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PubMed1975

The action of ether and methoxyflurane on synaptic transmission in isolated preparations of the mammalian cortex.

1. The actions of ether and methoxyflurane on the evoked potentials of in vitro preparations of the guinea-pig olfactory cortex were studied. Following stimulation of the lateral olfactory tract (l.o.t.) evoked potentials could be recorded from the cortical surface; these potentials consisted of an initial wave (the compound action potential of the l.o.t.) followed by a negative field potential which was associated with the synchronous excitation of many superficial excitatory synapses (population e.p.s.p.). Superimposed on the population e.p.s.p. was a number of positive peaks. These positive peaks reflect the synchronous discharge of many neurones and so have been called population spikes. 2. When ether or methoxyflurane was added to the gas stream that superfused the surface of the preparations, the population e.p.s.p.s. and population spikes were depressed at lower concentrations than those required to depress the compound action potential of the afferent fibres. 3. The evoked activity of individual cells in the cortex was depressed by ether and methoxyflurane. However, five of the twelve cells tested in ether showed an increase in their evoked activity at concentrations below 4-5%, but at higher concentrations these cells also became depressed. 4. Both ether and methoxyflurane depressed the sensitivity of cortical neurones to iontophoretically applied L-glutamate and may similarly depress the sensitivity of the post-synaptic membrane to the released transmitter substance. 5. Neither anaesthetic appeared to increase the threshold depolarization required for nerve impulse generation. Thus, the decrease of the discharge of the post-synaptic cells was primarily caused by a depression of chemical transmission. 6. Ether caused some cells in the cortex to alter their normal pattern of synaptically evoked discharge and both anaesthetics induced similar changes during excitation by glutamate.

Animals↗

PubMed1984

Age-related fine structural changes in axons and synapses during deafferentation of the rat pyriform cortex: a possible basis for plasticity.

The purpose of this study was to compare the sequence of axonal and synaptic alterations following deafferentating lesions at selected postnatal ages and relate these changes to synaptic organization in the olfactory cortex. Rats received unilateral olfactory bulb ablation at 2 1/2, 6, 9 and 13 days of age and were studied at survivals of 12 h to 30 days. At least three clearly different forms of acute degeneration were seen; flocculent, granular and dense with the granular form an intermediate form. The proportion of granular and especially dense degeneration increases after six days of age as does the presence of glia. The denser the type of degeneration, the greater the retention of remnants of this form of synaptic degeneration at deafferented postsynaptic sites. This as well as the increased presence of glia after six days may be important factors in the limitation of plastic reorganization or reinnervation in more mature individuals. The youngest operated animals show rapid vacating of the receptor site, relative absence of glia and striking evidence of competitive reoccupation of deafferented sites.

Age Factors↗

PubMed1983

Cortico-cortical connections reorganize in hamsters after neonatal transection of the callosal bridge.

Neonatal hamsters were subjected to transection of the callosal bridge. Later examination of the brains showed complete or partial absence of the corpus callosum and an anomalous bilateral longitudinal bundle of fibers. In addition, aberrant commissural fibers were seen to connect heterotopically the parietal cortex with the contralateral frontal cortex through a callosal remnant over the septum, and the olfactory cortex with the opposite frontal and parietal cortices through the anterior commissure.

Aging↗

PubMed1980

Double and triple labeling of neurons with fluorescent substances; the study of collateral pathways in the ascending raphe system.

A retrograde labeling procedure utilizing fluorescent substances (Granular Blue, Nuclear Yellow and propidium iodide) was used to establish the presence of branching axons in the ascending raphe system of young rats. After injections in septum, medial thalamus and olfactory cortex, the number of double-labeled cells in various combinations was found to be relatively large in the dorsal raphe nucleus, whereas triple-labeled cells occurred more rarely. Each class of neurons, i.e. single-, double- and triple-labeled, were shown to have a predominant distribution within specific parts of the nucleus.

Animals↗

PubMed1990

Chromogranin A in the olfactory system of the rat.

