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PubMed1983

Effects of delta 9-tetrahydrocannabinol on cat spinal motoneurons.

The influence of delta 9-tetrahydrocannabinol (delta 9-THC) on cat spinal motoneurons was investigated with intracellular recording techniques in order to identify possible mechanisms of action of the drug's central excitatory and depressant properties. delta 9-THC increased the amplitude of the excitatory postsynaptic potentials (EPSPs) and decreased the amplitude of the inhibitory postsynaptic potentials (IPSPs); these excitatory effects do not appear to be the result of changes in the afferent input. However, an observed increase in membrane resistance may account for, or contribute to, the enhanced EPSPs. The cannabinoid also concomitantly caused depression, as evidenced by a rise in the firing threshold for the motoneuron action potential. The responses of the motoneuron to the drug suggest synaptic sites and mechanisms of action.

Action Potentials↗
PubMed1991

Potentiation of inhibition with perforant path kindling: an NMDA-receptor dependent process.

Kindling produces a long-lasting enhancement of excitatory and inhibitory neurotransmission. Both long-term potentiation and kindling-induced potentiation of hippocampal excitatory neurotransmission are suppressed by N-methyl-D-aspartate (NMDA) receptor antagonists. These antagonists also greatly retard the development of electrical kindling. We have previously reported prolonged afterdischarges (AD) in animals stimulated in the perforant path and treated with the NMDA antagonist, dizocilpine maleate (MK-801), despite a retardation in the development of kindling. In the present study the potentiation of excitation and inhibition was assessed during perforant path kindling when NMDA channels were blocked with MK-801. Paired pulse inhibition at 8 interpulse intervals (IPI 20-1000 ms) was monitored before and during kindling development. MK-801 (1 mg/kg, i.p.) delivered 30 min prior to perforant path stimulation increased AD thresholds and delayed kindling development. Potentiation of the excitatory postsynaptic potential (EPSP) and of paired pulse inhibition measured 20-24 h after each drug administration/stimulation were suppressed in MK-801-treated animals. Paradoxically, AD durations were prolonged by MK-801. Longer AD durations could be accounted for by a higher incidence of secondary AD bouts in MK-801 relative to control animals. Development of potentiation of the early phase of paired pulse inhibition (IPI 20-30 ms) was delayed and the potentiation of the late phase of inhibition (IPIs of 200-1000 ms) was completely blocked by MK-801. Thus, some of the enhancement of inhibition seen with kindling is dependent upon NMDA neurotransmission. Suppression of this potentiated inhibition may account for prolonged focal ADs in the perforant path and dentate gyrus.

Animals↗
PubMed1995

Impairment of long-term potentiation in rats fed with vitamin E-deficient diet.

Our previous results indicate that alpha-tocopherol induces a slowly developing long-term potentiation (LTP) of excitatory postsynaptic potentials (EPSP) in hippocampal slices. In the present study on hippocampal slices obtained from rats fed with vitamin E-deficient diet for 3 months, a tetanic stimulation of the stratum radiatum or applied alpha-tocopherol phosphate failed to induce LTP of CA1 neuronal EPSPs. However, LTP could be induced in rats fed on a matching control diet. These results indicate that vitamin E-deficiency leads to an impairment in LTP induction.

Animals↗
PubMed1994

The action of synthetic cannabinoids on the induction of long-term potentiation in the rat hippocampal slice.

Incubation of rat hippocampal slices with the synthetic cannabinoid (-)-11-OH-delta 8-dimethylheptyl tetrahydrocannabinol (HU-210) (100 nM) prevented the induction of long-term potentiation of field excitatory postsynaptic potentials recorded in the CA1 region. However, in slices incubated with its non-psychoactive (+)-isomer HU-211 (100 nM), which is reported to be an NMDA receptor antagonist, high frequency stimulation evoked a long-lasting potentiation, comparable to control slices.

