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PubMed1991

Interaction between phorbol dibutyrate and anaesthetics on synaptic responses from olfactory cortex of rat.

Phorbol esters have been shown to enhance the release of transmitters and to potentiate the effect of local anaesthetics in olfactory cortex of the rat. This work examined the interaction between phorbol dibutyrate and a range of substances, which act on axonal conduction and synaptic transmission. Synaptically-evoked field responses were elicited by stimulation of the lateral olfactory tract of slices of olfactory cortex, maintained in vitro. Ketamine (0.2-1.0 mM), benzocaine (0.2-1 mM), atropine (0.1-2 mM) and tetrodotoxin (20-200 nM) depressed synaptic transmission and, in the presence of phorbol dibutyrate (1 microM), these substances were more potent by 3.7 +/- 0.5, 1.5 +/- 4, 2.6 +/- 0.6 and 5.5 +/- 1.8 fold, respectively. Pentobarbitone (0.1-2.0 mM) with or without bicuculline, urethane (10-200 mM), halothane (0.5-5.0 mM) (with bicuculline) and ethanol (50-500 mM) also depressed synaptic transmission but their effectiveness was not potentiated by phorbol dibutyrate. It is thought that the increased potency, produced by phorbol ester, was associated with a presynaptic action of those substances.

Anesthetics↗

PubMed1987

Ion activities and potassium uptake mechanisms of glial cells in guinea-pig olfactory cortex slices.

1. Double-barrelled ion-sensitive micro-electrodes were used to measure changes in the intracellular activities of K+, Na+ and Cl- (aiK, aiNa, aiCl) in glial cells of slices from guinea-pig olfactory cortex during repetitive stimulation of the lateral olfactory tract. 2. Base-line levels of aiK, aiNa and aiCl were about 66, 25 and 6 mM, respectively, for cells with resting potentials higher than -80 mV. During stimulation, intraglial aiK and aiCl increased, whereas aiNa decreased. Within about 2 min after stimulation the ion activities returned to their base-line levels. 3. The Cl- equilibrium potential was found to be close to the membrane potential (Em). There was also a strong correlation between changes of Em and aiCl. These observations indicate a high Cl- conductance of the glial cell membrane. 4. In the presence of Ba2+, the usual depolarizing response of the glial cells to a rise of the extracellular K+ activity (aeK) reversed into a membrane hyperpolarization. Furthermore, Ba2+ strongly reduced the stimulus-related rise of intraglial aiK. An additional application of ouabain blocked both the membrane hyperpolarization as well as the remaining rise of aiK. 5. In conclusion, our data show that glial cells in guinea-pig olfactory cortex slices possess at least two mechanisms of K+ accumulation. One mechanism is sensitive to the K+ channel blocker Ba2+ and might be a passive KCl influx. The other appears to be the electrogenic Na+/K+ pump, which can be activated by excess extracellular K+.

Action Potentials↗

PubMed1990

[Posttetanic and frequency potentiation in slices of the olfactory cortex from the rat brain].

A 15-sec tetanization of lateral olfactory tract at the frequency of 30/sec produced a short-term (20 min) posttetanic potentiation of the field potentials (FPs) in the rat olfactory cortex slices. Rhythmical stimulation of lateral olfactory tract (6 trains of 10 pulses each at the frequency of 10/sec, with 4-5 sec intertrain interval) evoked a progressive increase in the amplitude of postsynaptic components of the FPs (EPSP and IPSP) but not in amplitude of presynaptic component--the compound AP of lateral olfactory tract. The findings suggest the development of the 2-form functional plasticity: posttetanic and frequency potentiation in pyriform cortex.

Animals↗

PubMed1987

Calcium-dependent potassium conductance in guinea-pig olfactory cortex neurones in vitro.

