Partial antagonism of propofol anaesthesia by physostigmine in rats is associated with potentiation of fast (80-200 Hz) oscillations in the thalamus.

BACKGROUND: Positron emission tomography studies in human subjects show that propofol-induced unconsciousness in humans is associated with a reduction in thalamic blood flow, suggesting that anaesthesia is associated with impairment of thalamic function. A recent study showed that antagonism of propofol-induced unconsciousness by the anticholinesterase physostigmine is associated with a marked increase in thalamic blood flow, supporting the implication of the thalamus. The aim of the present study was to assess the role of the thalamus in the antagonistic effects of physostigmine during propofol anaesthesia using electrophysiological recordings in a rat model. METHODS: Local field potentials were recorded from the barrel cortex and ventroposteromedial thalamic nucleus in 10 chronically instrumented rats to measure spectral power in the gamma/high-gamma range (50-200 Hz). Propofol was given i.v. by target-controlled infusion at the lowest concentration required to abolish righting attempts. Physostigmine was given during anaesthesia to produce behavioural arousal without changing anaesthetic concentration. RESULTS: Compared with baseline, gamma/high-gamma power during anaesthesia was reduced by 31% in the cortex (P=0.006) and by 65% in the thalamus (P=0.006). Physostigmine given during anaesthesia increased gamma/high-gamma power in the thalamus by 60% (P=0.048) and caused behavioural arousal that correlated (P=0.0087) with the increase in power. Physostigmine caused no significant power change in the cortex. CONCLUSIONS: We conclude that partial antagonism of propofol anaesthesia by physostigmine is associated with an increase in thalamic activity reflected in gamma/high-gamma (50-200 Hz) power. These findings are consistent with the view that anaesthetic-induced unconsciousness is associated with impairment of thalamic function.

The use of fruiting synchrony by foraging mangabey monkeys: a 'simple tool' to find fruit.

Previous research has shown that a considerable number of primates can remember the location and fruiting state of individual trees in their home range. This enables them to relocate fruit or predict whether previously encountered fruit has ripened. Recent studies, however, suggest that the ability of primates to cognitively map fruit-bearing trees is limited. In this study, we investigated an alternative and arguably simpler, more efficient strategy, the use of synchrony, a botanical characteristic of a large number of fruit species. Synchronous fruiting would allow the prediction of the fruiting state of a large number of trees without having to first check the trees. We studied whether rainforest primates, grey-cheeked mangabeys in the Kibale National Park, Uganda, used synchrony in fruit emergence to find fruit. We analysed the movements of adult males towards Uvariopsis congensis food trees, a strongly synchronous fruiting species with different local patterns of synchrony. Monkeys approached within crown distance, entered and inspected significantly more Uvariopsis trees when the percentage of trees with ripe fruit was high compared to when it was low. Since the effect was also found for empty trees, the monkeys likely followed a synchrony-based inspection strategy. We found no indication that the monkeys generalised this strategy to all Uvariopsis trees within their home range. Instead, they attended to fruiting peaks in local areas within the home range and adjusted their inspective behaviour accordingly revealing that non-human primates use botanical knowledge in a flexible way.

Pilot study of the utility and acceptability of tampon sampling for the diagnosis of Neisseria gonorrhoeae and Chlamydia trachomatis infections by duplex realtime polymerase chain reaction in United Kingdom sex workers.

We aimed to evaluate the acceptability of self-collected tampon samples for the screening of female sex workers for sexually transmitted infections. We recruited 65 sex workers, and 63 agreed to provide tampon samples. The tampon samples were processed by realtime polymerase chain reaction (PCR) targeting Neisseria gonorrhoeae and Chlamydia trachomatis. Urethral and endocervical swabs were also obtained from 61 of 63 participants and tested using culture (N. gonorrhoeae) and the BD ProbeTec strand displacement amplification (SDA) (C. trachomatis) assay. Tampon sampling was preferred by 95% of the women and all favoured being tested away from genitourinary medicine clinics; the most common reasons cited were avoidance of embarrassment (40%) and convenience (30%). Besides near-universal acceptability of tampon sampling, the tampon sampling-PCR approach described in this study appeared to have enhanced sensitivity compared with conventional testing, suggesting the possibility of a residual hidden burden of N. gonorrhoeae and/or C. trachomatis genital infections in UK female sex workers.

Neither genetic nor observational data alone are sufficient for understanding sex-biased dispersal in a social-group-living species.