Animals↗
PubMed1993

Modulation of paired-pulse activation in the hippocampal dentate gyrus by cholecystokinin, baclofen and bicuculline.

Paired-pulse stimulation was used to evaluate the effects of the sulfated octapeptide of cholecystokinin (CCK8-S), the gamma-aminobutyric acidB (GABAB) agonist (-) baclofen, and the GABAA antagonist (-) bicuculline on hippocampal dentate gyrus (DG) granule cell excitability. Evoked action potentials (EAPs) and excitatory postsynaptic potentials (EPSPs) were recorded in response to orthodromic stimulation of the medial (MPP) or lateral (LPP) perforant pathway. Paired-pulse indices were determined using interpulse intervals (IPIs) across the range of 5-1000 ms. As reported by others, three phases of paired-pulse effects were revealed under control (drug-free ACSF) conditions: early paired-pulse inhibition (PPI), intermediate paired-pulse facilitation (PPF) and late PPI. With EAPs, CCK8-S enhanced only the intermediate PPF on both pathways, with no effect on the early or late PPIs. The effects of (-) baclofen were similar to CCK8-S. (-) Bicuculline attenuated the early and late PPI as well as the PPF. No differences were measured on the MPP- or LPP-evoked EPSPs in any of the drug conditions. These results indicate a similarity of CCK8-S- with GABAB-mediated modulation on neuronal activation in the DG. CCK8-S disinhibition of DG granule cells may play a role in the induction of long-lasting synaptic modifications.

Action Potentials↗
PubMed1990

Long-term potentiation in intact infant rat hippocampus.

In rats 14-28 days of age, high-frequency stimulation of the perforant path granule cell synapse in the dentate gyrus produced long-term potentiation of the population spike that was comparable in magnitude (150-250% of baseline) and duration (120 min) to that produced in adult animals with the same stimulation paradigm. In contrast, potentiation of the excitatory postsynaptic potential occurred inconsistently.

Action Potentials↗
PubMed1992

Impulse conduction in sympathetic nerve terminals in the guinea-pig vas deferens and the role of the pelvic ganglia.

Focal extracellular recording techniques were used to study nerve impulse propagation and the intermittent transmitter release mechanism in sympathetic nerve terminals of the guinea-pig vas deferens in vitro. In particular, the nature of impulse propagation in postganglionic nerve fibres was characterized following pre- or postganglionic stimulation. Conventional intracellular recording techniques were also used to study directly ganglionic transmission in cell bodies in the anterior pelvic ganglia. When brief electrical stimuli were applied to the hypogastric nerve trunk close to the prostatic end of the vas deferens, the nerve terminal impulses recorded extracellularly could be evoked either directly by stimulation of the parent axon (i.e. postganglionically) or indirectly by stimulation of the preganglionic nerve fibre. In 364 separate recordings, nerve terminal impulse conduction failure was not observed during trains of stimuli at 1 Hz. However, apparent "intermittent conduction" of nerve impulses was noted on 16 occasions. In these fibres, the degree of intermittent conduction decreased as the frequency of stimulation was increased. Conduction in these intermittent fibres was reversibly interrupted by removing calcium from the Krebs' solution or by the addition of the ganglion blocker, hexamethonium (30-100 microM). Thus, the cause of intermittent conduction is failure of the transmission of excitation in the sympathetic ganglia. Impulses evoked by postganglionic stimulation never failed to propagate into the nerve terminals, and changes in the shape or amplitude of the nerve terminal impulse during trains of stimuli were not detected. One effect of stimulation was a frequency-dependent increase in the latency of the nerve terminal impulse which developed during the train of stimuli. Thus, intermittence of transmitter release from individual varicosities cannot be attributed to failure of impulse propagation in sympathetic nerve terminals. Transmission in the anterior pelvic ganglia was investigated directly by making intracellular recordings from cell bodies whose terminals projected to the vas deferens. Many cell bodies received a strong synaptic input which generated an action potential in the postganglionic cell body on a one-to-one basis. However, in some cell bodies there was a low safety factor for the generation of the action potential by the excitatory postsynaptic potential. The safety factor for generating an action potential in the postganglionic cell body was raised by increasing the frequency of stimulation. These findings suggest that peripheral ganglia are not simple one-to-one relay stations, but may well play an important role in controlling the patterns of nerve impulse traffic in postganglionic sympathetic neurons.