1. Guinea-pig olfactory cortex neurones in vitro (23-25 degrees C) were voltage clamped by means of a single-micro-electrode sample-and-hold technique. 2. Under current clamp at the resting potential (approximately -80 mV), brief depolarizing stimuli evoked trains of action potentials with little visible after-potential. However, in 90% of recorded cells held at membrane potentials between -70 and -45 mV, depolarizing current pulses evoked a slow after-hyperpolarization (a.h.p.) (approximately 8 mV) lasting several seconds and accompanied by an increase in input conductance. 3. The outward membrane current underlying the a.h.p. was revealed either by switching rapidly to voltage clamp at the end of a spike train ('hybrid' clamp) or by applying brief depolarizing commands from potentials between -60 to -45 mV. The tail current showed a distinct rising phase (time to peak approximately 1 s) and exponential decay (tau approximately 3 s) and was suppressed by removal of external Ca2+, or adding Co2+ (1-2 mM), Cd2+ (200 microM) or Mg2+ (6 mM). The a.h.p. current reversal potential was -96 mV in 3 mM-K+ medium. 4. Low concentrations (1-2 microM) of muscarine, carbachol, oxotremorine or the muscarinic ganglion stimulant, McN-A-343 (1-10 microM) reduced the a.h.p. current and leak conductance and induced a steady inward current, without affecting M-current (IM) relaxations. IM inhibition generally required higher (greater than 10 microM) agonist concentrations, although oxotremorine remained ineffective at up to 50 microM. 5. The a.h.p. current was reduced by noradrenaline and tetraethylammonium (TEA), but not by apamin or tubocurarine. Apart from TEA, these agents had no effect on IM. 6. Addition of tetrodotoxin (TTX, 1 microM) or removing external Na+ depressed the a.h.p. current amplitude recorded under voltage clamp. The residual tail current could be further reduced by adding Cd2+ or muscarinic agonists. 7. Repolarizing tail currents induced following positive voltage commands consisted mainly of IM and slow a.h.p. current with little evidence of a 'fast' Ca2+-activated K+ current (IC). 8. It is concluded that the slow a.h.p. current that underlies the post-burst after-hyperpolarization of olfactory neurones, is a Ca2+-dependent K+ current distinct from IM. It is suggested that the cholinergic modulation of this current (rather than IM) may provide a more subtle control of cell excitability in cortical neurones.

Action Potentials↗

PubMed1978

Field potentials, inhibition and the effect of pentobarbitone in the rat olfactory cortex slice.

1. Field potentials were evoked in slices of rat olfactory cortex by stimulating the lateral olfactory tract. In addition to previously described components of the wave-form, a further distinct surface-negative potential of low amplitude and long duration (I-wave) has been described. 2. Pentobarbitone, at concentrations of 10(-5) M and above, markedly enhanced enhanced the amplitude and duration of the I-wave with only minimal effect on other components of the field potential. 3. The I-wave was reversibly reduced by the GABA antagonists bicuculline and picrotoxin and was also attenuated at rapid rates of stimulation. Low chloride medium usually caused a transient increase in amplitude of the I-wave followed by a gradual reduction, suggesting that a chloride-mediated depolarization was involved. 4. Evoked inhibition, which was most probably post-synaptic, occurred in parallel with the I-wave. This was monitored as a suppression of, or increase in latency of the population spike evoked by a second stimulus at appropriate intervals after the first. Pentobarbitone substantially increased the duration of the post-synpatic inhibition, without obvious changes in the presynaptic inhibitory phenomenon associated with antidromic firing in the lateral olfactory tract. 5. It is proposed that the I-wave is the field potential representation of a population depolarizing i.p.s.p. and that the main action of pentobarbitone is to enhance this inhibition.

Action Potentials↗

PubMed1985

Muscarinic depression of evoked surface-negative field potentials recorded from guinea-pig olfactory cortex in vitro.

The action of some cholinergic drugs has been studied on the field potentials evoked by orthodromic stimulation of the lateral olfactory tract (LOT) in guinea-pig olfactory cortex slices maintained in vitro. A reversible depression of the electrically evoked surface-negative field potential (N-wave) was seen following superfusion of muscarine (10-200 microM) or mixed-agonist choline esters but not nicotinic agonists. This depression was blocked by atropine and pirenzepine, but not d-tubocurarine or by antagonists active at gamma-aminobutyric acid or adenosine receptors. Little effect of muscarinic agonists was observed on the compound action potential recorded from the LOT, or on pial surface DC potential. A possible presynaptic site of action of muscarinic agonists in the olfactory cortex is discussed.

Acetylcholine↗

PubMed1989

Antagonism of monosynaptic excitations in the mouse olfactory cortex slice by 6,7-dinitroquinoxaline-2,3-dione.

