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PubMedDate not supplied

Effect of hydrocortisone on synaptic transmission in surviving rat olfactory cortex slices.

A study has been made of the effect of bath-applied hydrocortisone (10(-4) M) on excitatory transmission of the lateral olfactory tract (LOT), a superficial pyramidal cell synapse of the rat olfactory cortex slice. Populations EPSP and IPSP were depressed for 6-12 min and were then increased (60 min) by hydrocortisone. Recovery of evoked potentials was prolonged (40-60 min) when slices were washed with normal incubation medium. Habituation of synaptic potential during LOT repeated stimulation deteriorated as a result of hydrocortisone application in perfusion solution. The data obtained were considered to represent functions of adaption of the nervous system to a stressor.

Action Potentials↗
PubMed1979

Responses of the guinea-pig isolated olfactory cortex slice to gamma-aminobutyric acid recorded with extracellular electrodes.

1. Potential changes between the pial and cut surfaces of slices of guinea-pig olfactory cortex in vitro produced by gamma-aminobutyric acid (GABA) were recorded with extracellular electrodes. 2. GABA, superfused over the pial surface (0.1 to 10 mM), produced a pial-negative potential deflection, accompanied by inhibition of the postsynaptic response to lateral olfactory tract (LOT) stimulation. 3. This effect was replicated by the following compounds (potency relative to GABA = 1, in brackets): 3-aminopropanesulphonic acid (5.3), epsilon-aminovaleric acid (0.07), beta-alanine (0.07), beta-amino-nibutyric acid 0.05), epsilon-aminocaproic acid, alpha-amino-isobutyric acid, L-leucine (less than 0.02). 4. L-Glutamate (1 to 10 mM) produced a very large surface negative shift, with relatively less synaptic inhibition. Glycine (1 to 10 mM) produced less surface negatively, accompanied by synaptic inhibition. 5. Responses to GABA were antagonized more effectively than those to glycine by bicuculline (3 to 30 micrometer) and picrotoxin (1 to 30 micrometer). Strychnine (1 to 10 micrometer) incompletely inhibited responses to glycine. 6. It is concluded that, while the locus within the slice of these effects is uncertain, the preparation may be useful for testing the interaction of drugs with cerebral GABA receptors.

Action Potentials↗
PubMed1998

Muscarinic agonist-induced burst firing in immature rat olfactory cortex neurons In vitro.

Age-related changes in pre-/postsynaptic muscarinic (mAChR) and metabotropic-glutamate (mGluR) responsiveness were studied in slices of olfactory cortex from both immature [postnatal day 16-22 (P16-P22)] and adult (>/=P40) rats, using a conventional intracellular recording technique. In adult neurons, bath application of the mAChR agonist oxotremorine-M (OXO-M; 10 microM), or the selective mGluR agonist 1-aminocyclopentane-1S-3R-dicarboxylic acid (1S,3R-ACPD; 10 microM) evoked sustained membrane depolarizations, increases in input resistance, intense repetitive firing, and the appearance of a slow poststimulus afterdepolarizing potential (sADP). Excitatory postsynaptic potentials (EPSPs) evoked by local electrical stimulation of association fiber terminals were also depressed. In contrast, in neurons from immature slices, the 10 microM OXO-M-induced membrane depolarization was followed by the appearance of spontaneous rhythmic epileptiform activity, which was voltage independent and reversible on drug wash out. Epileptiform bursts were abolished or reduced by coapplication of tetrodotoxin (1 microM), atropine (1 microM), pirenzepine (100-200 nM), the N-methyl-D-aspartate (NMDA) receptor antagonist -amino-5-phosphonovaleric acid (-APV; 100 microM), the non-NMDA receptor antagonist 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX; 5-20 microM), the anesthetic-sedative barbiturate pentobarbitone (100 microM), or by raising the extracellular Mg2+ concentration, whereas a clear facilitatory effect was exhibited by the selective gamma-aminobutyric acid-A (GABAA) receptor blocker (-)-bicuculline methiodide (10 microM). The epileptogenic effects induced by OXO-M were indistinguishable from those produced by 4-aminopyridine (4-AP; 100-200 microM), although these latter actions were unaffected by atropine. In slices from immature animals, electrical stimulation of layer III association fibers in the presence of 10 microM OXO-M was accompanied by a dramatic prolongation of evoked depolarizing postsynaptic potentials (PSPs), with the appearance of recurrent superimposed spike discharges. This effect was readily reversed on wash out of OXO-M. No comparable age-dependent differences were observed in the nature or time course of 1S,3R-ACPD-evoked pre- (or post)synaptic responses, even in immature cells where muscarinic epileptiform activity had previously been demonstrated. We suggest that the overall susceptibility toward muscarinic-induced epileptiform discharge in immature olfactory cortical neurons may depend on the functional integrity of presynaptic inhibitory mAChRs; additional contributing mechanisms were also considered.