Animals↗
PubMed1992

In vivo modulation of N-methyl-D-aspartate receptor-dependent long-term potentiation by the glycine modulatory site.

The role of the glycine modulatory site in N-methyl-D-aspartate receptor function was examined by determining the effect of the glycine site antagonist, 7-chlorokynurenic acid, on the induction of long-term potentiation at the commissural-CA1 synapse in anesthetized rats. Robust long-term potentiation of population excitatory postsynaptic potentials and population spike responses recorded extracellularly in the stratum pyramidale and in stratum radiatum of CA1 developed after high frequency stimulation (100 Hz for 1 s) of commissural fibers during continuous intrahippocampal administration of vehicle solution (0.15 M NaCl). In contrast, infusion of either 7-chlorokynurenic acid (400 microM) or of the N-methyl-D-aspartate receptor antagonist, D-2-amino-5-phosphonovaleric acid (100 microM), significantly attenuated or completely blocked the development of long-term potentiation. When 7-chlorokynurenic acid was infused together with the glycine analog, D-serine (1 mM), long-term potentiation developed that was comparable to that observed in control animals. Intrahippocampal administration of D-serine alone was associated with slightly greater magnitude of long-term potentiation than observed in control animals. Collectively, these findings establish that in intact hippocampus, activity at the glycine modulatory site is necessary for activation of the N-methyl-D-aspartate receptor complex. Furthermore, these results suggest that the glycine modulatory site may not be fully saturated in vivo, and thus can serve to regulate N-methyl-D-aspartate receptor function.

2-Amino-5-phosphonovalerate↗
PubMed1997

Examination of persistent effects of repeated administration of pentylenetetrazol on rat hippocampal CA1: evidence from in vitro study on hippocampal slices.

The early and long-lasting effects of pentylenetetrazol-kindling on hippocampal CA1 synaptic transmission were investigated. Experiments were carried out in the hippocampal slices from control and kindled rats at two post-kindling periods, i.e. 48-144 h (early phase) and 30-33 days (long-lasting phase). Field potentials, i.e. population excitatory postsynaptic potential (pEPSP) and population spike (PS) were recorded at the stratum pyramidale following stimulation of the stratum radiatum. Kindling-induced changes in synaptic transmission were assessed by stimulus-response functions and paired-pulse responses. The results showed that 48-144 h after kindling, the PS amplitude in the CA1 of kindled slices enhanced, and a second PS appeared compared to control slices. But at 30-33 days after kindling, the pEPSP slope in the CA1 of kindled slices enhanced without any change in the PS compared with those in the control slices. Evaluation of paired-pulse responses showed a significant reduction in paired-pulse inhibition for PS 48-144 h after kindling and a significant increase in paired-pulse inhibition for pEPSP 30-33 days after kindling. Our results suggest that pentylenetetrazol-kindling is accompanied by enhanced excitability and a reduction of paired-pulse inhibition in hippocampal CA1. The increased paired-pulse inhibition one month after kindling, may be interpreted as an adaptive process to cope with subsequent seizures.

Analysis of Variance↗
PubMed1999

Calexcitin transformation of GABAergic synapses: from excitation filter to amplifier.