Complex sex-biased dispersal patterns often characterize social-group-living species and may ultimately drive patterns of cooperation and competition within and among groups. This study investigates whether observational data or genetic data alone can elucidate the potentially complex dispersal patterns of social-group-living black and white colobus monkeys (Colobus guereza, "guerezas"), or whether combining both data types provides novel insights. We employed long-term observation of eight neighbouring guereza groups in Kibale National Park, Uganda, as well as microsatellite genotyping of these and two other neighbouring groups. We created a statistical model to examine the observational data and used dyadic relatedness values within and among groups to analyse the genetic data. Analyses of observational and genetic data both supported the conclusion that males typically disperse from their natal groups and often transfer into nearby groups and probably beyond. Both data types also supported the conclusion that females are more philopatric than males but provided somewhat conflicting evidence about the extent of female philopatry. Observational data suggested that female dispersal is rare or nonexistent and transfers into neighbouring groups do not occur, but genetic data revealed numerous pairs of closely related adult females among neighbouring groups. Only by combining both data types were we able to understand the complexity of sex-biased dispersal patterns in guerezas and the processes that could explain our seemingly conflicting results. We suggest that the data are compatible with a scenario of group dissolution prior to the start of this study, followed by female transfers into different neighbouring groups.

Extracting impedance changes from a frequency multiplexed signal during neural activity in sciatic nerve of rat: preliminary study in vitro.

OBJECTIVE: To establish suitable frequency spacing and demodulation steps to use when extracting impedance changes from frequency division multiplexed (FDM) carrier signals in peripheral nerve. APPROACH: Experiments were performed in vitro on cadavers immediately following euthanasia. Neural activity was evoked via stimulation of nerves in the hind paw, while carrier signals were injected, and recordings obtained, with a dual ring nerve cuff implanted on the sciatic nerve. Frequency analysis of recorded compound action potentials (CAPs) and extracted impedance changes, with the latter obtained using established demodulation methods, were used to determine suitable frequency spacing of carrier signals, and bandpass filter (BPF) bandwidth and order, for a frequency multiplexed signal. MAIN RESULTS: CAPs and impedance changes were dominant in the frequency band 200 to 500 Hz and 100 to 200 Hz, respectively. A Tukey window was introduced to remove ringing from Gibbs phenomena. A ±750 Hz BPF bandwidth was selected to encompass 99.99% of the frequency power of the impedance change. Modelling predicted a minimum BPF order of 16 for 2 kHz spacing, and 10 for 4 kHz spacing, were required to avoid ringing from the neighbouring carrier signal, while FDM experiments verified BPF orders of 12 and 8, respectively, were required. With a notch filter centred on the neighbouring signal, a BPF order of at least 6 or 4 was required for 2 and 4 kHz, respectively. SIGNIFICANCE: The results establish drive frequency spacing and demodulation settings for use in FDM electrical impedance tomography (EIT) experiments, as well as a method for their selection, and, for the first time, demonstrates the viability of FDM-EIT of neural activity on peripheral nerve, which will be a central aspect of future real-time neural-EIT systems and EIT-based neural prosthetics interfaces.

Amphetamine induces dendritic growth in ventral tegmental area dopaminergic neurons in vivo via basic fibroblast growth factor.

Dopaminergic neurons of the ventral tegmental area are implicated in the physiology of reward, and long-lasting changes in their function induced by exposure to psychostimulant drugs are related to the pathophysiology of drug abuse. It is not known, however, whether such changes are accompanied by morphological changes in these neurons. We characterized and labeled cells in slices containing the ventral tegmental area using whole-cell electrophysiological methods. Injections of saline or amphetamine were given to rats on postnatal days 10, 12 and 14 and individual neurons were examined one to four weeks later. We show that repeated exposure to amphetamine induces substantial dendritic growth of ventral tegmental area dopaminergic neurons in vivo. Furthermore, we show, by immuno-neutralization of endogenous basic fibroblast growth factor, that the amphetamine-induced increase in astrocytic basic fibroblast growth factor in the ventral tegmental area is essential for these morphological changes. We propose that the amphetamine-induced elaboration of the dendritic arbor of dopaminergic neurons leads to their increased excitability and contributes to compulsive drug-seeking and relapse.

Long-term depression in the sensorimotor cortex induced by repeated delivery of 10 Hz trains in vivo.

