepinephrine mediated by locus coeruleus activity appear to enhance the influence of extrinsic input on cortical representations, allowing a pulse of norepinephrine in an arousing context to mediate formation of memories with a strong influence of environmental variables.

Acetylcholine↗
PubMed2002

Protein tyrosine phosphatase sigma-deficient mice show aberrant cytoarchitecture and structural abnormalities in the central nervous system.

Protein tyrosine phosphatase sigma (PTPsigma) is a member of the LAR family of receptor tyrosine phosphatases and is highly expressed in the nervous system during development. PTPsigma is homologous to the Drosophila DLAR, which plays a key role in the targeting of axonal growth cones in flies. We have previously inactivated the Ptprs gene in mice and demonstrated stunted growth, developmental delays, and neurological and neuroendocrine defects in the PTPsigma null animals. Here, we mapped the expression of the lac-Z reporter gene included in the knockout cassette and surveyed the development of the CNS in these mice after birth. The strongest expression of beta-galactosidase (PTPsigma) was observed in the hippocampus, cerebral cortex, olfactory bulbs, and subependymal layer. Our analysis reveals hippocampal dysgenesis, reductions in the thickness of the corpus callosum and the cerebral cortex, and late expression of the growth-associated protein 43 (GAP-43) in the knockout animals. Architectural abnormalities in the brain and spinal cord were confirmed by immunoreactivity to neurofilament and glial fibrillary acidic protein (GFAP) antibodies. Several of these neural abnormalities were corrected with age, suggesting a delay in neurological development related to the knockout of the Ptprs gene. These data suggest that PTPsigma is likely involved in neurogenesis, axonal growth, and axonal pathfinding in the maturation of the mammalian CNS.

Agenesis of Corpus Callosum↗
PubMed1993

Associative long-term potentiation in piriform cortex slices requires GABAA blockade.

Previous studies have demonstrated that NMDA-dependent, long-term potentiation (LTP) can be induced in both afferent and intrinsic association fiber systems in the piriform (primary olfactory) cortex. In this report we demonstrate that an associative form of LTP can be induced by coactivation of these two systems, which terminate on adjacent apical dendritic segments of pyramidal cells. Potentiating stimulus trains were delivered to either afferent or association fibers, and weak shocks, which were nonpotentiating when delivered alone, were delivered to the other pathway. Under control recording conditions where homosynaptic (single pathway) LTP is consistently evoked, coincident application of these stimuli failed to induce LTP of the weak shock response. However, after local blockade of the fast, GABAA-mediated IPSP, associative LTP was consistently produced in both directions. Induction was blocked by D-2-amino-5-phosphonovaleric acid, indicating that it is dependent on activation of NMDA receptors. It is speculated that afferent and association fibers are segregated on different dendritic segments of pyramidal cells in piriform cortex to allow regulation of associative LTP by way of centrifugal inputs that modulate the activity of GABAergic interneurons.

2-Amino-5-phosphonovalerate↗
PubMed1997

GABAA-mediated IPSCs in piriform cortex have fast and slow components with different properties and locations on pyramidal cells.

GABAA-mediated IPSCs in piriform cortex have fast and slow components with different properties and locations on pyramidal cells. J. Neurophysiol. 78: 2531-2545, 1997. A recent study in piriform (olfactory) cortex provided evidence that, as in hippocampus and neocortex, gamma-aminobutyric acid-A (GABAA)-mediated inhibition is generated in dendrites of pyramidal cells, not just in the somatic region as previously believed. This study examines selected properties of GABAA inhibitory postsynaptic currents (IPSCs) in dendritic and somatic regions that could provide insight into their functional roles. Pharmacologically isolated GABAA-mediated IPSCs were studied by whole cell patch recording in slices. To compare properties of IPSCs in distal dendritic and somatic regions, local stimulation was carried out with tungsten microelectrodes, and spatially restricted blockade of GABAA-mediated inhibition was achieved by pressure-ejection of bicuculline from micropipettes. The results revealed that largely independent circuits generate GABAA inhibition in distal apical dendritic and somatic regions. With such independence, a selective decrease in dendritic-region inhibition could enhance integrative or plastic processes in dendrites while allowing feedback inhibition in the somatic region to restrain system excitability. This could allow modulatory fiber systems from the basal forebrain or brain stem, for example, to change the functional state of the cortex by altering the excitability of interneurons that mediate dendritic inhibition without increasing the propensity for regenerative bursting in this highly epileptogenic system. As in hippocampus, GABAA-mediated IPSCs were found to have fast and slow components with time constants of decay on the order of 10 and 40 ms, respectively, at 29 degrees C. Modeling analysis supported physiological evidence that the slow time constant represents a true IPSC component rather than an artifactual slowing of the fast component from voltage clamp of a dendritic current. The results indicated that, whereas both dendritic and somatic-region IPSCs have both fast and slow GABAA components, there is a greater proportion of the slow component in dendrites. In a companion paper, the hypothesis is explored that the resulting slower time course of the dendritic IPSC increases its capacity to regulate the N-methyl--aspartate component of EPSPs. Finally, evidence is presented that the slow GABAA-mediated IPSC component is regulated by presynaptic GABAB inhibition whereas the fast is not. Based on the requirement for presynaptic GABAB-mediated block of inhibition for expression of long-term potentiation, this finding is consistent with participation of the slow GABAA component in regulation of synaptic plasticity. The lack of susceptibility of the fast GABAA component to the long-lasting, activity-induced suppression mediated by presynaptic GABAB receptors is consistent with a protective role for this process in preventing seizure activity.

