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Identifying geochemical paleo‐proxies of vegetation type in watersheds could become a powerful tool for paleoecological studies of ecosystem dynamics, particularly when commonly used proxies, such as pollen grains, are not suitable. In order to identify new paleological proxies to distinguish ecosystem types in lake records, we investigated the differences in the sediment geochemistry of lakes surrounded by two boreal forest ecosystems dominated by the same tree species: closed‐canopy black spruce‐moss forests (MF) and open‐canopy black spruce‐lichen woodlands (LW). This study was designed as a first calibration step between terrestrial modern soils and lacustrine sediments (0–1000 cal yr BP) on six lake watersheds. In a previous study, differences in the physical and geochemical properties of forest soils had been observed between these two modern ecosystems. Here we show that the geochemical properties of the sediments varied between the six lakes studied. While we did not identify geochemical indicators that could solely distinguish both ecosystem types in modern sediments, we observed intriguing differences in concentrations of C:N ratio, carbon isotopic ratio, and aluminum oxide species, and in the stabilization of their geochemical properties with depth. The C accumulation rates at millennial scale were significantly higher in MF watersheds than in LW watersheds. We suggest that these variations could result from organic matter inflows that fluctuate depending on forest density and ground vegetation cover. Further investigations on these highlighted geochemistry markers need to be performed to confirm whether they can be used to detect shifts in vegetation conditions that have occurred in the past. Lake sediments of closed‐canopy moss forest and open‐canopy lichen woodland watersheds showed different geochemical propertiesOrganic matter accumulation in lake sediments at long‐time scales depend on the tree density of the forests surrounding the watershedGeochemical proxies could be useful to detect changes in ecosystem structure over time

While post‐harvest residue (“slash”) is increasingly viewed as a source of biofuel, few studies have considered the potential ecological impact of the spatial distribution of forest harvest residue. We hypothesized that slash piles create islands of high soil fertility and light, leading to greater abundance, growth, and reproduction of plants. In 6‐yr‐old intensively managed hybrid poplar (Populus balsamiferaL. × P. maximowicziiA. Henry) plantations, we showed that soluble organic N, NO3–N, NH4–N, and P decreased as a negative exponential function with distance from the pile. Pin cherry (Prunus pensylvanicaL. f.) relative growth rate was fastest near piles in the first few years after harvest. We found significantly greater stem size, flowers per plant, and foliar P near piles for cherry, and this inverse gradient sharpened in a 16‐yr‐old white spruce [Picea glauca(Moench) Voss] plantation. For the two other flowering species, strawberry (Fragaria virginianaMill.) and raspberry (Rubus idaeusL.), flower and fruit abundance were also significantly and strongly negatively correlated with distance to the pile. Further, directly correlating soil nutrient availability with plant traits, we found significant positive relationships between plant growth, reproductive output, and N availability. Partial correlation analysis indicated that more of the variance in plant traits was explained by distance than by soil nutrition. We conclude that in industrial forests, piles replace canopy gaps as sites where understory plant species can episodically reproduce and are therefore important for many plant species as well as the pollinators and frugivores dependent on them.

The effects of harvesting and slash treatments on soil nutrient dynamics were assessed in boreal aspen stands growing on mesic clayey sites. Stem‐only harvested stands were compared with unharvested controls according to a complete block design with three replications. Within harvested areas, four slash treatments (stem‐only harvesting [SOH], whole‐tree harvesting [WHT], wood chip application, and slash burns) were compared. Treatments created a gradient of slash that ranged from 52.3 Mg ha−1in stem‐only to 13.8 Mg ha−1in control stands. The amount of slash had no effect on wood decomposition rates but was strongly associated with higher forest floor organic C, Kjeldahl N and base cation concentrations (Caeand Mge), base saturation, pH, and effective cation exchange capacity (CEC) and lower microbial C/N when control stands were compared with stem‐only harvested stands. Slash burn severity was too low to significantly reduce slash loads and induce base cation release but severe enough to reduce forest floor microbial C and N concentrations (−48 and −55%, respectively) for at least one complete growing season. Slash burn also induced increases in forest floor available P (54%) concentration compared with other slash treatments. Chipping reduced forest floor microbial N concentration by 25% and increased microbial C/N by 28% but had no impact on nutrient availability. Differences between WTH and SOH were linked to the abundance of slash. Finally, the results illustrate that whatever the treatment, the amount of slash left on the ground is the main factor found to affect soil microbial community characteristics and soil nutrient availability.