Memory consolidation in the neocortex is thought to be mediated in part by bi-directional modifications of synaptic strength. The sensorimotor cortex shows marked spontaneous activity near 10 Hz during both waking and sleep in the form of electroencephalographic spindle waves, and is also sensitive to electrical activation of inputs at 10 Hz. Induction of long-term synaptic depression in corpus callosum inputs to layer V of the sensorimotor cortex of the awake, adult rat requires repeated low-frequency stimulation over many days. To determine if 10 Hz stimulation may facilitate the induction of long-term depression, we compared the amounts of long-term depression induced by conventional 1 Hz trains, repeated delivery of 450 pairs of stimulation pulses using a 100 ms interpulse interval, and 45 short, 2 s, 10 Hz trains. Each pattern was delivered daily for 10 days and was matched for total duration and number of pulses. Changes in synaptic responses were assessed by monitoring field potentials evoked by stimulation of the corpus callosum. A facilitation of synaptic responses in layer V was observed during delivery of both paired-pulse trains and 10 Hz trains. There was no significant difference in long-term depression induced by 1 Hz stimulation and repeated paired-pulse stimulation, but 10 Hz trains induced significantly greater long-term depression than 1 Hz trains in both the early monosynaptic and late polysynaptic field potential components. The effectiveness of short 10 Hz trains for the induction of long-term depression suggests that synchronous population activity at frequencies near 10 Hz such as spindle waves may contribute to endogenous synaptic depression in sensorimotor cortex.

Cholinergic induction of theta-frequency oscillations in hippocampal inhibitory interneurons and pacing of pyramidal cell firing.

Cholinergic and GABAergic medial septal afferents contribute to hippocampal theta activity in part by actions on local interneurons. Interneurons near the border between stratum radiatum and stratum lacunosum-moleculare (LM) display intrinsic membrane potential oscillations at theta frequency when depolarized near threshold. First, whole-cell current-clamp recordings in rat hippocampal slices were used to examine effects of the cholinergic agonist carbachol on biocytin-labeled LM interneurons. At resting membrane potential, cells were depolarized by bath application of 25 microM carbachol, and the depolarization was sufficient to induce membrane potential oscillations (2.4 +/- 0.2 mV) that paced cell firing. Carbachol also depolarized LM interneurons in the presence of 6-cyano-7-nitroquinoxaline-2,3-dione, (+/-)-2-amino-5-phosphonopentanoic acid, and bicuculline, indicating that cholinergic depolarization of LM cells does not depend on ionotropic glutamate or GABA(A) synaptic transmission in local circuits. Atropine blocked the depolarization, indicating that muscarinic receptors were involved. Minimal stimulation applied to visually identified LM interneurons was then used to determine if spontaneous activity in CA1 pyramidal cells can be paced by rhythmic inhibition generated by LM cells at theta frequency. Inhibitory postsynaptic potentials evoked in pyramidal cells by single minimal stimulations were followed by rebound depolarizations and action potentials. When trains of minimal stimulation were delivered, membrane potential oscillations of depolarized pyramidal cells followed the stimulation frequency. Minimal stimulation led pyramidal cell firing with an average phase of 177 degrees. Thus, muscarinic induction of theta-frequency membrane potential oscillations in LM interneurons may contribute to the generation of rhythmic inhibition that paces intrinsically generated theta activity in CA1 pyramidal cells.

Long-term depression and depotentiation in the sensorimotor cortex of the freely moving rat.

Activity-dependent reductions in synaptic efficacy are central components of recent models of cortical learning and memory. Here, we have examined long-term synaptic depression (LTD) and the reversal of long-term potentiation (depotentiation) of field potentials evoked in sensorimotor cortex by stimulation of the white matter in the adult, freely moving rat. Prolonged, low-frequency stimulation (1 Hz for 15 min) was used to induce either depotentiation or LTD. LTD was expressed as a reduction in the amplitude of both monosynaptic and polysynaptic field potential components. Both LTD and depotentiation were reliably induced by stimulation of the ipsilateral white matter. Stimulation of the contralateral neocortex induced only a depotentiation effect, which decayed more rapidly than that induced by ipsilateral stimulation (hours vs days). Although ipsilateral LTD was effectively induced by a single session of low-frequency stimulation, multiple sessions of stimulation, either massed or spaced, induced LTD effects that were larger in magnitude and longer lasting. Previously, we showed that the induction of long-term potentiation in the neocortex of chronic preparations required multiple, spaced stimulation sessions to reach asymptotic levels. Here, we report that LTD also required multiple stimulation sessions to reach asymptotic levels, but massed and spaced patterns of low-frequency stimulation were equally effective.