Encoding an experience into a lasting memory is thought to involve an altered operation of relevant synapses and a variety of other subcellular processes, including changed activity of specific proteins. Here, we report direct evidence that co-applying (associating) membrane depolarization of rat hippocampal CA1 pyramidal cells with intracellular microinjections of calexcitin (CE), a memory-related signaling protein, induces a long-term transformation of inhibitory postsynaptic potentials from basket interneurons (BAS) into excitatory postsynaptic potentials. This synaptic transformation changes the function of the synaptic inputs from excitation filter to amplifier, is accompanied by a shift of the reversal potential of BAS-CA1 postsynaptic potentials, and is blocked by inhibiting carbonic anhydrase or antagonizing ryanodine receptors. Effects in the opposite direction are produced when anti-CE antibody is introduced into the cells, whereas heat-inactivated CE and antibodies are ineffective. These data suggest that CE is actively involved in shaping BAS-CA1 synaptic plasticity and controlling information processing through the hippocampal networks.

Animals↗
PubMed2004

Effect of static magnetic fields on the amplitude of action potential in the lateral giant neuron of crayfish.

PURPOSE: To investigate whether exposure to static magnetic field (SMF) affects the passive properties of neurons that mediate tail-flip escape behavior in crayfish. MATERIALS AND METHODS: A permanent magnet was placed under the isolated nerve cord of crayfish to experience SMF at 4.74 to 43.45 mT intensity for various period of time (20 seconds to 3 hours). An intracellular electrode was impaled on the axon of the lateral giant neuron (LG) of the last abdominal ganglion of crayfish to record the evoked action potential (AP) and excitatory postsynaptic potential (EPSP). The amplitudes of evoked AP and EPSPs before and after SMF exposure were measured to study the effect of SMF exposure. RESULTS: The exposure to SMF increased the amplitude of AP in the LG depending upon both the intensity of field and duration of field exposure. The changes in AP by field exposure are likely to be mediated by the increasing level of intracellular Ca2+ in the LG because the chelating of intracellular Ca2+ would block the effects by SMF exposure, while the injection of Ca2+ into the LG could mimic the effects of SMF exposure. SMF exposure also increases the input resistance of the LG membrane. Therefore, the magnitude of the EPSP in LG evoked by electrical shock on the sensory nerves was found to be enhanced after SMF exposure. CONCLUSION: SMF is usually considered to be safe for the biological issues since no electrical current is induced via the Faraday effect. Our results showed that some passive membrane properties of neurons are affected by SMF exposure. The increase in magnitude of evoked AP and EPSP suggests an increase in the sensitivity of the LG neuron. These changes by SMF exposure may not necessarily to be harmful to animals; however, further study is needed to address the biological effects from SMF exposure, especially in nervous systems.

Action Potentials↗
PubMed1996

Effects of the uncompetitive NMDA receptor antagonist memantine on hippocampal long-term potentiation, short-term exploratory modulation and spatial memory in awake, freely moving rats.

Chronic treatment of adult male F-344 rats (9-12 months old) with therapeutically relevant doses of memantine (30 mg/kg/day in chow for > 8 weeks) increased the maintenance of long-term potentiation of field excitatory postsynaptic potentials from perforant path-granule cell hippocampal synapses recorded in the fascia dentata in vivo. In contrast, there was no effect of memantine on baseline synaptic responses or population spikes. Likewise, short-term exploratory modulation of these hippocampal evoked responses was not different between memantine-treated and control rats. Both groups of rats were able to learn the spatial version of the Morris water task equally well, but the memantine-treated group showed a strong tendency to show more selective spatial search patterns in the training quadrant of the water pool during a final probe trial. As such, these studies provide the first electrophysiological evidence that memantine can increase the durability of synaptic plasticity and provide preclinical confirmation of the cognitive improvement seen with memantine in the treatment of demented patients.

Animals↗
PubMed1972

Analysis of the mechanism of action of some ganglion-blocking drugs in the rabbit superior cervical ganglion.