In classical fear conditioning, a neutral sensory stimulus (CS) acquires the ability to elicit fear responses after pairing to a noxious unconditioned stimulus (US). As amygdala lesions prevent the acquisition of fear responses and the lateral amygdaloid (LA) nucleus is the main input station of the amygdala for auditory afferents, the effect of auditory fear conditioning on the sensory responsiveness of LA neurons has been examined. Although conditioning was shown to increase CS-evoked LA responses, the specificity of the changes in responsiveness was not tested. Because conditioning might induce nonspecific increases in LA responses to auditory afferents, we re-examined this issue in conscious, head-restrained cats using a differential conditioning paradigm where only one of two tones (CS(+) but not CS(-)) was paired to the US. Differential conditioning increased unit and field responses to the CS(+), whereas responses to the CS(-) decreased. Such changes have never been observed in the amygdala except in cases where the CS(-) had been paired to the US before and fear responses not extinguished. This suggests that fear conditioning is not only accompanied by potentiation of amygdalopetal pathways conveying the CS(+) but also by the depression of sensory inputs unpaired to noxious stimuli.

Summary: Several experimental results indicate that the peribrachial (PB) cholinergic area of the pedunculopontine nucleus is the final relay for the transfer of brainstem-generated pontogeniculo-occipital (PGO) waves to the thalamus. However, the mechanisms underlying the PGO-related activity of PB neurons remain unknown. In order to study these mechanisms, single unit recordings in the PB area were performed in reserpinized cats. Because PGO waves are closely related to rapid eye movements, our microelectrode explorations were also aimed to some structures of the preoculomotor network, namely, the superior colliculus (SC) and parts of the central tegmental field (FTC). We have found several classes of PGO-on cells in the PB area, most of them descharging 80 ms or less before the peak of PGO waves. These cell-classes comprised high-frequency bursting cells, slow-frequency bursting cells, and neurons discharging single spikes or doublets. Intracellular recordings showed that PGO-on single spikes arise from conventional excitatory postsynaptic potentials. Among PGO-related cells in structures outside the PB limits, it was found that most SC cells discharge during or after the PGO, whereas FTC cells increase their discharge rate several hundreds of ms before PGO waves, thus indicating that PGO waves are elaborated long before the activition of PB neurons. Massive retrograde labeling was found in FTC following horseradish peroxidase injections into the PB area. We suggest that long-lead FTC neurons provide an excitatory input to PGO-on PB neurons.

In contrast with most dorsal thalamic nuclei, the anterior thalamic (AT) complex is devoid of input from the reticular (RE) thalamic nucleus. Instead, it is interposed in a limbic circuit linking the mammillary bodies (MB) to various allo- and periallocortical fields. To investigate the electrophysiological consequences of this peculiar pattern of connectivity, a sample of 92 AT cells, physiologically identified by their short-latency response to MB stimulation, was recorded in chronically-implanted animals and compared to a group of rostral intralaminar centralis-paracentralis (CL-PC) thalamic neurons receiving a dense innervation from the RE nucleus. Numerous similarities were found between the state-related fluctuations in spontaneous and evoked activities of AT and CL-PC neurons. For instance, both types of cells displayed stereotyped, high-frequency (250–300 Hz) bursts of 2–4 spikes in S and a more tonic discharge pattern in W and D. However, the high-frequency bursts of the S state occurred randomly in AT cells, whereas in CL-PC neurons they appeared rhythmically in clusters closely related to spindle waves. In addition, we found that a period of decreased responsiveness consistently followed the ortho- or antidromic activation of AT an CL-PC cells. This inhibitory period lasted less than 80 ms in AT cells and contrasted with the much longer (?120ms) period of decreased excitability observed in CL-PC neurons during S. We suggest that these differences reflect the lack of RE input to the AT group. Since the AT complex is, through the MB, intimately linked to the hippocampal formation, it was expected that such prominent hippocampal activities as the theta rhythm would be channeled to the AT nuclei. Surprisingly, no theta-related modulation of neuronal activity was observed in identified AT cells during D epochs. This finding suggests that dramatic transformations are made on the signals emitted by the hippocampal formation somewhere along the pathway linking the hippocampal formation to the AT complex.