Induction of long-term potentiation leads to increased reliability of evoked neocortical spindles in vivo.

Large amplitude electroencephalographic spindle waves (7-14 Hz) occur spontaneously in the neocortex during both sleep and awake immobility, and it has been proposed that synchronous neuronal activation during spindles may contribute to learning-related synaptic plasticity. Spindles can also be evoked in the sensorimotor cortex by electrical stimulation of cortical or thalamic inputs in the rat. To determine if strengthening cortical synapses can affect the initiation and maintenance of electrically evoked spindles, stimulation pulses were delivered at a range of intensities to the corpus callosum or ventrolateral thalamus in the awake rat before and after the induction of long-term potentiation (LTP) by tetanization of the corpus callosum. The morphology of evoked spindles was similar to that of naturally occurring spindles. Spindles were evoked less reliably during slow-wave sleep than during waking, and this was correlated with smaller synaptic responses during slow-wave sleep. Similar to previous findings, daily tetanization of the corpus callosum for 15 days decreased the early component and increased the late component of synaptic responses evoked by corpus callosum stimulation, but did not significantly affect synaptic responses evoked by thalamic stimulation. Similarly, LTP induction increased the reliability with which low-intensity corpus callosum stimulation evoked spindles, but increases in spindles evoked by thalamic stimulation were not significant. Synaptic potentiation and the increased reliability of spindles developed with a similar time-course over the 15-day LTP induction period. These results reflect strong correlations between the strength of cortical layer V activation and the initiation of spindles in the sensorimotor cortex, and support the idea that monosynaptic and polysynaptic horizontal collaterals of layer V neurons can play a significant role in the initiation of spindles.

Motor cortex and pyramidal tract axons responsible for electrically evoked forelimb flexion: refractory periods and conduction velocities.

Double-pulse methods are used here to measure the refractory periods and conduction velocities of the pyramidal tract axons which cause forelimb flexion in pentobarbital anesthetized rats. In the refractory period experiments, conditioning and test pulses were delivered to the motor cortex, the ipsilateral internal capsule, or the ipsilateral pyramid, and the maximum force exerted by the contralateral forelimb was measured at various conditioning-test intervals. The movements increased as conditioning-test interval increased from 0.5 to 1.0 ms in pyramid sites, from 0.6 to 1.5 in internal capsule sites, and from 0.6 to 2.0 ms in surface cortical sites, suggesting longer refractory periods for the substrates at more rostral sites. In cortical sites, as the conditioning-test interval increased from 4.0 to 20.0 ms, the movements decreased gradually to the single-pulse level, suggesting decreasing temporal summation at longer conditioning-test intervals. In the collision experiments, when conditioning pulses were delivered to one site and test pulses to a second site, the movements increased at conditioning-test intervals that were longer by 0.5-1.3 ms than the refractory periods in either site. This suggests that collisions occurred between orthodromic and antidromic action potentials in the pyramidal tract axons responsible for the limb movement. The collision-like increase was greater between internal capsule and pyramid than between cortex and pyramid, or between cortex and internal capsule. The estimated conduction times were 0.9-1.5 ms between cortex and pyramid, 0.4-0.8 ms between cortex and internal capsule, and 0.5-0.8 ms between internal capsule and pyramid. The range of conduction velocities, therefore, was quite narrow between all pairs (8.8-16.8 m/s). The largest pyramidal tract axons appear to be responsible for most of the force of forelimb flexion in pentobarbital anesthetized rats.

Beta-frequency (15-35 Hz) electroencephalogram activities elicited by toluene and electrical stimulation in the behaving rat.