1. Mechanisms of action of hexamethonium, mecamylamine and (+)-tubocurarine on the rabbit superior cervical ganglion were investigated by intracellular recording techniques.2. In concentrations up to 1 mM, none of these drugs affected the resting membrane potential nor altered the excitability of the postganglionic neurone to direct or antidromic stimulation.3. Post-tetanic potentiation of the excitatory postsynaptic potential (e.p.s.p.) was inhibited by mecamylamine (10-100 muM) but not affected by either hexamethonium (5-100 muM) or (+)-tubocurarine (10-50 muM).4. The decline in amplitude of successive e.p.s.ps in a train (40 Hz) was not influenced by hexamethonium or (+)-tubocurarine but was greatly exaggerated in the presence of mecamylamine; desensitization of the receptors for acetylcholine was excluded as a possible explanation for this latter finding.5. Mecamylamine depressed the quantal content of e.p.s.ps in a train, with the exception of the first e.p.s.p. which had an increased quantal content.6. Reduction in quantal content was attributed to a substantial fall in the size of the store of quanta of transmitter immediately available for release and to a reduction in the rate of mobilization of acetylcholine into that store; mecamylamine also caused a simultaneous increase in the fractional release.7. Hexamethonium and (+)-tubocurarine had no effect on transmitter release.8. The time-course of presynaptic effects of mecamylamine was similar to the duration of its postsynaptic blocking action.9. It is concluded that inhibition of ganglionic transmission by mecamylamine is due to both presynaptic and postsynaptic inhibitory actions; in contrast, hexamethonium and (+)-tubocurarine reduce transmission solely by their postsynaptic actions.

Animals↗
PubMed2005

An inverse agonist selective for alpha5 subunit-containing GABAA receptors enhances cognition.

Alpha5IA is a compound that binds with equivalent subnanomolar affinity to the benzodiazepine (BZ) site of GABA(A) receptors containing an alpha1, alpha2, alpha3, or alpha5 subunit but has inverse agonist efficacy selective for the alpha5 subtype. As a consequence, the in vitro and in vivo effects of this compound are mediated primarily via GABA(A) receptors containing an alpha5 subunit. In a mouse hippocampal slice model, alpha5IA significantly enhanced the burst-induced long-term potentiation of the excitatory postsynaptic potential in the CA1 region but did not cause an increase in the paroxysmal burst discharges that are characteristic of convulsant and proconvulsant drugs. These in vitro data suggesting that alpha5IA may enhance cognition without being proconvulsant were confirmed in in vivo rodent models. Hence, alpha5IA significantly enhanced performance in a rat hippocampal-dependent test of learning and memory, the delayed-matching-to-position version of the Morris water maze, with a minimum effective oral dose of 0.3 mg/kg, which corresponded to a BZ site occupancy of 25%. However, in mice alpha5IA was not convulsant in its own right nor did it potentiate the effects of pentylenetetrazole acutely or produce kindling upon chronic dosing even at doses producing greater than 90% occupancy. Finally, alpha5IA was not anxiogenic-like in the rat elevated plus maze nor did it impair performance in the mouse rotarod assay. Together, these data suggest that the GABA(A) alpha5-subtype provides a novel target for the development of selective inverse agonists with utility in the treatment of disorders associated with a cognitive deficit.

Animals↗
PubMed1983

Integration of biphasic synaptic input by electrotonically coupled neuroendocrine caudodorsal cells in the pond snail.