Summary: The projections of cholinergic and noncholinergic neurons of the rostral brainstem reticular formation to the visual thalamic nuclei (dorsal lateral geniculate — LG, lateral posterior — LP, and perigeniculate — PG) were studied in cat by using the retrograde transport of horseradish peroxidase conjugated with wheat germ agglutinin (WGA-HRP) combined with choline acetyltransferase (ChAT) immunohistochemistry. After thalamic injections, less than 10% of all retrogradely labeled neurons in the upper brainstem reticular core were located at most rostral (perirubral) levels where there are virtually no cholinergic elements. Approximately 75–80% of all HRP-positive neurons in the reticular formation were found between stereotaxic planes anterior 1 and posterior 2, in the peribrachial (PB) area of the pedunculopontine nucleus and in the laterodorsal tegmental (LDT) nucleus. The brainstem afferents to LG and PG thalamic nuclei essentially derive from PB neurons, with a small contribution from LDT cells, whereas the LP thalamic nucleus receives massive inputs from both PB and LDT brainstem nuclei. Of all HRP-positive elements visualized in the PB nucleus after an LG or a PG injection, 87% and 73%, respectively, were also ChAT-positive. Of all HRP-positive elements in the PB and LDT nuclei after an LP injection, 82% and 92%, respectively, were also ChAT-positive. The numbers of labeled neurons in the contralateral brainstem reticular nuclei reach 30% to 50% of the numbers found in the ipsilateral reticular formation. These findings reveal the existence of a prominent cholinergic projection from the brainstem reticular formation to the visual thalamic nuclei. Such a chemospecific projection is probably involved in phasic and tonic events of activated behavioral states.

1. To characterize the physiological properties of lateral and basolateral (BL) amygdaloid neurons, intracellular recordings were performed in barbiturate-anesthetized cats. Morphological identification of recorded cells was achieved by intracellular injection of neurobiotin. Two types of physiologically identified projection neurons were distinguished in the BL and lateral nuclei. 2. The first type of neurons prevailed in the BL nucleus (80% of BL cells). Their resting membrane potential (Vm) averaged -66 +/- 4.9 (SE) mV. They generated stereotyped spike doublets or bursts in response to threshold depolarizing pulses. In most cells, depolarizing pulses of higher amplitude elicited spike bursts or doublets at a shorter latency followed by a nonadapting train of single spikes whose frequency rose with the amplitude of the current pulses. However, 15% of BL bursting neurons generated repetitive spike bursts or doublets in response to prolonged depolarizing current pulses. The response of BL bursting neurons to hyperpolarizing current pulses revealed the presence of slow inward rectification in the form of a depolarizing sag, thus suggesting the presence of a hyperpolarization-activated current. 3. The second type of neurons prevailed in the lateral nucleus. Their resting Vm was quite polarized (-74 +/- 2.85 mV) and they generated slow Vm oscillations (2-10 Hz) upon steady depolarization beyond congruent to -62 mV. The frequency of the oscillation increased with the amount of depolarizing current. In the majority of cells, analysis of voltage responses to subthreshold current pulses revealed the presence of voltage- and time-dependent rectification in the depolarizing direction. Current pulses that brought the Vm to -65 mV and beyond elicited a voltage response that reached an early peak and then decayed. Increasing the amplitude of the pulse decreased the latency of the early peak until it triggered an action potential. Current-voltage plots demonstrated inward rectification in the depolarizing direction. At the break of hyperpolarizing current pulses applied at depolarized levels, the Vm overshot prepulse values and generated one or more oscillatory cycles. 4. An important proportion of bursting and oscillating neurons (45.8% and 29%, respectively) were physiologically identified as projection neurons by antidromic invasion from the basal forebrain, entorhinal cortex, or perirhinal cortex. The conduction velocity of bursting and oscillating neurons estimated from the latency of antidromic spikes was low (< or = 2.5 m/s). 5. Most bursting and oscillating neurons of the BL nucleus were spiny cells with a pyramidal morphology. Four to eight dendritic trunks emerged from the apex, base, and sides of their triangular soma.(ABSTRACT TRUNCATED AT 400 WORDS)