The effects of 6,7-dinitroquinoxaline-2,3-dione (DNQX) have been tested in slices of olfactory cortex of the mouse against responses evoked by N-methyl-D-aspartate, kainate and quisqualate and on the surface field potentials evoked on electrical stimulation of the lateral olfactory tract. At a concentration of 5 microM, DNQX competitively antagonized responses evoked by kainate and quisqualate, with only a small reduction in the responses to N-methyl-D-aspartate. In contrast, DL-(+-)-2-amino-5-phosphonopentanoic acid (APP, 50 microM) selectively antagonized depolarizations to N-methyl-D-aspartate. The amplitude of the field potential known as the N-wave was reduced by DNQX in a concentration-dependent reversible manner (IC50 = 2.92 +/- 0.33 microM; mean +/- SE mean, n = 4). DL-(+-)-2-Amino-5-phosphonopentanoic acid (50 microM) did not significantly affect this action of DNQX. It is concluded that DNQX inhibits monosynaptic excitations in the olfactory cortex by selectively blocking kainate and/or quisqualate receptors, although it is unclear whether the receptors are located at pre- and/or postsynaptic sites.

Animals↗

PubMed1986

Plasticity in the olfactory cortex: age-dependent effects of deafferentation.

In order to assess the role of input-target interactions in the development of olfactory cortex, the primary afferent fibers from the olfactory bulb to the superficial part of layer I of the cortex (layer Ia) were removed in developing and mature rats. After survival periods that vary from a few days to 2-6 months, changes were assessed in (1) the radial thickness of layer I, (2) the laminar distribution of intracortical associational fibers, which normally terminate in a deep part of layer I (layer Ib), and (3) the distribution of glia in layer I. The findings indicate that the lamination of fibers within layer I is not intrinsically prespecified, but gradually becomes "set" during the first month after birth. If the fibers from the olfactory bulb are removed, the dendrites of cortical cells are capable of accepting inputs from other fiber systems, depending on the maturational state of the dendrites and the ingrowing axons. Development of the abnormal inputs is associated with relatively normal dendritic growth, whereas lack of adequate input results in dendritic atrophy. Thus, after neonatal bulb ablation, the intracortical fibers occupy both superficial and deep parts of layer I, and a normal synaptic density is established throughout the layer. Layer I also develops to nearly its normal adult thickness, although the high density of glia that normally characterizes layer Ia is not apparent. With bulb ablation at progressively older ages (from postnatal day (P-) 3 to 21), the cortical associational fibers show progressively less extension into the denervated layer Ia. Layer I continues to grow, but not to the same extent as after P-1 ablations. In these experiments the glia distribution resembles the pattern present at the time of denervation. After adult olfactory bulb ablation, the long intracortical fibers extend very little into layer Ia, which undergoes pronounced shrinkage and becomes filled with a high concentration of glia. However, partial reinnervation of layer Ia is accomplished by the proliferation of a normally sparse native fiber system, which has been identified only with the Timm method. These results are interpreted as evidence that the normal development of lamination of afferent fibers to the olfactory cortex depends on axodendritic interaction during development.

Age Factors↗

PubMed1990

General anaesthetics and field currents in unclamped, unmyelinated axons of rat olfactory cortex.

1. The effects of seven general anaesthetics and one local anaesthetic having a wide range of physical and chemical properties were studied on nerve terminal Na- and K-mediated currents in slices of olfactory cortex. These currents were measured from the groups of fine unmyelinated axons traversing the surface of the olfactory cortex and which give off synapses en passant. The amplitude of the K-current was visualized by depolarizing the axons via an electrode polarization. 2. The anaesthetics tested were ketamine (0.1-2 mM), pentobarbitone (0.1-5 mM), urethane (5-200 mM), halothane (0.5-5 mM), ether (10-200 mM), alphaxalone (0.001-0.05 mM), diisopropylphenol (0.05-0.5 mM) and lignocaine (0.01-0.5 mM). All had depressant effects on the axonal Na-current (at the higher concentrations tested) and on the K-current (at slightly lower concentrations). The apparent lower potency on the Na-current was considered to be due to a masking of effect as a consequence of the reduction in the K-mediated membrane rectification rather than any real difference in the susceptibilities of the Na and K-currents. 3. Some of the depressant effect of pentobarbitone and alphaxalone was gamma-aminobutyric acid (GABA)-mediated as indicated by the reduced potency in the presence of bicuculline. The actions of ketamine and halothane were unaffected by bicuculline. 4. For some anaesthetics these axonal depressant effects might contribute to general anaesthesia, while for other substances the relatively high concentrations necessary would suggest that this mode of action does not produce effective anaesthesia in vivo.