Animals↗
PubMed1997

The density of 5-hydoxytryptamine2A receptors in forebrain is increased at pro-oestrus in intact female rats.

We have shown previously that in ovariectomised rats, oestradiol-17beta, in its positive-feedback mode for luteinizing hormone (LH) release, induces a significant increase in the density of 5-hydroxytryptamine2A (5-HT2A) receptors in the forebrain. Here we investigated whether there are any changes in 5-HT2A receptor density in relation to the spontaneous surge of oestradiol-17beta in female COB Wistar rats between dioestrus and pro-oestrus. Using [3H]RP62203-binding and autoradiography, we found that 5-HT2A binding sites were significantly increased at 1630-1800 h on pro-oestrus compared with 0900-1130 h on dioestrus in frontal and cingulate cortex, olfactory tubercle and nucleus accumbens. The densities of 5-HT2A binding sites in male rats were similar to dioestrous female values in cortex, and to pro-oestrous female values in nucleus accumbens. The changes in the density of 5-HT2A binding sites in the forebrain of female rats may be relevant to oestrogen effects on mood and mental state.

Animals↗
PubMed1999

The olfactory bulb: coding and processing of odor molecule information.

Olfactory sensory neurons detect a large variety of odor molecules and send information through their axons to the olfactory bulb, the first site for the processing of olfactory information in the brain. The axonal connection is precisely organized so that signals from 1000 different types of odorant receptors are sorted out in 1800 glomeruli in the mouse olfactory bulb. Individual glomerular modules presumably represent a single type of receptor and are thus tuned to specific molecular features of odorants. Local neuronal circuits in the bulb mediate lateral inhibition among glomerular modules to sharpen the tuning specificity of output neurons. They also mediate synchronized oscillatory discharges among specific combinations of output neurons and may contribute to the integration of signals from distinct odorant receptors in the olfactory cortex.

Action Potentials↗
PubMed2000

[The cerebral cortex: structure, interrelations of neurons, functional columnar organization].

The cerebral cortex develops from a portion of the telencephalic vesicle. Cells originating from the germinal zone surrounding the lumen migrate peripherally to form the cortical mantle. During the fetal life, cortical neurons begin to form six horizontal layers. Cells formed at the same time migrate to the same cortical layer, cells migrating later pass through deep layers to form more superficial laminae. A six layer cellular organization is characteristic of the entire neopallium, which is referred to as the neocortex. The paleopallium--olfactory cortex--and the archipallium--hippocampal formation and dentate gyrus--have three basic layers and collectively constitute the allocortex. Through the course of evolution, the cerebral cortex has increased enormously in surface area but not in thickness, a trend that can be seen even in the relatively short period of primate evolution. The human cortex is only about 15% thicker than that of the macaque monkey but is at least 10 times greater in area. To understand how this complex structure functions we need to examine its unique internal cellular arrangement.

Cell Movement↗
PubMed1995

Olfactory bulb transplants establish afferent and efferent connections with host forebrain in rat.

We are using wheat germ agglutinin-conjugated horseradish peroxidase (WHRP) to study reconnectivity in the transplanted (TX) olfactory bulb (OB) in Sprague-Dawley rats. Tritium-labeled OBs from fetal rat donors of Embryonic Days 14-15 were immediately grafted into neonatal rats in the site from which the host OB had been removed. Following survival times of 7 weeks and longer, WHRP solution was injected into the TX OB, and subjects were perfused after 24 h. The WHRP transport is seen in fibers from the TX OB into layer I of the host olfactory peduncle (OP) and olfactory cortex (OC) and in cell bodies in layers II and III of the OP and OC, the lateral hypothalamus, and the contralateral anterior olfactory nucleus (AON). These findings reaffirm that the axons from a TX OB make connections with some appropriate areas of the host brain and also indicate that axons from cells in the target areas of the host brain, including contralateral AON, reinnervate the TX OB.