1. Amygdala neurons were recorded extracellularly during the sleep-waking cycle in chronically implanted cats. Neurons were identified as projection cells when they could be antidromically invaded from the perirhinal and/or entorhinal cortices. 2. In contrast with other nuclei of the amygdala, few spontaneously active neurons were encountered in the lateral nucleus. However, when hunting stimuli were applied to the parahippocampal cortices, we noticed the presence of numerous projection cells that would have otherwise remained undetected because they had little or no spontaneous activity. 3. In the states of waking, slow-wave sleep, and paradoxical sleep, the discharge rate of antidromically invaded neurons averaged 0.09 +/- 0.07 Hz (mean +/- SE) with 82% of cells firing at < 0.01 Hz in all states. However, they transiently increased their firing rate when cats were presented complex sensory stimuli, which apparently were specific to each cell. In contrast to projection cells, spontaneously active neurons of the lateral nucleus that could not be backfired from the parahippocampal cortices had an average firing rate of 4.34 +/- 1.15 Hz with 38% of cells firing at > or = 6 Hz in at least one state. 4. These results on the extremely low firing rates of identified projection cells suggest that previous extracellular studies of lateral amygdaloid neurons were biased toward a class of spontaneously active cells which probably includes local-circuit cells.

Foliar analysis of maple sugar (Acer saccharumMarsh.) saplings having low foliar K (5.4 g kg−1) and P (1.2 g kg−1) was carried out for 3 yr to investigate the effects of a single application of fertilizer P triple superphosphate [TSP], K (K2SO4) and Ca [Ca(OH)2]. Also, soll, water‐saturated soil extract, resin sacks buried in situ, and lysimeter solution analysis methods were used. Potassium and P additions significantly increased foliar K (1.81 g kg−1increase) and P (0.25 g kg−1increase) for the 3 yr that the observations were conducted. Calcium addition had no effect on foliar element concentrations. A Diagnosis and Recommendation Integrated System (DRIS) analysis corroborated the foliar analysis: K indices increased with increased K fertilization (from −47 to ‐23) and P indices increased with increased P fertilization (from ‐25 to −15). Calcium application significantly increased the effective cation‐exchange capacity (CEC), exchangeable Ca and Mg and water‐extractable Ca and decreased the acidity in the rooting zone for a 3‐yr period. Conventional soil analysis and resin sacks detected significant effects of P and K fertilizers on their respective elements. However, these effects did not last more than 2 yr after fertilizer application in the surface soil horizon (Ah). Lysimeter solution analysis showed that K2SO4fertilizer caused short‐term increases in SO4and Ca leaching. The duration of fertilizer P and K on foliar nutrition and the behavior of soil nutrients suggested that biochemical cycles are important mechanisms perpetuating fertilizer effects.