4-Aminopyridine↗
PubMed1990

[The neurotropic effects of hydrocortisone in surviving slices of the rat olfactory cortex].

The effects of hydrocortisone on short-term habituation, post-tetanic potentiation, fluctuations of the amplitude of focal potentials (FPs) and slow after-hyperpolarization were studied in the olfactory cortex slice preparations. Hydrocortisone (10(-5)-10(-4) M) inhibited the habituation but facilitated and prolonged the post-tetanic potentiation of the FPs. The hormone increased the fluctuations of the FPs and exerted no effect on slow after-hyperpolarization evoked by a brief orthodromic stimulation. The neurotrophic effects of the hydrocortisone seem to reflect adaptive reactions of nervous system under stress conditions.

Animals↗
PubMed1984

An unlikely role for cyclic AMP in the mediation of the excitatory and inhibitory effects of noradrenaline on transmission in the olfactory cortex.

Simultaneous measurements have been made of the actions of noradrenaline and other agonists, alone and in the presence of appropriate antagonists, on synaptic transmission and cyclic AMP levels in the rat olfactory cortex. The possible role of cyclic AMP as an obligatory mediator of the excitatory and inhibitory actions of noradrenaline is discussed.

Animals↗
PubMedDate not supplied

Peroxidative oxidation of lipids in slices of olfactory cortex of the rat brain during long-term potentiation.

The content of the products of the peroxidative oxidation of lipids (POL) in slices of olfactory cortex of the rat brain during long-term potentiation was investigated. The phasic character of the changes in the level of POL as a function of the duration of potentiation was demonstrated. The initial stages of potentiation (5 min) is characterized by an increase in POL; the stationary phase (15 min) is accompanied by inhibition of free-radical oxidation of lipids; the concluding phase of long-term potentiation (30 min) leads to the normalization of POL. The dynamics of the change in POL reflect the adaptive character of the development of potentiation in the slices.

Animals↗
PubMed1995

Excitotoxic increase of xanthine dehydrogenase and xanthine oxidase in the rat olfactory cortex.

Excitotoxic lesions induced by systemic injection of kainic acid, resulted in 2-3-fold increase of xanthine dehydrogenase and xanthine oxidase activities in the rat olfactory cortex 48-72 h after drug administration. A significant increase of the xanthine oxidase/dehydrogenase ratio was also observed at 4 and 48 h post-injection. No similar changes were noticed in the hippocampus. The enhancement of enzyme activity seems to be primarily a consequence of the altered cell composition in damaged area. Free radicals produced by the increased oxygen-dependent form of the enzyme could in turn aggravate the excitotoxic brain injury.

Animals↗
PubMed1978

A barbiturate induced intensification of the inhibitory potential in slices of guinea-pig olfactory cortex.

1. A study has been made of the effect of barbiturates on membrane constants and synaptic potentials of neurones in the isolated guinea-pig olfactory cortex slice. 2. Normally, a long depolarizing i.p.s.p. follows the e.p.s.p. Pentobarbitone (0.1 mM) produced a tenfold increase in the duration of the high conductance phase of this i.p.s.p. 3. The i.p.s.p. was potentiated increasingly with higher barbiturate concentrations from 0.02 to 1.0 mM-pentobarbitone and 0.2 to 5 mM-phenobarbitone. 4. The resting membrane conductance, the initial phase of the e.p.s.p. and the threshold for the action potential were unaffected at lower concentrations. 5. The highest barbiturate doses increased the resting membrane conductance. This was associated with a depolarization of about 14 mV maximally and resulted in smaller synaptic potentials. The effect was probably generated by the same mechanism as the i.p.s.p. 6. This fortifies the idea that barbiturates have a primary action on prolonging inhibition rather than a depression in the excitatory potential.

Action Potentials↗
PubMed2006

RETRACTED: Combinatorial effects of odorant mixes in olfactory cortex.