Afferent Pathways↗
PubMed2006

Neurotrophin B receptor kinase increases Kv subfamily member 1.3 (Kv1.3) ion channel half-life and surface expression.

Kv subfamily member 1.3 (Kv1.3), a member of the Shaker family of potassium channels, has been found to play diverse roles in immunity, metabolism, insulin resistance, sensory discrimination, and axonal targeting in addition to its traditional role in the stabilization of the resting potential. We demonstrate that the neurotrophin B receptor (TrkB) causes an upregulation of Kv1.3 ion channel protein expression in the absence of the preferred ligand for the receptor (brain-derived neurotrophic factor; BDNF) and oppositely downregulates levels of Kv subfamily member 1.5. Although the effect occurs in the absence of the ligand, Kv1.3 upregulation by TrkB is dependent upon the catalytic domain of the TrkB kinase as well as tyrosine (Y) residues in the N and C terminus of the Kv1.3 channel. Using pulse-chase experiments we find that TrkB alters the half-life residence of the channel by approximately 2x and allows it to sustain activity as reflected in an increased current magnitude without alteration of kinetic properties. TrkB and Kv1.3 co-immunoprecipitate from tissue preparations of the mouse olfactory bulb and olfactory cortex, and by immunocytochemical approaches, are found to be co-localized in the glomerular, mitral cell, and internal plexiform layers of the olfactory bulb. These data suggest that Kv1.3 is not only modulated by direct phosphorylation in the presence of BDNF-activated TrkB kinase, but also may be fine tuned via regulation of surface expression while in the proximity of neurotrophic factor receptors. Given the variability of TrkB expression during development, regeneration, or neuronal activation, modulation of surface expression and turnover of Kv channels could significantly impact neuronal excitability, distinct from that of tyrosine kinase phosphorylation.

Blotting, Western↗
PubMed2002

Imaging of brain activation by odorants in humans.

Application of positron emission tomography and magnetic resonance imaging has provided several new insights into various olfactory functions. One is that sniffing and smelling engage separate subsystems in the human olfactory cortex. Another is that perception of odorous compounds (odorants) is mediated by a set of core regions, which are partly different for pure olfactory than for olfactory plus trigeminal odorants. Depending on the task associated with odor perception, the core regions are recruited together with other circuits, in a parallel and hierarchical manner. The sense of smell seems, therefore, to be organized similarly to other sensory modalities, and the specific psychophysical characteristics of olfaction should be attributed to an early involvement of the limbic system rather than to a conceptually different mode of processing.

Brain↗
PubMed2005

The sniff is part of the olfactory percept.

In this review, we use data obtained primarily from humans to argue that sniffs are not merely a stimulus carrier but are rather a central component of the olfactory percept. We argue that sniffs 1) are necessary for the olfactory percept, 2) affect odorant intensity perception and identity perception, 3) drive activity in olfactory cortex, 4) are rapidly modulated in an odorant-dependent fashion by a dedicated olfactomotor system, and 5) are sufficient to generate an olfactory percept of some sort even in the absence of odor.

Humans↗
PubMed1986

Efferent projections of the basolateral amygdala in the opossum, Didelphis virginiana.

The autoradiographic anterograde axonal transport technique was used to study efferent projections of the opossum basolateral amygdala. All nuclei of the basolateral amygdala send topographically organized fibers to the bed nucleus of the stria terminalis (BST) via the stria terminalis (ST). Injections into rostrolateral portions of the basal nuclei label fibers that surround the commissural bundle of the ST, cross the midline by passing along the outer aspect of the anterior commissure, and terminate primarily in the contralateral BST, anterior subdivision of the basolateral nucleus (BLa), ventral putamen, and olfactory cortex. Each of the basal nuclei project ipsilaterally to the anterior amygdaloid area, substantia innominata and topographically to the ventral part of the striatum and adjacent olfactory tubercle. The posterior subdivision of the basolateral nucleus (BLp), but not the basomedial nucleus (BM), projects to the ventromedial hypothalamic nucleus. BLa and BLp have projections to the nucleus of the lateral olfactory tract and also send fibers to the central nucleus, as does the lateral nucleus (L). The lateral nucleus also has a strong projection to BM and both nuclei project to the amygdalo-hippocampal area. BLa and BLp send axons to the ventral subiculum and ventral lateral entorhinal area whereas L projects only to the latter area. The lateral nucleus and BLp project to the perirhinal cortex and the posterior agranular insular area. The BLa sends efferents to the anterior agranular insular area. Rostrally this projection is continuous with a projection to the entire frontal cortex located rostral and medial to the orbital sulcus. All of the nuclei of the basolateral amygdala project to areas on the medial wall of the frontal lobe that appear to correspond to the prelimbic and infralimbic areas of other mammals. Despite the great phylogenetic distance separating the opossum from placental mammals, the projections of the opossum basolateral amygdala are very similar to those seen in other mammals. The unique frontal projections of the opossum BLa to the dorsolateral prefrontal cortex appear to be related to the distinctive organization of the mediodorsal thalamic nucleus and prefrontal cortex in this species.