The ovulation hormone-producing caudodorsal cells (CDCs) of the pond snail Lymnaea stagnalis form two clusters of electrotonically coupled cells, each containing a few specialized (ventral) cells that connect the clusters. The hormone is secreted during a pacemaker-driven discharge. The CDCs receive a biphasic cholinergic postsynaptic potential (PSP), consisting of a rapid excitatory postsynaptic potential (EPSP) and a slow inhibitory postsynaptic potential (IPSP) that is elicited by stimulation of nerves. The effect of the synaptic input on the discharge of the CDCs is described and the location of the synapse investigated by a combination of electrophysiological recordings and morphological techniques. The PSP interrupts the discharge and hastens its termination. In addition, it causes a reversal of the temporal order of the spikes of ventral cells (that normally lead) and dorsal cells (that lead only after the PSP). Ion-substitution experiments indicate that the ionic mechanism underlying the biphasic PSP is conventional, involving a conductance increase for Na+ (EPSP) and K+ (IPSP). Receptors mediating the inhibitory component occur only on the proximal axons of the ventral cells, both components are larger and reverse more readily in ventral cells. These findings suggest that the PSP is generated in the ventral cells. The biphasic PSP has no effect on electrical coupling, suggesting that it is not generated along the electrical pathways among the cells. Horseradish peroxidase (HRP) staining reveals that the lateral branches emerge from the proximal axons of the ventral cells only. In HRP-filled preparations processed for electron microscopy (EM) acetylcholinesterase is demonstrated at these branches where it occurs associated with synapses. The location on fine branches of the ventral cells explains the absence of an effect on electrotonic transmission, whereas the reluctance of components of the PSP to reverse at the expected potentials is due to the distribution of the synapses over more than one cell. It is concluded that the biphasic PSP is received only by the ventral cells and that it is conveyed electrotonically to the other cells.

Acetylcholinesterase↗
PubMed1983

Rat hippocampal neurons in culture: responses to electrical and chemical stimuli.

Intracellular activity was recorded from dissociated rat hippocampal neurons maintained in tissue culture conditions for 4-6 wk. The cells developed dense interconnections and had typical morphological characteristics similar to hippocampal neurons in situ. The recorded neurons possessed similar electrophysiological properties to those observed in situ or in a slice preparation. Their input resistance (42 M omega), resting membrane potential (-60 mV), membrane time constant (16.2 ms), total electrotonic length (0.92), and spike size (68.3 mV) were similar to values obtained in hippocampal cells in a slice. The connections among adjacent neurons were largely inhibitory. The inhibitory postsynaptic potentials (IPSPs) had longer durations than excitatory postsynaptic potentials (EPSPs) when these were detected. Synaptic delay varied between 0.3 and 3.0 ms. There were no electrotonic connections among neurons. Reciprocal connections were common. Most neurons reacted to acetylcholine (ACh) by an increase in frequency of spontaneous EPSPs, action-potential discharges, and IPSPs. Concurrently, there was a marked reduction in the magnitude of the evoked PSPs tested in pairs of cells. This effect is probably presynaptic to the recorded neurons. A statistical analysis of quantal properties of the synaptic interactions among neurons revealed that ACh causes a reduction of magnitude of PSPs by reducing the number of releasing elements (m). This effect is different from the reduction of evoked PSPs caused by postsynaptic depolarization.

Acetylcholine↗
PubMed1988

Characterization of synaptically mediated fast and slow inhibitory processes in piriform cortex in an in vitro slice preparation.

