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Depth-profile, current-source-density (CSD) and impedance analysis were used to determine the current generators of secondary waves "a" and "b" in the response evoked in pyriform cortex (PC) of the urethane anesthetized rat following OB or LOT stimulation. Positive peaks (sinks) in the second-derivative curves of the "a" and "b" waves were localized at 50-75 and 225-250 microns deep, respectively. Cortical impedance was significantly (p less than 0.01) correlated with the cell packing density of PC layers, being maximal close to the zero dipole point of the gross evoked response; magnitude of conductivity gradients was, however, insufficient to alter the interpretation of positive and negative peaks in terms of net membrane currents. Post-tetanic and/or frequency potentiation of PC responses but not long-term potentiation were found in the majority of animals tested. Recovery of the test "b" wave was faster when using paired-shock stimulation at 3.0 Hz than at 0.3 Hz; suppression of this component following a conditioning OB volley could be overcome and the "b" wave facilitated if either a long-latency component (i.e., 65-100 msec) was present in the priming response, or if the conditioning stimulus was delivered to the mediodorsal thalamic nucleus (MDT). These results confirm and extend similar ones in other species, suggesting that following OB or LOT stimulation three successive excitatory processes take place in PC neural elements of the rat under urethane anesthesia: an initial monosynaptic excitation of distal segments of apical dendrites of layer II cells, and to a lesser extent, also of layer III neurons ("a" wave), followed by action potentials in their respective somas (PS wave); subsequently, long association axons give rise to a di or polysynaptic compound EPSP in proximal apical and possibly also, in basal pyramidal dendrites ("b" wave; early reactivation process). Finally, a "late" reactivation takes place in PC involving neurons which participated in the early reactivation process (late component). In addition, heterosynaptic facilitation of the "b" wave in the PC evoked response follows MDT conditioning stimulation.
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Corticoliberin may induce protective effects via its specific receptors or unspecifically by means of the glutamate receptors. A combined action of these mechanisms is also possible.
How do we smell? Our knowledge of how odor information from the environment is perceived has greatly advanced since the discovery of approximately 1,000 genes for odorant receptors in the mammalian genome. From the combination of molecular-genetic, electrophysiological, and optical imaging studies a better understanding of how we smell is emerging.
Within 15 min after addition of picrotoxin to incubation medium, a reduction of the phosphatidylethanolamine methylation occurred. The reduction seems to be related to opening of ion channels since during this period of the picrotoxin action the maximal membrane depolarisation takes place.
The initial stationary phase of the LTP was followed by a decrease in the Na(+),K(+)-ATPase activity of neurons and an augmentation of enzyme activity in the glial cells. Decay of the LTP tends to normalize the above types of activity.
Long-term potentiation (LTP) was shown to be accompanied by an increase in the lipid peroxidation at the initial stage. Stationary phase resulted in inhibition of the free radical lipid peroxidation. A decline of the LTP is accompanied by normalising of the lipid peroxidation level. The latter's dynamics seems to express the adaptive character of the LTP development in the rat brain slices.
We studied the effect of in vivo exposure to hypobaric hypoxia of different depth on the resistance of neurons in brain slices to 10-min anoxia in vitro. Severe hypoxia simulating ascent to 11,000 m above sea level potentiated the adverse effect of 10-min anoxia and caused profound suppression of synaptic transmission. Moderate preconditioning hypoxia simulating ascent to 5000 m above sea level produced a long-lasting protective effect on synaptic activity.
In a previous work (Ballain et al., 1998. Biol. Cyber. 79, 323-336) we reported the analysis of a model for the piriform cortex activity in rats based on experimental data. In this paper, we study an extension of this model by supplementing it with equations for the post-synaptic conductance and/or the pre-synaptic activation threshold. We use the present model's outputs to account for experimental data based on paired stimulation in the opossum or the rat, obtained either through electrical recording or optical mapping of the cortex activity. The model exhibits great robustness when it comes to large variation in synaptic characteristics. Model outputs mimic satisfactorily the three kind of responses to paired stimuli (Litaudon and Cattarelli, 1996. Eur. J. Neurosci. 8, 21-29) and the recovery of the excitable capacities as demonstrated by Haberly (1973. J. Neurophysiol. 36 (4), 789-802) and Ferreyra-Moyano et al. (1985. Brain Res. Bull. 15, 237 248).