This study tested the hypothesis that neurons of thalamic nuclei, which are normally devoid of inputs from the reticular thalamic nucleus, do not display spindle oscillations and related rhythmic spike bursts. This proposal derived from our recent studies indicating that the reticular nucleus is the generator of spindling rhythmicity. We used retrograde tracing methods, intracellular recordings in barbiturized cats, and extracellular recordings of single neurons and field potentials in anteroventral (AV), anteromedial (AM), ventroanterior (VA), ventrolateral (VL), and central lateral (CL) thalamic nuclei in cats with rostral brain stem transections (cerveau isolé preparations), before and after administration of barbiturates. The observation that AV and AM nuclei do not receive inputs from the reticular nucleus was confirmed by using injections of horseradish peroxidase conjugated to wheat germ agglutinin confined within the limits of anterior nuclei. Such injections led to massive retrograde labeling in mammillary nuclei and layer VI of the retrosplenial cortex but left free of labeling the neurons of the reticular thalamic nucleus. Intracellular recordings showed that AV-AM neurons discharge tonically in response to a depolarizing current applied at rest, whereas they give rise to a slow spike that underlies a burst of fast action potentials when the membrane is hyperpolarized by 5-12 mV. Despite the fact that they share similar properties with other thalamic neurons, intracellularly recorded AV-AM neurons do not exhibit spindle waves under barbiturate anesthesia, whereas VA-VL, CL, and other thalamocortical neurons that receive afferents from the reticular nucleus commonly display such oscillations. With extracellular recordings performed simultaneously in CL and AV or AM nuclei of the unanesthetized cerveau isolé preparation, focal spindle oscillations and related rhythmic high-frequency spike bursts of single CL cells contrasted with absence of spindles and spike bursts in AV or AM neurons. Spindling could be induced in AV-AM nuclei only after administration of barbiturates at doses exceeding 3 mg/kg, and it appeared approximately 35-40 s after the barbiturate effect was detected in the simultaneously recorded CL nucleus. Moreover, the spike bursts that were elicited in AV-AM neurons after barbiturate administration were not temporally related with focal spindles. Since spindle oscillations did not appear intracellularly in AV-AM neurons, the possibility was envisaged that barbiturate-induced spindles were the passive reflection of field potentials actively generated in neighboring thalamic nuclei.(ABSTRACT TRUNCATED AT 400 WORDS)

1. The responses of thalamocortical neurons to stimulation of mesopontine [peribrachial (PB) and laterodorsal (LDT)] cholinergic nuclei were studied intracellularly in urethan-anesthetized cats. Neurons recorded from anterior thalamic (AT), ventroanterior-ventrolateral (VA-VL) and rostral intralaminar centrolateral (CL) nuclei were physiologically identified by their orthodromic responses to prethalamic stimulation and/or antidromic activation from the cerebral cortex. 2. Besides early excitatory and inhibitory postsynaptic potentials (EPSPs and IPSPs) that were not sensitive to cholinergic antagonists, two types of cholinergic responses were elicited by PB/LDT stimulation: a short-lasting and a late, long-lasting depolarization. All these components survived monoamine depletion by reserpine. 3. The latency of the short-lasting depolarizing response was 147.4 +/- 27.3 (SE) ms. The response lasted for 1.3 +/- 0.1 s and had a peak amplitude of 4.2 +/- 0.3 mV. This component was associated with 10-30% increase in membrane conductance and was abolished by systemic administration of the nicotinic antagonist mecamylamine. 4. The long-lasting depolarizing response had a latency of 1.2 +/- 0.1 s, a duration of 20.8 +/- 2.2 s, and a peak amplitude of 5.4 +/- 0.4 mV. Similar values were found in decorticated animals. The duration and amplitude of the late depolarizing component were dependent on stimulation parameters and membrane potential. This response increased under depolarizing current, decreased and eventually disappeared under hyperpolarizing current, and was associated on average with 40% increase in apparent input resistance. After systemic administration of the muscarinic antagonist scopolamine, the long-lasting depolarization disappeared; the surviving short-lasting depolarization was subsequently abolished by mecamylamine. 5. The prolonged depolarizing response of thalamocortical neurons to mesopontine cholinergic stimulation was accompanied by a desynchronization of the electroencephalogram (EEG). These two phenomena had a similar time course. Stimulation of deep cerebellar nuclei, whose axons traverse the PB area, did not induce a long-lasting depolarization of target thalamic cells, nor an EEG desynchronization. 6. These data demonstrate that, in addition to an initial nicotinic excitation, brain stem cholinergic stimulation elicits a late, long-lasting muscarinic depolarization of thalamocortical neurons. We suggest that the prolonged depolarization plays an important role in cortical activation.