Anesthetics↗

PubMed1982

Some effects of excitatory amino acid receptor antagonists on synaptic transmission in the rat olfactory cortex slice.

A study has been made of the effects of a series of excitatory amino acid receptor antagonists on the field potentials evoked on electrical stimulation of the lateral olfactory tracts of olfactory cortex slices perfused in vitro. The antagonists studied included (+/-)-2-amino-5-phosphonovaleric acid, a potent, specific antagonist of N-methyl-D-aspartate (NMDA) receptors, gamma-D-glutamylglycine, an antagonist of NMDA and kainate receptors and (+/-)-cis-2,3-piperidine dicarboxylic acid and 2-amino-4-phosphonobutyric acid, drugs which in addition to antagonizing NMDA and kainate receptors also block responses to quisqualic acid. From the patterns of effects of the drugs it is proposed that quisqualate and NMDA but not kainate receptors are involved in mediating excitatory transmission in the olfactory cortex; quisqualate receptors are located at the lateral olfactory tract - superficial pyramidal cell synapse whereas NMDA receptors are present at the synapses of the superficial pyramidal cell collaterals with the deep pyramidal cell dendrites and/or at the synapses of the pyramidal cell collaterals and inhibitory interneurones. The results are discussed in terms of possible presynaptic and/or postsynaptic sites of antagonist action.

2-Amino-5-phosphonovalerate↗

PubMed1989

Antigenic abnormalities in fiber tract astrocytes of myelin-deficient rats: an immunocytochemical study in the olfactory cortex.

Intrafascicular oligodendrocytes in myelin-deficient (md) rats typically fail to form myelin sheaths or survive to maturity. The present study of the md olfactory cortex compares astrocytes that develop either among populations of pathological oligodendrocytes in a fiber tract or that develop in neuropil, which normally contains few oligodendrocytes. Antigenic profiles for md and normal astrocytes were defined by the monoclonal antibody Rat 401, and by antibodies that recognize vimentin and glial fibrillary acidic protein. In the olfactory cortex, antigenic abnormalities were typically restricted to astrocytes located in the vicinity of pathological oligodendrocytes.

Animals↗

PubMed1979

Mono-and multi-synaptic origin of the early surface-negative wave recorded from guinea-pig olfactory cortex in vitro.

1. Silices of guinea-pig olfactory cortex were cut at 550 micrometer nominal thickness and preincubated at 24 +/- 0.5 degrees C for than 2 1/2 hr. They were then stimulated via the lateral olfactory tract, and field potential recordings were made from all regions of the slice. 2. Potentials recorded resembled those described previously, but it was noticed the early N-wave had two distinct components, which we designated the N'a' wave (earlier) and N'b' wave (later). Evidence was obtained that this was not a consequence of the division of a single population e.p.s.p. (N-wave) into two by a P notch (synchronous discharge of post-synaptic action potentials). 3. In some slices the N'a' wave and N'b' wave had similar thresholds, and in others the N'a' wave had the slightly lower threshold. 4. The N'b' wave was best developed at low frequencies of stimulation (less than 0.1 Hz), and considerably depressed with stimulation above 1 Hz. This was most evident with submaximal stimulation. 5. Exploration of the distribution of peak amplitudes and latencies of the N'a' and N'b' waves showed that the N'a' wave could have been directly initiated by lateral olfactory tract action potentials, while the N'B' wave could not. The N'b' wave amplitude was relatively larger towards the periphery of the slices, away from the tract. In a few cases, an N'b' wave could be recorded in the absence of an N'a' wave at that site. 6. Depth studies showed that the origin of the N'b' wave lay deeper in the slice than that of the N'a' wave. 7. The effect of conditioning stimulation on the N'a' and N'b' waves was examined. The N'b' wave was more depressed at short conditioning intervals than the N'a' wave, and showed less later potentiation. The recovery of the N'b' wave from conditioning was much slowed with submaximal stimulation, and when trials were repeated at low frequency. 8. The N'a' and N'b' components persisted when the slice was warmed to near-physiological temperatures, and showed a similar pattern of response to conditioning stimulation as had been found at lower temperatures. 9. N'a' and N'b' waves could still be recorded when slices were incubated in a medium containing 1.2 mM-Mg2+ and 1.2 mM-Ca2+. These physiological concentrations were about half those routinely employed. There was little or no depression of the N'b' component by conditioning stimulation in this medium. 10. The N'a' wave is probably a result of e.p.s.p.s in apical dendrites of superficial pyramidal cells, initiated by transmitter release from lateral olfactory tract axon collaterals. The N'b' wave may reflect e.p.s.p.s in the apical dendrites of deeper pyramidal cell elicited by firing in recurrent collaterals from superficial pyramidal cell axons.