The olfactory bulb of the rat contains chromogranin A at a similar level as the adrenal gland or the hypophysis as revealed by immunoblots. Olfactory chromogranin A also displays the same size as chromogranin A of endocrine cells. In the hippocampus and other brain regions, we could not detect chromogranin A by immunoblotting. In contrast, chromogranin A messenger ribonucleic acid (using S1 nuclease protection assays) was observed in all brain regions examined, including the olfactory bulb. By in situ hybridization histochemistry with a complementary ribonucleic acid probe (280 nucleotides), and by immunocytochemistry, chromogranin A synthesis could be localized to cell bodies of the mitral cell layer, of the external plexiform layer and of the periglomerular region of the olfactory bulb. Immunocytochemically, chromogranin A was also detected in the central projection areas of mitral and tufted cells in the primary olfactory cortex and the anterior amygdaloid area but not in the olfactory glomeruli, where the incoming olfactory nerve fibers of the primary olfactory neurons establish synaptic contacts. Taken together the data show that chromogranin A, following biosynthesis in the perikarya of the mitral and tufted cells, is specifically transported into their axonal terminals but not into their primary dendrites. We propose that the rat olfactory system could serve as a model for the study of chromogranin A regulation and function in neurons.

Adrenal Glands↗

PubMed2001

Activation and habituation in olfaction--an fMRI study.

This study investigated human BOLD responses in primary and higher order olfactory cortices following presentation of short- and long-duration odorant stimuli using a 3-T MR scanner. The goal was to identify temporal differences in the course of the response that might underlie habituation. A short-duration stimulus (9 s) consistently activated the primary olfactory cortex (POC). After a long stimulus (60 s), the temporal form of the response differed in different parts of the olfactory network: (1) The POC (piriform, entorhinal cortex, amygdala) and, interestingly, the hippocampus and, to a certain degree, the anterior insula show a short, phasic increase in the signal, followed by a prolonged decrease below baseline. (2) In the orbitofrontal cortex a sustained increase in activation was seen. This increase lasted approximately as long as the duration of odorant presentation ( approximately 60 s). (3) The mediodorsal nucleus of the thalamus and the caudate nucleus responded with an increase in signal which returned to baseline after approximately 15 to 30 s. The correlated biphasic hemodynamic response in the POC, hippocampus, and anterior insula during prolonged olfactory stimulation suggests that these three areas may interact closely with each other in the control of habituation. These results extend recent data which showed habituation of the rat piriform cortex and dissociation between the POC and the orbitofrontal cortex.

Adult↗

PubMed1991

Selective suppression of afferent but not intrinsic fiber synaptic transmission by 2-amino-4-phosphonobutyric acid (AP4) in piriform cortex.

Differences in the glutaminergic modulation of afferent and intrinsic fiber synaptic transmission in piriform (olfactory) cortex were investigated using extracellular and intracellular recording techniques in a transverse slice preparation. 2-Amino-4-phosphonobutyric acid (AP4) strongly suppressed synaptic potentials evoked by afferent fiber stimulation in layer 1a, while having a much weaker effect on synaptic potentials evoked by intrinsic fiber stimulation in layer 1b. Both the racemic mixture and L-(+)-enantiomer of AP4 showed this differential effect. Suppression of afferent fiber synaptic potentials was accompanied by an increase in paired pulse facilitation, suggesting a pre-synaptic mechanism, while intrinsic fiber synaptic potentials showed little change in facilitation. Previous work has shown that cholinergic modulation in piriform cortex appears selective for intrinsic fiber synapses. The present data describes a pre-synaptic glutaminergic modulation complementary to the cholinergic modulation.

Afferent Pathways↗

PubMed2000

Neural activity in the horizontal limb of the diagonal band of broca can be modulated by electrical stimulation of the olfactory bulb and cortex in rats.

Previously published theoretical models of olfactory processing suggest that cholinergic modulatory inputs to the olfactory system should be regulated by neural activity in the olfactory bulb. We tested these predictions using in vivo electrophysiology in rats. We show that the activity of approximately 20% of neurons recorded in the horizontal limb of the diagonal band of Broca (HDB), which is the source of cholinergic projections to the olfactory system, can be modulated by electrical stimulation of either the lateral olfactory tract or the cell body layer of piriform cortex. These data suggest a possible physiological pathway for the proposed regulation of neural activity in the HDB by activity in the olfactory bulb or cortex.

Animals↗

PubMed1994

Blocking effects of ethanol on stress-induced activation of rat mesoprefrontal dopamine neurons.