1. These experiments were carried out to study how thalamic interneurons generate inhibitory postsynaptic potentials (IPSPs) in relay cells. Intracellular recordings were performed in the anterior thalamic (AT) nuclei, a nuclear group in which interneurons constitute the only intrathalamic source of gamma-aminobutyric acid (GABA). 2. In the AT complex, as in most dorsal thalamic nuclei, interneurons can influence relay cells through their presynaptic dendrites (PSDs) and their axons. This dual mode of action is paralleled by a different termination pattern of prethalamic fibers and cortical axons on interneurons. Prethalamic fibers, which in the AT nuclei arise in the mammillary bodies (MBs), end mostly on PSDs, whereas cortical terminals usually synapse on the parent dendrites of PSDs. We therefore took advantage of the differential mode of termination of cortical and MB afferents on interneurons to infer the respective roles of the axons and PSDs of interneurons in the genesis of the IPSPs recorded from relay cells. 3. In all responsive AT cells, cortical stimuli delivered at low frequency (less than or equal to 0.5 Hz) evoked a biphasic IPSP, with an early and a late phase, having a total duration of 221.96 +/- 8.18 ms (mean +/- SE). The early part of the IPSP (termed A) had a reversal potential (ER) close to the equilibrium potential for Cl- ions: -79.25 +/- 2.14 mV. Furthermore, it reversed in polarity after impalement of the cells with KCl-filled pipettes. The late IPSP (termed B) always began before the end of the early IPSP, 45.93 +/- 2.50 ms after the onset of the A-IPSP. The B-IPSP had an ER of -109 +/- 2.4 mV and was not affected by Cl- injection. 4. By contrast, MB stimuli delivered at low frequency (less than or equal to 0.5 Hz) evoked a triphasic IPSP having a total duration of 220.5 +/- 9.42 ms in most (61.2%) AT cells. The IPSP with the shortest latency (termed a) was evoked only by MB stimuli. Before the return of the membrane potential to the resting level, a second hyperpolarizing potential began (7.41 +/- 0.46 ms after the onset of the a-IPSP). This second inhibitory phase was biphasic and had electrophysiological characteristics similar to the biphasic A- and B-IPSP evoked by cortical stimulation. Both the MB-evoked a- and A-IPSPs had an ER close to the equilibrium potential for Cl- ions (-72.22 +/- 0.68 and -72 +/- 0.82 mV, respectively) and reversed in polarity after impalement of the cells with KCl-filled pipettes.(ABSTRACT TRUNCATED AT 400 WORDS)

Previous investigations in various motor and sensory cortical areas have shown that fast oscillations (20-80 Hz) of focal electroencephalogram and multiunit activities occur spontaneously during increased alertness or are dependent upon optimal sensory stimuli. We now report the presence of 20- to 40-Hz rhythmic activities in intracellularly recorded thalamocortical cells of the cat. In some neurons, subthreshold oscillations were triggered by depolarizing pulses and eventually gave rise to action potentials. In other neurons, the oscillations consisted of fast prepotentials, occasionally generating full spikes that arose from the resting or even from hyperpolarized membrane potential levels, and leading to trains of spikes at more depolarized levels. The rhythmic nature of these fast prepotentials was confirmed by means of an autocorrelation study, which demonstrated clear peaks at 25-ms intervals (40 Hz). In view of the recent evidence that mesopontine cholinergic nuclei trigger and maintain activation processes in thalamocortical systems, we tested the possibility that stimulation of these brainstem nuclei potentiates the 40-Hz waves on the background of the cortical electroencephalogram. This was indeed the case. The potentiation outlasted the stimulation by 10-20 s. The brainstem-induced facilitation of cortical 40-Hz oscillations was blocked by scopolamine, a muscarinic antagonist. That this facilitation was transmitted by brainstem-thalamic cholinergic projections was confirmed by persistence of the phenomenon after large excitotoxic lesions of the nucleus basalis of Meynert.