The existence of neurons with intrinsic oscillations does not in itself explain the synchronization of local populations of neurons, but it is likely to pace population rhythms when the neurons are suitably coupled by chemical and/or electrical synapses. In the present study, we have investigated the role of spontaneously active cells as noisy or pacemaker units in setting global oscillations in a three-layered cortical model. The presence of a small number of noisy (spontaneously active) units induce oscillations at the network level in the range of the gamma rhythm. The number of noisy units in the network and their type (excitatory or inhibitory or excitatory and inhibitory together) determines the emergence of regular oscillations or aperiodic (chaotic) behaviour. It also determines the onset of the global behaviour. On replacing a noisy unit by a pacemaker unit, similar gamma oscillations were generated. With both noisy and pacemaker units, we found that certain characteristics of the spontaneous activity determine the delay period for the onset of global activity. Preliminary studies have been carried out with spontaneously active units having a chaotic dynamics but the results are much similar to that with a noisy burst. Different functional roles have been suggested for cortical oscillations, such as determining global functional states and specifying connectivity during development. Oscillations at different frequency bands, in particular in the gamma band (around 40 Hz), have also been associated with memory and attention. The presence of spontaneously active neurons, either with noisy or oscillatory activity, could be responsible for global oscillations in the absence of external stimuli in certain cortical areas in the mature brain.
1. Differences in the cholinergic suppression of afferent and intrinsic fiber synaptic transmission were studied in the rat piriform cortex. Extracellular and intracellular recording techniques were applied in an in vitro transverse slice preparation. Afferent and intrinsic fiber systems were differentially stimulated with electrodes placed in layer Ia or layer Ib, respectively. Synaptic responses were monitored in the presence of cholinergic agonists and antagonists. 2. Afferent and intrinsic fiber synaptic potentials measured extracellularly showed large differences in sensitivity to micromolar concentrations of the cholinergic agonists carbachol or (+/-)-muscarine, or to acetylcholine combined with neostigmine. Intrinsic fiber synaptic responses in layer Ib were strongly reduced in the presence of cholinergic agonists, whereas afferent fiber synaptic responses in layer Ia were largely unaffected. At a concentration of 100 microM, all three agonists caused a greater than 60% decrease in the height of the intrinsic fiber synaptic potential but less than 15% reduction in the afferent fiber synaptic potential. 3. Intracellular recordings confirmed that the cholinergic agonist carbachol selectively suppresses intrinsic fiber synaptic potentials but not afferent fiber synaptic potentials recorded from the same pyramidal cell. 4. Dose-response curves to carbachol were obtained for both fiber systems using extracellular recording of evoked field potentials. Carbachol suppressed intrinsic fiber synaptic potentials with a coefficient of dissociation (KD) estimated at 2.9 microM and an inhibitory concentration for 50% response estimated at 6.6 microM. 5. Carbachol produced a proportionately greater suppression of the first pulse than the second pulse of a pulse pair. This increase in the level of facilitation accompanying suppression suggests a presynaptic mechanism.(ABSTRACT TRUNCATED AT 250 WORDS)
We performed whole-cell recordings of layer III non-pyramidal neurons in the piriform cortex of Sprague-Dawley rats. For comparison purposes, recordings were made from deep pyramidal cells, which are also present in layer III. These two cell types could be distinguished both anatomically and physiologically. Anatomically, the layer III non-pyramidal neuron displayed smooth beady dendrites, while deep pyramidal cells showed thicker dendrites with spines. The dendrites of the layer III non-pyramidal neuron also tended to be restricted to layer III while deep pyramidal cells had long apical dendrites that spanned layers I and II. Although the resting membrane potentials of both cell types were very similar, significant differences were noted in other physiological measures. Layer III non-pyramidal neurons typically displayed higher input resistances, faster time constants, smaller spike amplitudes, shorter spike widths, and higher spike thresholds. In addition, layer III non-pyramidal neurons were able to spike at much higher rates when stimulated with the same level of threshold normalized current injection. The most dramatic differences in physiology were seen in the pattern of spiking in response to increasing levels of positive constant current pulses. Layer III non-pyramidal neurons showed qualitatively different responses at low and high levels of stimulation. At low levels, spikes occurred with long latency and the firing frequency increased throughout the duration of the current pulse. At high levels, non-pyramidal neurons started spiking with short latency, followed by a decrease in firing frequency, which in turn was followed by an increase in firing frequency. Deep pyramidal neurons differed dramatically from this pattern, displaying a qualitatively similar response at all levels of current injection. This response was characterized by short latency spikes and spike adaptation for the duration of the current pulse.