Animals↗

PubMed1988

A quantitative study of the effects of some muscarinic antagonists on the guinea-pig olfactory cortex slice.

1. Muscarinic depression of the electrically-evoked surface-negative field potential (N-wave) was measured in guinea-pig olfactory cortex slices maintained in vitro. 2. The effects of three muscarinic receptor antagonists, pirenzepine, atropine and gallamine on this muscarinic response were analysed in detail. 3. Pirenzepine was a potent competitive antagonist of carbachol (CCh)-evoked responses. Schild plot analysis yielded a pA2 value of 7.9 (Schild slope constrained to unity). A similar analysis for atropine versus CCh responses gave a pA2 of 8.9. 4. Combination experiments using pirenzepine and atropine produced dose-ratio shifts close to those expected for two antagonists competing for a similar receptor site. 5. Gallamine was only a weak antagonist of responses to CCh. 6. Oxotremorine behaved as a competitive antagonist at this muscarinic receptor (pA2 = 6.1). 7. It is concluded that the presynaptic muscarinic receptor mediating depression of the N-wave in the olfactory cortex slice is of the M1-subtype.

Animals↗

PubMed1990

Muscarinic suppression of the evoked N-wave by oxotremorine-M recorded in the guinea-pig olfactory cortex slice.

The effect of the muscarinic agonist oxotremorine-M has been studied on the surface-negative field potential (N-wave) evoked by orthodromic stimulation of the lateral olfactory tract in slices of guinea-pig olfactory cortex. Bath-application of oxotremorine-M (5-80 microM) or carbachol (10-300 microM) produced a reversible depression of the N-wave amplitude without affecting the lateral olfactory tract compound action potential. Oxotremorine-M was approximately 5 times more potent than carbachol in this respect, and the effects of both agonists were competitively blocked by telenzepine (5-100 nM), a selective M1-receptor antagonist. In contrast, methoctramine or AF-DX 116, two 'cardioselective' M2-receptor antagonists, had little or no blocking effect on the agonist responses. It is suggested that oxotremorine-M (like carbachol) inhibits the evoked field potential by activating presynaptic M1-type muscarinic receptors in the olfactory cortex slice.

Action Potentials↗

PubMed1993

Frequency-dependent plasticity of potentials evoked by repetitive stimulation of the lateral olfactory tract in rat olfactory cortex slices.

Habituation and sensitization were demonstrated in slices of olfactory cortex. One of the habituation properties, its dependence on the frequency of the lateral olfactory tract (LOT) stimulation, was tested. It was used in the frequency ranges (1, 10, 20, 30, 40, 50 and 100 impulses/s) which imitated the spontaneous activity of pyriform cortex (PC). Monosynaptic field potentials (FPs) were recorded in PC. Repeated stimulation with one of the frequencies of this range evoked different types of reactions in the PC populations of neurons. Three groups of neuronal reactions were distinguished. The first group of neurons manifested habituation (H-group), while the second one demonstrated sensitization (S-group). In the third group primary sensitization was observed, which then transformed into a short-term phase, when the amplitude of FPs did not change. After that the habituation was found to develop (S-H-group). In the H-group, it was more difficult to evoke habituation at the frequencies of 20-40/s and the number of stimuli in a trial of repeated stimuli (n) being equal to 10 and 150. In the S-group, it was more difficult to induce sensitization at the frequencies of 30-40/s and n equal to 10 and 150. This data proves that the development of habituation and sensitization depends on two factors at least: on the frequency of stimulation and on the type of excited synapse/cell population. Thus, in the PC neuronal populations, a property of habituation suggested by Thompson and Spencer [Psychol. Rev., 73 (1966) 16-43] (higher stimulation frequency causes more rapid and/or pronounced habituation) is not true for all ranges of frequencies.