1. Intracellular recordings were obtained from anatomically verified layer II pyramidal cells in slices from rat piriform cortex cut perpendicular to the surface. 2. Responses to afferent and association fiber stimulation at resting membrane potential consisted of a depolarizing potential followed by a late hyperpolarizing potential (LHP). Membrane polarization by current injection revealed two components in the depolarizing potential: an initial excitatory postsynaptic potential (EPSP) followed at brief latency by an inhibitory postsynaptic potential (IPSP) that inverted with membrane depolarization and truncated the duration of the EPSP. 3. The early IPSP displayed the following characteristics suggesting mediation by gamma-aminobutyric acid (GABA) receptors linked to Cl- channels: associated conductance increase, sensitivity to increases in internal Cl- concentration, blockage by picrotoxin and bicuculline, and potentiation by pentobarbital sodium. The reversal potential was in the depolarizing direction with respect to resting membrane potential so that the inhibitory effect was exclusively via current shunting. 4. The LHP had an associated conductance increase and a reversal potential of -90 mV in normal bathing medium that shifted according to Nernst predictions for a K+ potential with changes in external K+ over the range 4.5-8 mM indicating mediation by the opening of K+ channels and ruling out an electrogenic pump origin. 5. Lack of effect of bath-applied 8-bromoadenosine 3',5'-cyclic monophosphate (8-Br-cAMP) or internally applied ethylene glycol-bis(beta-aminoethyl ether)-N,N,N',N'-tetraacetic acid (EGTA) on the LHP and failure of high amplitude, direct membrane depolarization to evoke a comparable potential, argue against endogenous mediation of the LHP by a Ca2+ activated K+ conductance [gK(Ca)]. However, an apparent endogenously mediated gK(Ca) with a duration much greater than the LHP was observed in a low percent of layer II pyramidal cells. Lack of effect of 8-Br-cAMP also indicates a lack of dependence of the LHP on cAMP. 6. Other characteristics of the LHP that were demonstrated include: a lack of blockage by GABAA receptor antagonists, a probable voltage sensitivity (decrease in amplitude in the depolarizing direction), and an apparent brief onset latency (less than 10 ms) when the early IPSP was blocked by picrotoxin. The LHP was unaffected by pentobarbital sodium when the early IPSP was blocked by picrotoxin. 7. Both the LHP and early IPSP were blocked by low Ca2+/high Mg2+, consistent with disynaptic mediation.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1992

Dendritic origin of late events in optical recordings from salamander olfactory bulb.

1. Optical recordings of membrane-potential changes were used to characterize the origin and properties of the electrical signals from the dendritic level in slices of the salamander olfactory bulb. 2. The optical events were correlated with field-potential waves recorded simultaneously. Both responses exhibited patterns similar to those found in other species. 3. Orthodromic stimulation evoked a compound action potential in the olfactory nerve fibers, followed by two additional principal waves (N1 and N2). These field-potential waves reflected excitatory postsynaptic potentials at the primary mitral/tufted and granule cell dendrites, respectively. 4. Extrinsic optical signals from horizontal slices stained with the pyrazo-oxonal dye RH-155 showed a characteristic sequence of depolarizing and hyperpolarizing events. All of the signals exhibited a wavelength dependence expected for this dye and were abolished in the presence of high K+ in the bath. 5. According to their time courses, depolarizing responses under normal recording conditions were divided into two components, fast and slow. Orthodromic stimuli evoked a fast presynaptic response that represents synchronous compound action potentials from olfactory nerve fibers. At subglomerular levels, additional fast responses could often be recorded at the peri/subglomerular level and in the mitral/tufted somata region. These postsynaptic responses partially coincided with the rising phase of a different depolarizing signal, a slow component characterized by its prolonged time course. 6. With orthodromic stimulation, this slow signal attained its largest amplitude in the zone between the glomeruli and the superficial part of the external plexiform layer (EPL). Antidromic stimuli evoked a signal with some similarities to the one evoked orthodromically, but originating in deeper EPL regions. 7. Slow components were characterized by their Ca dependence. Low Ca2+ medium, or calcium channel blockers, suppressed this optical component, whether evoked orthodromically, antidromically, or by direct stimulation. In addition, Ba2+ (2.5-3.6 mM) in the bath did not abolish these responses, suggesting that they do not reflect a glial depolarization in response to elevated extracellular K+ concentration ([K+]o). 8. Locally applied stimuli next to the glomerular layer elicited these signals in 5-10 microM tetrodotoxin (TTX) or in low extracellular Na+ concentration ([Na+]o) medium, but antidromic or orthodromic stimuli failed to evoke the response under these conditions. The sizes of the responses to local stimuli remained constant, but an increase in their duration was observed in either TTX or low [Na+]o. 9. gamma-Aminobutyric acid (GABA) and baclofen reduced the size of the slow components in a dose-dependent manner.(ABSTRACT TRUNCATED AT 400 WORDS)

Action Potentials↗