Amygdala↗
PubMed2005

Perception without a thalamus how does olfaction do it?

The olfactory system has generated considerable interest in recent years, mainly focused on receptor genes and early olfactory processing. In this issue of Neuron, Mori et al. focus centrally, providing evidence for slow- and fast-wave states in olfactory cortex that appear to gate the inflow of information underlying conscious smell perception.

Olfactory Bulb↗
PubMed1995

Noise-enhanced performance in a cortical associative memory model.

Spontaneous neuronal activity and synaptic noise are well-known phenomena, but their biological significance has not yet been assessed. Using a computer model of the olfactory cortex we show that such activity, expressed as temporal noise in the model, can reduce recall time in associative memory tasks. We investigate both additive and multiplicative noise, and find optimal noise levels for which the recall time reaches a minimum. In addition, we demonstrate that noise can induce state transitions, such that the system is pushed from one attractor state to another. For high enough noise levels the dynamics can change dramatically and, for example, switch from an oscillatory to a chaos-like behavior. We discuss these findings in light of their significance for neural information processing.

Association Learning↗
PubMed1996

Kindling-induced epileptiform potentials in piriform cortex slices originate in the underlying endopiriform nucleus.

1. Previous studies in vivo and in vitro have shown that kindling from several locations in the limbic system induces the onset of epileptiform activity in the piriform (olfactory) cortex in the rat. In the present study we tested the hypothesis that kindled epileptiform events in piriform cortex are initiated in the underlying endopiriform nucleus. The experiments were performed in slices taken from rats that were previously kindled by conventional means. 2. Both stimulus-evoked and spontaneous interictal-like epileptiform events were observed in most slices from the anterior piriform cortex, but in few slices from the posterior piriform cortex. These events resembled those described in unanesthetized and urethan-anesthetized rats in previous studies. 3. Findings in support of the hypothesis were as follows. Epileptiform events in the endopiriform nucleus preceded those in the piriform cortex. Epileptiform events could occur in endopiriform nucleus alone, but were only observed in the piriform cortex following occurrence in the endopiriform nucleus. A buildup in population activity preceded the onset of all-or-none epileptiform events in the endopiriform nucleus. Epileptiform events could be triggered by local application of glutamate in the endopiriform nucleus and adjacent claustrum, but not from the piriform cortex. Finally, local application of Co2+ in the endopiriform nucleus, but not in the piriform cortex or elsewhere in the slices, blocked the occurrence of epileptiform events. 4. Additional experiments were performed to further characterize the generation process. 6,7-Dinitroquinoxaline-2,3-dione (DNQX) blocked epileptiform events and the preceding accelerating buildup in multiunit activity at a concentration below that required to block the monosynaptic excitatory postsynaptic potential (EPSP). This suggests that EPSPs mediated by alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptors underlie epileptiform events in slices of piriform cortex, and that multisynaptic interactions within the endopiriform nucleus are required for generation of these epileptiform EPSPs. By contrast, block of N-methyl-D-aspartate (NMDA) receptors decreased the amplitude of epileptiform EPSPs but did not block their occurrence, indicating that NMDA receptors contribute to generation but are not required. When membrane potential was depolarized to increase driving force, fast inhibitory postsynaptic potentials were found to consistently accompany the buildup process and epileptiform EPSPs. This indicates that if initiation of epileptiform activity in the endopiriform nucleus results from a compromise in feedback inhibition, this compromise is partial rather than complete. 5. Epileptiform EPSPs in slices of piriform cortex from kindled rats displayed similarities in properties, locus of origin, and mechanism of generation to those previously studied in slices from normal rats in which epileptiform activity was induced by a brief period of bursting activity. These similarities suggest that study of bursting-induced epileptiform EPSPs may provide insight into certain aspects of kindling-induced epileptogenesis.

Amygdala↗