Animals↗

PubMed1979

Presynaptic gamma-aminobutyric acid responses in the olfactory cortex.

1. Potential changes were recorded from the lateral olfactory tract in slices of rat olfactory cortex in vitro at room temperature. 2. Superfused gamma-aminobutyric acid (GABA) usually produced dose-related depolarization of the lateral olfactory tract. Muscimol and 3-aminopropanesulphonic acid appeared more potent depolarizing agents than GABA, and glycine and taurine appeared less potent. Carbachol and glutamate were virtually ineffective. 3. The GABA responses were at least partially Cl- dependent. 4. (+)-Bicuculline and higher concentrations of strychnine antagonized the GABA but not the glycine-induced depolarizations. Paradoxically, responses to high doses of GABA were sometimes potentiated by both bicuculline and strychnine. 5. It is suggested that GABA receptors could occur as widely on nerve terminals as they do postsynaptically in the CNS, where GABA could be involved in the modulation of transmitter output.

Animals↗

PubMed1988

Presynaptic Na/Ca action potentials in unmyelinated axons of olfactory cortex.

(1) Pial surface slices of guinea-pig olfactory cortex were cut to have a thickness of 150 micron. Action potentials were recorded from the sectioned ends of the unmyelinated afferent axons originating from the lateral olfactory tract (LOT). These potentials were prolonged by the K-channel blocker 3,4-diaminopyridine (0.1 mmol/l) and further lengthened by tetraethylammonium (10 mmol/l). The action potential was also greatly prolonged by partly replacing the K+ in the bathing solution by Cs+. (2) These prolonged action potentials were shortened by Cd2+; Gd3+ (gadolinium); Ni2+; Mn2+; Co2+, in order of potency. The residual early component of the action potential was tetrodotoxin (TTX) sensitive. In contrast, the LOT action potential was little affected by Ca-channel blockade. (3) Organic Ca-channel blockers either had no effect (0.05 mmol/l nifedipine), or depressed the early and later phases of the prolonged action potential equally (0.05-0.5 mmol/l verapamil or 0.05-0.2 mmol/l diltiazem). (4) A propagated action potential was also obtained in solution containing TTX and low Na+. This potential was supported by Ca2+, Sr2+ or Ba2+ and completely suppressed by Cd2+. (5) The later parts of the action potential, after K-channel blockade, had a pharmacological sensitivity towards Ca-channel blockers matching that of synaptic transmission. This suggests the falling phase of the action potential is caused by charge carrier (mainly Ca2+) passing through Ca-channels that have similar properties to, or are the same as those which open prior to transmitter release.

4-Aminopyridine↗

PubMed1980

Release of endogenous amino acid neurotransmitter candidates from rat olfactory cortex slices: possible regulatory mechanisms and the effects of pentobarbitone.

A study has been made of the regulation of evoked release of the amino acid neurotransmitter candidates (aspartate, GABA and taurine) from rat olfactory cortex slices. The effects of pentobarbitone (10-1000 microM) on release have also been assessed. Release of aspartate, the presumed excitatory transmitter of some of the lateral olfactory tract fibres, is reduced by muscimol (10 microM) and this effect is antagonized by picrotoxin (15 microM): it is concluded that presynaptic GABA receptors may modulate aspartate release. Low concentrations of pentobarbitone also reduce aspartate release, but this effect is picrotoxin-insensitive. Release of GABA, the presumed transmitter of inhibitory interneurones, is reduced by muscimol (10 microM) and this effect is antagonized by picrotoxin (15 microM): it is suggested that GABA release may be regulated by presynaptic autoreceptors. Pentobarbitone significantly increases release of GABA when slices are synaptically activated although the mechanism of this effect is unclear. Release of taurine, not hitherto considered a neurotransmitter in this brain area, is depressed by muscimol (10 microM) and pentobarbitone and increased by picrotoxin (15 microM). Results are discussed in terms of (i) mechanisms of regulation of amino acid release in the olfactory cortex, (ii) effects of pentobarbitone on release and (iii) the compatibility of the present results with previously published electrophysiological studies.

Animals↗