In mammals, each odorant is detected by a combination of different odorant receptors. Signals from different types of receptors are segregated in the nose and the olfactory bulb, but appear to be combined in individual neurons in the olfactory cortex. Here, we report that binary odorant mixes stimulate cortical neurons that are not stimulated by their individual component odorants. We propose that cortical neurons require combinations of receptor inputs for activation and that merging the receptor codes of two odorants provides novel combinations of receptor inputs that stimulate neurons beyond those activated by the single odorants. These findings may explain why odorant mixtures can elicit novel odor percepts in humans.

Animals↗
PubMed1979

Depolarization of neurones in the isolated olfactory cortex of the guinea-pig by gamma-aminobutyric acid.

1 Effects of gamma-aminobutyric acid (GABA) on single neurones in slices of guinea-pig olfactory cortex maintained in vitro were recorded with single intracellular microelectrodes. The average resting potential of 52 cells was -75 mV and apparent input resistance ranged from 20 to 200 MOmega.2 Superfusions of GABA over the slice invariably depolarized the neurones and reduced their input resistance. The minimum effective concentration was 50 to 200 muM.3 The reversal potential for the depolarization produced by 0.1 mM GABA (E(g)) was -66 +/- 2 mV. At concentrations >0.1 mM the reversal potential became progressively more positive (-55 to -50 mV).4 Reduction of external chloride, with isethionate as the substitute anion, increased the amplitude of the depolarization.5 GABA reduced the amplitude of the excitatory postsynaptic potential produced by lateral olfactory tract stimulation, and occluded or reversed the subsequent depolarizing recurrent inhibitory postsynaptic potential.6 Action potentials elicited by injection of depolarizing current or by focal antidromic stimulation were slowed and reduced in amplitude by GABA.7 The effects of GABA on membrane conductance (potency = 1) were duplicated by 3-aminopropanesulphonic acid (potency = 20), beta-alanine (0.5), beta-amino-n-butyric acid (0.5), glycine (0.3) and L-2,4-diaminobutyric acid (0.2). For a given conductance change, 3-aminopropanesulphonic acid, glycine and beta-alanine produced less depolarization than did GABA.8 It is concluded that the action of GABA on the neurones is compatible with a role in mediating recurrent postsynaptic inhibition.

Action Potentials↗
PubMed1993

Persistent muscarinic excitation in guinea-pig olfactory cortex neurons: involvement of a slow post-stimulus afterdepolarizing current.

The persistent excitatory effects of the muscarinic agonist oxotremorine-M were investigated in guinea-pig olfactory cortex neurons in vitro (28-30 degrees C) using a single-microelectrode current-clamp/voltage-clamp technique. In 40% of recorded cells (type 1), bath-application of oxotremorine-M (2-10 microM; 1-2 min) induced a strong membrane depolarization, an increase in input resistance and a sustained neuronal discharge lasting over 30 min following agonist washout. A large depolarizing stimulus applied during the action of oxotremorine-M, evoked a slow post-stimulus afterdepolarization (approximately 10-15 mV) lasting approximately 30 s. Injection of steady negative current at the peak of this response produced a slow repolarization of the membrane potential (half-time approximately 0.6 min) towards a plateau level ("hyperpolarization recovery"); these effects of oxotremorine-M were slowly reversed on washout or by application of atropine (1 microM). In a second population of neurons (type 2; 39% of total), oxotremorine-M produced a large depolarization, a resistance increase and repetitive firing that did not persist after agonist washout; these neurons failed to generate a prominent slow afterdepolarization on stimulation, and showed no hyperpolarization recovery effect. Their resting membrane properties were not significantly different from those of type 1 cells. The remaining proportion of cells (type 3) elicited little or no muscarinic response to oxotremorine-M and no slow afterdepolarization; these cells showed characteristics spike fractionation (pre-potentials) during an evoked train of action potentials.(ABSTRACT TRUNCATED AT 250 WORDS)

4-Aminopyridine↗
PubMed1991

[The effect of the tripeptide melanostatin on phospholipid metabolism in the olfactory cortex of rats].

The incubation of the brain slices with melanostatine for 15 min increased the contents and reduced the metabolism intensity of phosphatidylcholine and phosphatidyletanolamine in the rat olfactory cortex. The sphingomyelin metabolism intensity was increased. These shifts in the metabolism of membraneous components may cause considerable modifications in the membranes properties and can be a material basis for long-term changes in the unit activity.