We investigated the effects of ethanol on stress-induced activation of the brain dopamine (DA) systems in rats. Ethanol (0.5 and 1.0 g/kg) was injected IP 25 min before sacrifice (5 min before 20-min immobilization stress). Ethanol treatment by itself did not affect the levels of either DA or its major metabolite, 3,4-dihydroxyphenylacetic acid (DOPAC), in the mesoprefrontal cortex, cingulate cortex, olfactory tubercle, or caudate putamen. Immobilization stress for 20 min caused increases in DOPAC levels in the prefrontal cortex (160% of control) and cingulate cortex (135% of control), but not in the olfactory tubercle or caudate putamen. The stress had no effects on DA levels in any of the four brain regions studied. Pretreatment with ethanol blocked, in a dose-dependent manner, the stress-induced increases in DOPAC levels in the mesoprefrontal cortex. The present data suggest that ethanol exhibits a blocking effect on stress-induced activation of the mesoprefrontal DA neurons. This blocking effect may be related to the anxiolytic action of ethanol.

3,4-Dihydroxyphenylacetic Acid↗

PubMed2001

Immunocytochemical analysis of basket cells in rat piriform cortex.

Basket cells, defined by axons that preferentially contact cell bodies, were studied in rat piriform (olfactory) cortex with antisera to gamma-aminobutyric acid (GABA)ergic markers (GABA, glutamate decarboxylase) and to peptides and calcium binding proteins that are expressed by basket cells. Detailed visualization of dendritic and axonal arbors was obtained by silver-gold enhancement of staining for vasoactive intestinal peptide (VIP), cholecystokinin (CCK), parvalbumin, and calbindin. Neuronal features were placed into five categories: soma-dendritic and axonal morphologies, laminar distributions of dendritic and axonal processes, and molecular phenotype. Although comparatively few forms were distinguished within each category, a highly varied co-expression of features from different categories produced a "combinatorial explosion" in the characteristics of individual neurons. Findings of particular functional interest include: dendritic distributions suggesting that somatic inhibition is mediated by feedforward as well as feedback pathways, axonal variations suggesting a differential shaping of the temporal aspects of somatic inhibition from different basket cells, evidence that different principal cell populations receive input from different combinations of basket cells, and a close association between axonal morphology and molecular phenotype. A finding of practical importance is that light microscopic measurements of boutons were diagnostic for the molecular phenotype and certain morphological attributes of basket cells. It is argued that the diversity in basket cell form in the piriform cortex, as in other areas of the cerebral cortex, reflects requirements for large numbers of specifically tailored inhibitory processes for optimal operation that cannot be met by a small number of rigidly defined neuronal populations.

Animals↗

PubMed2005

Variable coupling between olfactory system activity and respiration in ketamine/xylazine anesthetized rats.

In this study, we have characterized slow and fast oscillations at several stages of olfactory processing under light and deep ketamine/xylazine anesthesia in the albino rat. While monitoring the animal's respiration, we also obtained field potentials from the olfactory bulb and piriform (olfactory) cortex and simultaneously recorded membrane potentials in piriform cortex pyramidal cells. Our results demonstrate that oscillations are generally found at higher frequencies under lighter and lower frequencies under deeper anesthesia. In previous studies of cerebral cortex, similar results in ketamine/xylazine anesthetized animals have been interpreted to correspond with the higher frequencies found during waking and lower frequencies found in the sleep state. Correlation and coherence analysis between data obtained in the bulb and cortex reveals a clear difference in coupling depending on the anesthetic state of the animal. Specifically, activity recorded in the whole system is highly correlated with respiration during deep anesthesia, whereas only the olfactory bulb, and not the cortex, is correlated with respiration during light anesthesia. These data suggest that global activity in the piriform cortex is actually more directly tied to peripheral slow respiratory input during slow wave than fast wave states and that the coupling between olfactory structures can be dynamically modulated by the level of anesthesia and therefore presumably by different brain states as well.

Analgesics↗

PubMedDate not supplied

Influence of perfusates of tetanized donor slices on the induction of long-term potentiation in recipient slices.

A perfusate collected from donor slices of the olfactory cortex of the brain of rats during tetanization of the lateral olfactory tract (100 imp/sec, 30 sec) induced prolonged changes in the amplitudes of various components of the focal potentials (FP) in recipient slices. When the perfusates are divided in relation to the reactions arising in the donor slices into three types, "potentiated," "depressive," and "nonpotentiated," the reactions of the recipient slices prove to be diverse. The potentiated perfusate induced the development of depression. The depressive induced potentiation. The reactions of the recipient slices to the nonpotentiated perfusate were indeterminate. The data obtained suggest the secretion of active substances during the electrical tetanization of donor slices. These factors are capable of inducing reactions in the recipient slices which the donor slices had "experienced."