Lang, E. J. and D. Paré.Synaptic and synaptically activated intrinsic conductances underlie inhibitory potentials in cat lateral amygdaloid projection neurons in vivo. J. Neurophysiol.77: 353–363, 1997. The companion paper demonstrated that the responses of lateral amygdaloid (LAT) projection neurons to the stimulation of major input and output structures are dominated by monophasic hyperpolarizing potentials of large amplitude. To characterize the mechanisms underlying these inhibitory potentials, intracellular recordings of cortically evoked responses were obtained from morphologically and/or physiologically identified LAT projection neurons in barbiturate anesthetized cats. The reversal potential of the cortically evoked hyperpolarization was measured at its peak, and 115 ms later (tail), an interval corresponding to the peak latency of the γ-aminobuturic acid-B (GABAB) response previously recorded in vitro. When recorded with K-acetate (KAc) pipettes, these reversal potentials were −86.9 ± 1.6 mV (peak; mean ± SE) and −90.7 ± 1.7 mV (tail), suggesting that both Cl−and K+conductances contribute throughout the cortically evoked hyperpolarization. The small, but consistent, difference between the two reversal potentials suggested that an additional slowly activating K+-mediated component contributed to the inhibitory postsynaptic potential (IPSP) tail. To determine whether Cl−conductances contributed to the evoked hyperpolarization, recordings were performed with KCl; the peak (−57.8 ± 2.2 mV) and tail (−61.3 ± 2.1 mV) reversal potentials were ∼15–20 mV more depolarized than those recorded with KAc pipettes. However, the difference between the peak and tail reversals remained. In an attempt to block the Cl−conductance, recordings were obtained with pipettes filled with KAc or KCl and 4,4′-diisothiocyanostilbene-2,2′-disulphonic acid (DIDS), a Cl−pump blocker that also was reported to block GABAAresponses. With KAc and DIDS, the initial depolarization was prolonged and the amplitude of the hyperpolarization decreased relative to that seen with KAc alone. However, with KCl and DIDS, the reversal potential was shifted to an even greater extent than with KCl pipettes with the evoked response consisting entirely of a large depolarization, which produced a spike burst. These results suggest that LAT neurons have a Cl−pump that is blocked by DIDS, but that their Cl−channels are not blocked by DIDS. To assess the contribution of K+conductances to cortically evoked hyperpolarizing potentials, recordings were obtained with Cs-acetate pipettes. Under these conditions, the response reversed at more depolarized potentials (peak, −71.9 ± 1.0 mV; tail,−72.0 ± 0.9 mV) compared with KAc recordings, with no difference between the peak and tail reversal potentials. These cells also had depolarized resting potentials (−66.2 ± 1.8 mV) compared with those of cells recorded with KAc pipettes (−73.6 ± 1.8 mV); however, this difference was too small to attribute the shift in reversals to a redistribution of Cl−ions across the membrane. The action potentials generated by LAT neurons under Cs+had a shoulder that prolonged their falling phase. The increased duration of the spikes was presumably due to a dendritic Ca2+conductance because LAT amygdaloid neurons are known to possess such conductances and Cs+blocks the delayed rectifier and some Ca2+-dependent K+currents. The dramatic reduction of this shoulder by spontaneous and evoked IPSPs suggests that the activation of dendritic conductances by back-propagating somatic action potentials is regulated tightly by synaptic events. Intracellular injection of the Ca2+chelating agent, 1,2-bis(2-aminophenoxy)ethane-N,N,N′,N′-tetraacetic acid (100 mM) caused a depolarization of the peak (−75.3 ± 1.3 mV) and tail (−77.7 ± 1.7 mV) reversal potentials during a time course of 15–45 min. Concurrently, the amplitude of the excitatory postsynaptic potential increased whereas that of the hyperpolarization decreased, suggesting that a Ca2+-dependent K+conductance contributes significantly to the evoked hyperpolarization. In conclusion, the large hyperpolarizing potentials that regulate the excitability of LAT projection neurons appear to be mediated primarily by a Cl−, presumably GABAA, IPSP, and a synaptically activated Ca2+-dependent K+conductance. A relatively weak K+-mediated, possibly GABAB, IPSP makes a small contribution to the later portions of the response.