1. The effects of agonists of on the evoked N-wave complex in slices of mouse have been studied: most experiments were carried out using slices perfused with Mg(2+)-free solution to which 10 microM of either 6,7-dinitroquinoxaline-2,3-dione or 6-cyano-7-nitroquinoxaline-2,3-dione was applied. 2. Following agonist washout, a slowly developing, long lasting potentiation of the complex occurred which was confined to the mediated component of the potential. The relative agonist potencies were 1S,3R-1-aminocyclopentane-1,3-dicarboxylic acid (1S,3R-ACPD, 5-250 microM) = quisqualate (5-50 microM) > 1RS,3RS-cis-1-aminocyclopentane-1,3-dicarboxylic acid (ACPD, 25-1000 microM) > L-glutamate (0.25-2.5 mM); NMDA, alpha-amino-3-hydroxy-5-methyl-4-isoxazole-propionate (AMPA) and L-aspartate were inactive. 3. Potentiation of the NMDA receptor-mediated component by 1S,3R-ACPD (0.1 mM) was non-competitively antagonised by S-(+)- but not R-(-)-2-amino-3-phosphonopropionate (AP3, 0.125 mM), equally by D-(-) and L-(+)-2-amino-4-phosphonobutyrate (0.25 mM) and also by the protein kinase C inhibitors sphingosine, (25 microM), sangivamycin (25 microM) and 5-(isoquinolinylsulphonyl)-3-methylpiperazine (50 microM). 4. In a series of input-output experiments, 1S,3R-ACPD (0.1 mM) reversibly reduced the latency to peak of the NMDA receptor-mediated component at submaximal stimulus intensities, an effect blocked by S-(+)-AP3 (0.125 mM). On agonist washout, there was an increase in the area of the receptor-mediated component over all stimulus intensities, an effect blocked by the inhibitors of protein kinase C and by S-(+)-AP3 (0.125mM). 4-beta-Phorbol-12,13-diacetate (2.5 muM) also potentiated the component, an action inhibited by protein kinase C inhibitors but not by S-(+)-AP3. IS,3R-ACPD (0.1mM) had no significant effect on postsynaptic responses evoked by NMDA, AMPA and kainate, but significantly reversed a partial antagonism of NMDA responses produced by 7-chlorokynurenate (2.5 muM). The K+evoked release of glycine was selectively and significantly increased in the presence 0.1mM 1S,3R-ACPD(antagonized by 0.125 mM S-(+)-AP#) whereas following agonist washout, release of glycine fell to control levels but there was a significant increase in release of aspartate(antagonized by 25 muM sangivamycin and 0.125 muM S-(+)-AP3). It is concluded that mediate (i) a reduction in the latency of the mediated component of potentials by a mechanism that is independent of protein kinase C but which may depend on increased glycine release release and (ii) a long lasting increase in the total area of the potential by increasing transmitter (possibly aspartate) release by a mechanism that is protein kinase C-dependent.
The behavior of the Lynch-Granger model for layer-II piriform cortex is reviewed, and a simple neural model with similar properties is introduced. This model allows us to understand the observed functionality of the Lynch-Granger model intuitively, and suggests which of the many biological facts introduced into the original model are relevant to this particular behavior.