Animals↗

PubMed1991

BDNF mRNA expression is increased in adult rat forebrain after limbic seizures: temporal patterns of induction distinct from NGF.

We have localized brain-derived neurotrophic factor (BDNF) mRNA in rat brain and examined its regulation by seizure activity. In situ hybridization of BDNF 35S-cRNA most prominently labeled neurons in hippocampal stratum pyramidale and stratum granulosum, superficial olfactory cortex, pyramidal cell layers of neocortex, amygdala, claustrum, endopiriform nucleus, anterior olfactory nucleus, and ventromedial hypothalamus. Hybridization to BDNF mRNA was markedly increased in all of these regions after lesion-induced recurrent limbic seizures and within dentate gyrus granule cells following one electrically stimulated epileptiform afterdischarge. In contrast to seizure-elicited changes in nerve growth factor (NGF) mRNA expression, increases in BDNF mRNA occur in a greater number of different neuronal populations and develop several hours more rapidly in extrahippocampal loci. These results indicate that regulation by physiological activity may be an intrinsic property of this class of neurotrophic factor but that, in the recurrent seizure paradigm, different mechanisms mediate increased expression of mRNAs for BDNF and NGF outside hippocampus.

Animals↗

PubMed2004

The delta-opioid receptor agonist (+)BW373U86 regulates BDNF mRNA expression in rats.

delta-Opioid receptor agonists have antidepressant-like effects in behavioral models of depression. Chronic administration of classical antidepressants upregulates mRNA expression of brain-derived neurotrophic factor (BDNF) and its high-affinity tyrosine kinase receptor, TrkB in the frontal cortex and hippocampus of rats. Increases in BDNF and TrkB levels are thought to be important for the therapeutic effects of these drugs. Therefore, we examined the ability of the delta-opioid receptor agonist (+)BW373U86 to regulate BDNF and TrkB mRNA expression in frontal cortex, hippocampus, as well as, basolateral amygdala, endopiriform nucleus, and primary olfactory cortex. At 3 h after a single administration of (+)BW373U86 animals were killed and BDNF and TrkB mRNA levels were examined by in situ hybridization. BDNF mRNA levels produced by (+)BW373U86 were compared to acute administration of the antidepressants desipramine and bupropion. A behaviorally antidepressant dose of 10 mg/kg (+)BW373U86 increased BDNF mRNA expression in all regions examined; a smaller dose of (+)BW373U86 (1 mg/kg) significantly increased BDNF mRNA expression only in frontal cortex. The delta-opioid receptor antagonist naltrindole blocked (+)BW373U86-mediated increases in BDNF mRNA expression. In addition, tolerance developed to increased BDNF mRNA expression with repeated injection, except in frontal cortex. Midazolam was administered to some animals to prevent the convulsions produced by (+)BW373U86, but midazolam did not block delta-opioid receptor-mediated increases in BDNF mRNA expression in frontal cortex, hippocampus, or amygdala. Unlike desipramine and bupropion, (+)BW373U86 upregulated BDNF mRNA expression acutely (within 3 h after a single administration). These data support the concept that delta-opioid receptor agonists may have antidepressant potential, and could be good targets for the development of faster-acting antidepressants.

Analysis of Variance↗

PubMed1989

Effects of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine in the dog: effect of pargyline pretreatment.

Adult beagle dogs of either sex were injected with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-HCl (2.5 mg/kg, i.v.) alone or after pretreatment with pargyline (5.0 mg/kg, s.c., twice), with pargyline alone, or were uninjected. Groups were killed 2 h, 3 weeks, or 3 months after injection, and several brain areas were assayed for biogenic amines and their synthetic and degradative enzymes. MPTP caused a massive and permanent loss of striatal dopamine, tyrosine hydroxylase, and 3,4-dihydroxyphenylalanine decarboxylase activities and the loss of cells within the substantia nigra pars compacta. Dopamine and norepinephrine also were depleted to various degrees in cortex, olfactory bulb, and hypothalamus; however, dopamine beta-hydroxylase activity in cortex was normal. There was no cell loss in the ventral tegmental area or locus ceruleus. The activities of monoamine oxidase (MAO)-A and MAO-B in cortex and caudate were not affected by MPTP. Despite a permanent loss of the nigrostriatal system, the dogs exhibited only a transient hypokinesia lasting 1-2 weeks. Pargyline pretreatment prevented the loss of striatal dopamine and cells from the substantia nigra, but did not prevent a prolonged but reversible decrease in the concentration of dopamine metabolites. It is argued that this apparent inhibition of MAO is due not to suicide inactivation of the enzyme by MPTP, but to reversible inhibition by accumulation of the pyridinium metabolite, 1-methyl-4-phenylpyridinium, selectivity in aminergic terminals.