Lang, E. J. and D. Paré. Similar inhibitory processes dominate the responses of cat lateral amygdaloid projection neurons to their various afferents. J. Neurophysiol.77: 341–352, 1997. To investigate the impact of inhibitory processes on responses of lateral amygdaloid (LAT) neurons, intracellular recordings were obtained from identified LAT projection neurons in barbiturate-anesthetized cats. Synaptic responses evoked by perirhinal (PRH), entorhinal (ENT), basomedial, and LAT stimulation were investigated. Regardless of stimulation site, responses consisted of an excitatory postsynaptic potential (EPSP) that either preceded and was truncated by an inhibitory postsynaptic potential (IPSP) or occurred just after the IPSP onset. IPSPs were monophasic, lasted hundreds of milliseconds, and were of such large amplitude and rapid onset that they effectively opposed the EPSPs, generally preventing orthodromic spikes. All sites elicited IPSPs with relatively negative reversal potentials around −85 mV. Experiments analyzing the underlying ionic mechanisms are presented in the companion paper. Evoked responses were similar to synaptic potentials associated with spontaneous EEG events, known as simple (small, monophasic) and complex (large, triphasic) ENT sharp potentials (SPs), with no difference between the reversals of evoked and SP-related IPSPs (−83.2 ± 2.7 mV). IPSPs coinciding with complex SPs truncated SP-related EPSPs more rapidly and had larger amplitudes and longer durations than those related to simple SPs. These differences reflected the fact that the amplitude and duration of SP-related IPSPs were correlated with SP amplitude. Similar variations were reproduced in evoked IPSPs by varying the stimulus intensity. Low intensities generated predominantly excitatory responses consisting of EPSPs sometimes followed by small IPSPs, whereas high intensities evoked predominantly inhibitory responses comprised of a large IPSP that truncated or occluded the EPSPs. Orthodromic spikes were elicited only in a narrow range of intermediate intensities. These changes in the evoked response primarily reflected increases in the IPSP evoked at high intensities. PRH stimulation at different rostro-caudal levels demonstrated that rostral sites elicited larger EPSPs and IPSPs with shorter latencies and longer durations than caudal sites. These differences probably reflect contrasting patterns of activity spread through the PRH cortex, suggesting that the intact cortical circuitry allowed a temporally distributed activation of inhibitory interneurons and thereby partly explains the long duration and monophasic nature of the IPSPs. Inhibition, thus, plays a primary role in shaping LAT neuronal responses. The profuse intrinsic connectivity of the LAT nucleus and parahippocampal cortices may underlie the relatively invariant response pattern of LAT neurons and suggests a common mode of information processing, based upon quantitative, rather than qualitative, differences in activation of LAT circuitry. Therefore we propose that effective transmission of signals through the LAT nucleus may require activation of specifically sized neuronal ensembles, rather than widespread afferent excitation.

The amygdaloid complex plays an essential role in auditory fear conditioning of the Pavlovian type. The available evidence suggests that the lateral nucleus is the input station of the amygdala for auditory conditioned stimuli, whereas the central medial nucleus is the output for conditioned fear responses. However, the intrinsic pathway transmitting auditory information about the conditioned stimulus from the lateral to the central medial nuclei is unknown as there are no direct projections between these nuclei. The present study was undertaken to determine if the main intra-amygdaloid targets of the lateral nucleus, namely the basomedial and basolateral nuclei, project to the central medial nucleus. To this end, iontophoretic injections of the anterograde tracer Paseolus vulgaris-leucoagglutinin were performed in these nuclei. To rule out the possibility that the anterograde labeling reflected passing fibers merging with the major fiber bundles that course in and around the central medial nucleus, labeled terminals and varicosities were observed in the electron microscope.