Acetates↗
PubMedDate not supplied

Carbachol-evoked suppression of excitatory neurotransmission in guinea-pig olfactory cortex slices is unlikely to involve an M4-muscarinic receptor subtype.

Depression of the electrically-evoked surface-negative field potential (N-Wave) by bath-superfusion of carbachol was measured in guinea-pig olfactory cortex slices maintained in vitro. The possibility that this response, previously proposed to be mediated via a presynaptic M1: muscarinic receptor, might in fact be due to M4 receptor activation, was investigated by testing the effectiveness of himbacine (a proposed M4-selective antagonist) on our cortical preparation. Himbacine (100 nM-1 microM) had no effect on the N-wave potential alone, but it induced a clear competitive-type inhibition of carbachol effects. Schild plot analysis (regression slope constrained to unity) of pooled data yielded a pA2 value of 7.2 for this antagonist (n = 7 slices). This value accords more with that expected for the interaction of himbacine with M1 receptors (approximately 7.2) than with functionally expressed M4 receptors (approximately 8.5-8.5). We therefore conclude that M4-type muscarinic receptors are unlikely to be involved in mediating this presynaptic carbachol response.

Alkaloids↗
PubMed1996

Effects of felbamate on muscarinic and metabotropic-glutamate agonist-mediated responses and magnesium-free or 4-aminopyridine-induced epileptiform activity in guinea pig olfactory cortex neurons in vitro.

The effects of the anticonvulsant agent felbamate (FBM) were examined on muscarinic and metabotropic-glutamate receptor agonist-induced responses and chemically induced epilepti-form activity, in guinea pig olfactory cortex slices in vitro. FBM (100-500 microM) had little effect on neuronal membrane properties and on postsynaptic potentials evoked by electrical stimulation of lateral olfactory tract terminals, whereas it reduced the duration of presumed Ca++ spikes induced by intracellular Cs+ loading. In contrast, the muscarinic receptor agonist oxotremorine-M (10 microM) or the metabotropic glutamate receptor agonist 1-aminocyclopentane-1S-3R-dicarboxylic acid (10 microM) induced a sustained membrane depolarization with repetitive firing, an increase in input resistance and the appearance of a slow poststimulus afterdepolarizing potential. These effects were reversibly reduced in the presence of FBM (100-500 microM). After preincubation of slices with Mg+(+)-free solution or 200 microM 4-aminopyridine, neurons exhibited spontaneous and stimulus-evoked epileptiform potentials that were suppressed by FBM (1 mM). We conclude that FBM can interfere with muscarinic and metabotropic-glutamate response generation and slow after-depolarization induction in olfactory cortical neurons, most likely by blocking Ca++ influx through voltage-sensitive Ca++ channels. A possible interaction of FBM with other voltage-insensitive Ca++ conductances is also considered. We also suggest that FBM can suppress epileptiform activity induced by Mg+(+)-free or 4-aminopyridine exposure primarily through inhibition of N-methyl-D-aspartate-gated ion channels, although additional actions on non-N-methyl-D-aspartate receptor sites and/or presynaptic transmitter release mechanisms cannot be excluded.

4-Aminopyridine↗
PubMedDate not supplied

Na+,K(+)-ATPase activity in neurons and glial cells of the olfactory cortex of the rat brain during the development of long-term potentiation.

Na+,K(+)-ATPase and Mg(2+)-ATPase activities were studied in neurons and glial cells of the olfactory cortex of the rat by quantitative cytophotometry in conditions of long-term potentiation (LTP), and significant changes in direction and extent were found. Na+,K(+)-ATPase activity decreased in neurons in the first 15 min after LTP, with subsequent elevation by 30 min. Mg(2+)-ATPase activity remained unchanged in these conditions. Glial cells showed significant increases in Na+,K(+)-ATPase activity in the initial period after LTP, with return to control by 30 min. Again, there were no significant changes in Mg(2+)-ATPase activity. The formation and persistence of LTP in neurons and glial cells was accompanied by significant changes in Na+,K(+)-ATPase activity, which were reciprocal in nature.

Animals↗
PubMed1986

"Desensitization" of excitatory amino acid responses in the rat olfactory cortex.