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗

PubMed1996

Bulbocortical interplay in olfactory information processing via synchronous oscillations.

Emergence of synchronous oscillatory activity is an inherent feature of the olfactory systems of insects, mollusks and mammals. A class of simple computational models of the mammalian olfactory system consisting of olfactory bulb and olfactory cortex is constructed to explore possible roles of the related neural circuitry in olfactory information processing via synchronous oscillations. In the models, the bulbar neural circuitry is represented by a chain of oscillators and that of cortex is analogous to an associative memory network with horizontal synaptic connections. The models incorporate the backprojection from cortical units to the bulbar oscillators in particular ways. They exhibit rapid and robust synchronous oscillations in the presence of odorant stimuli, while they show either nonoscillatory states or propagating waves in the absence of stimuli, depending on the values of model parameters. In both models, the backprojection is shown to enhance the establishment of large-scale synchrony. The results suggest that the modulation of neural activity through centrifugal inputs may play an important role at the early stage of cortical information processing.

Animals↗

PubMed1990

NMDA-dependent induction of long-term potentiation in afferent and association fiber systems of piriform cortex in vitro.

Long-term potentiation (LTP) was demonstrated in a slice preparation of piriform (olfactory) cortex. LTP could be reliably induced in both afferent and association fiber pathways. The magnitude of the observed potentiation was greater in the association fiber pathway. 2-Amino-5-phosphonovalerate (APV) blocked induction of LTP in both pathways, indicating that N-methyl-D-aspartate (NMDA) receptor activation is required for induction.

2-Amino-5-phosphonovalerate↗

PubMed2005

Entorhinal cortex stimulation modulates amygdala and piriform cortex responses to olfactory bulb inputs in the rat.

The rodent olfactory bulb sends direct projections to the piriform cortex and to two structures intimately implicated in memory processes, the entorhinal cortex and the amygdala. The piriform cortex has monosynaptic projections with the amygdala and the piriform cortex and is therefore in a position to modulate olfactory input either directly in the piriform cortex, or via the amygdala. In order to investigate this hypothesis, field potential signals induced in anesthetized rats by electrical stimulation of the olfactory bulb or the entorhinal cortex were recorded simultaneously in the piriform cortex (anterior part and posterior part) and the amygdala (basolateral nucleus and cortical nucleus). Single-site paired-pulse stimulation was used to assess the time courses of short-term inhibition and facilitation in each recording site in response to electrical stimulation of the olfactory bulb and entorhinal cortex. Paired-pulse stimulation of the olfactory bulb induced homosynaptic inhibition for short interpulse interpulse intervals (20-30 ms) in all the recording sites, with a significantly lower degree of inhibition in the anterior piriform cortex than in the other structures. At longer intervals (40-80 ms), paired-pulse facilitation was observed in all the structures. Paired-pulse stimulation of the entorhinal cortex mainly resulted in inhibition for the shortest interval duration (20 ms) in anterior piriform cortex, posterior piriform cortex and amygdala basolateral but not cortical nucleus. Double-site paired-pulse stimulation was then applied to determine if stimulation of the entorhinal cortex can modulate responses to olfactory bulb stimulation. For short interpulse intervals (20 ms) heterosynaptic inhibition was observed in anterior piriform cortex, posterior piriform cortex and amygdala basolateral but not cortical nucleus. The level of inhibition was greater in the basolateral nucleus than in the other structures. Taken together these data suggest that the entorhinal cortex exerts a main inhibitory effect on the olfactory input via the amygdala basolateral nucleus and to a lesser extent the piriform cortex. The potential role of these effects on the processing of olfactory information is discussed.

Amygdala↗