Repeated application of the excitatory amino acid transmitter candidates, L-aspartate and L-glutamate and of N-methyl-D-aspartate, kainate and quisqualate to slices of olfactory cortex evoked progressively smaller depolarizations. These "desensitizations" were concentration-dependent, essentially irreversible and non-selective, although responses to gamma-aminobutyric acid (GABA) and to potassium ions were not significantly depressed. The specific N-methyl-D-aspartate receptor antagonist 2-amino-5-phosphonopentanoic acid, partially blocked the reduction in responses to amino acids which accompanied "desensitization" by N-methyl-D-aspartate, suggesting that activation of receptors is an obligatory step in provoking the phenomenon. "Desensitization" of responses was not prevented by the lectin concanavalin A but was potentiated by ouabain, an inhibitor of the sodium-potassium pump. It is proposed that the phenomenon does not reflect a true desensitization of receptors but is possibly the result of accumulation of intracellular sodium because of overloading the sodium pump. Under circumstances where responses to N-methyl-D-aspartate, quisqualate and kainate were "desensitized" by approx. 96%, depolarizations evoked by L-aspartate and L-glutamate were reduced by only 55%: these residual responses were not antagonized by the excitatory amino acid receptor blockers, (+/-)cis-2,3-piperidine dicarboxylate and 2-amino-4-phosphonobutyrate or by dihydrokainate, an inhibitor of the uptake of glutamate and aspartate. One possibility is that the residual responses reflect an interaction between L-aspartate and L-glutamate and an as yet unknown category of receptors.

Amino Acids↗
PubMed1991

Muscarinic inhibition of excitatory neurotransmission in guinea-pig olfactory cortex slices: weak antagonism by M3-muscarinic receptor antagonists.

Dose-dependent depression of the electrically evoked surface-negative field potential (N-wave) produced by bath-superfusion of carbachol was measured in guinea-pig olfactory cortex slices maintained in vitro. The possible involvement of M3 (smooth muscle/glandular) type muscarinic receptors in partly mediating this response was investigated by testing the effectiveness of the muscarinic M3 receptor antagonists hexahydro-sila-difenidol (HHSiD) and p-fluoro-hexahydro-sila-difenidol (p-F-HHSiD). Low doses of HHSiD (10-100 nM) or p-F-HHSiD (up to 1 microM), pre-applied for 30 min, produced no obvious antagonism of carbachol responses. However, a clear competitive-type inhibition of carbachol effects was observed in 250 nM-1 microM HHSiD or 10-50 microM p-F-HHSiD respectively. Schild plot analysis (regression slope constrained to unity) of pooled data yielded pA2 values of 6.6 for HHSiD (n = 6 slices) and 5.5 for p-F-HHSiD (n = 6 slices) respectively, suggesting a weak competitive antagonism by both compounds. In addition, combination experiments using either HHSiD or p-F-HHSiD with atropine, produced dose-ratio shifts close to those predicted for two antagonists competing for a common receptor site. By comparison, another suggested M3-receptor antagonist, 4-diphenyl-acetoxy-N-methyl-piperidine methiodide (4-DAMP) was a potent competitive blocker of carbachol responses. Schild analysis for 4-DAMP versus carbachol gave a pA2 of 7.9 (n = 6 slices). It is concluded that the muscarinic receptors involved in the suppression of the olfactory cortical N-wave possess a low affinity for HHSiD and particularly for p-F-HHSiD, but not 4-DAMP.(ABSTRACT TRUNCATED AT 250 WORDS)

Action Potentials↗
PubMed1980

Potentiation of inhibition by general anaesthetics in neurones of the olfactory cortex in vitro.

Pentobarbitone, phenobarbitone, methohexitone, chloralose and alphaxalone produced 10-fold increases in the duration of an inhibitory post-synaptic conductance (i.p.s.c.) as recorded intracellularly from neurones of the guinea-pig olfactory cortex in vitro. Higher concentrations slightly depolarised these neurones and reduced their input resistance (Ri), presumably a spontaneous activation of the inhibitory conductance. The excitatory potentials were also depressed. Ketamine, halothane and urethane doubled the i.p.s.c. duration. Higher concentrations depressed synaptic activity and the action potential, as did lignocaine. Ketamine also increased Ri. These results confirm the idea that these compounds produce anaesthesia by prolonging inhibition (accompanied by a depression of the e.p.s.p. with some anaesthetics).

Anesthetics↗