Bursts of beta-frequency (15-35 Hz) electroencephalogram activity occur in the olfactory system during odour sampling, but their mode of propagation within the olfactory system and potential contribution to the mechanisms of learning and memory are unclear. We have elicited large-amplitude beta activity in the rat olfactory system by applying noxious olfactory stimuli (toluene), and have monitored the bursts via chronically-implanted electrodes. Following exposure to toluene, coherent bursts with a peak frequency of 19.8 +/- 0.9 Hz were observed in the olfactory bulb, piriform cortex, entorhinal cortex and dentate gyrus. The timing of the bursts and the phases of electroencephalogram cross-spectra indicate that beta bursts propagate in a caudal direction from the olfactory bulb to the entorhinal cortex. The time delays between peaks of bursts in these structures were similar to latency differences for field potentials evoked by olfactory bulb or piriform cortex test-pulses. Peaks of burst cycles in the dentate region, however, were observed just prior to those in the entorhinal cortex. Surprisingly, power in toluene-induced beta-frequency oscillations was not increased following long-term potentiation induced by tetanic stimulation of the olfactory bulb, piriform cortex and entorhinal cortex. The activity of local inhibitory mechanisms may therefore counteract the effects of synaptic enhancements in afferent pathways during beta bursts. Low-frequency electrical stimulation of the piriform cortex was most effective in inducing coherent oscillatory responses in the entorhinal cortex and dentate gyrus at stimulation frequencies between 12 and 16 Hz. The results show that repetitive polysynaptic volleys at frequencies in the beta band induced by either toluene or electrical stimulation are transmitted readily within the olfactory system. The propagation of neural activity within this frequency range may therefore contribute to the transmission of olfactory signals to the hippocampal formation, particularly for those odours which induce high-amplitude bursts of beta activity.

Increased striatal dopamine efflux follows scopolamine administered systemically or to the tegmental pedunculopontine nucleus.

The cholinergic cells of the tegmental pedunculopontine nucleus monosynaptically excite dopaminergic neurons of the substantia nigra. In vivo electrochemical methods were used to monitor dorsal striatal dopamine efflux in awake rats following intraperitoneal scopolamine injections and following the direct application of scopolamine to the tegmental pedunculopontine nucleus. Systemic injections of scopolamine (1.0, 3.0 or 10.0 mg/kg) resulted in dose-related increases in peak striatal dopamine oxidation currents of between 1.1 and 2.0 nA. Increases began within 10-20 min after injection and peaked after 40-90 min. Unilateral microinjections of scopolamine into the tegmental pedunculopontine nucleus (10, 50 or 100 micrograms/0.5 microliter) resulted in dose-related increases in dopamine oxidation currents that peaked 60-90 min postinjection (2.9-5.0 nA). Carbachol (4.0 micrograms/0.5 microliter) injected unilaterally into the tegmental pedunculopontine nucleus 20 min before 100 micrograms tegmental pedunculopontine nucleus scopolamine, or injected bilaterally 20 min before 3.0 mg/kg systemic scopolamine, attenuated the increases produced by scopolamine alone. The carbachol preinjection tests suggest that the effects of both systemic and tegmental pedunculopontine nucleus scopolamine treatments are mediated largely by muscarinic receptors near the tegmental pedunculopontine nucleus. These findings are consistent with the proposal that enhanced activation of substantia nigra dopamine cells results from scopolamine-induced disinhibition of the tegemental pedunculopontine nucleus cholinergic cell group via blockade of their inhibitory autoreceptors.

Differential induction of long-lasting potentiation of inhibitory postsynaptic potentials by theta patterned stimulation versus 100-Hz tetanization in hippocampal pyramidal cells in vitro.

Tetanization of Schaffer collaterals, which induces long-term potentiation of excitatory transmission in the hippocampus of the rat, also affects local inhibitory circuits. Mechanisms controlling plasticity of early and late components of inhibitory postsynaptic potentials in CA1 pyramidal cells were studied using intracellular recordings and Ca2+ imaging in rat hippocampal slices. High-frequency stimulation (100 Hz/s) of Schaffer collaterals resulted in no change in the mean amplitude of early or late inhibitory postsynaptic potentials 30 min post-tetanus. However, intracellular injection of the Ca2+ chelator 1,2-bis(2-aminophenoxy)ethane-N,N,N',N'-tetra-acetate unmasked a significant increase in mean amplitude of both inhibitory postsynaptic potentials 30 min post-tetanus and the induction of this potentiation was blocked by the N-methyl-D-aspartate receptor antagonist(+/-)-2-amino-5-phosphopentanoic acid. In contrast to high-frequency tetanization, "theta-burst" stimulation in normal medium resulted in a significant potentiation of the mean amplitude of both early and late inhibitory postsynaptic potentials 30 min post-tetanus. This potentiation was blocked by the N-methyl-D-aspartate receptor antagonist. The more physiological tetanization pattern, which mimics the endogenous theta rhythm, therefore resulted in an N-methyl-D-aspartate-dependent increase in inhibition 30 min post-tetanus. Calcium imaging during whole-cell recordings from pyramidal cells revealed differences in the Ca2+ signal associated with high-frequency and theta-burst stimulations. During theta-burst stimulation of Schaffer collaterals, the mean time to peak of Ca2+ signals was significantly longer, and the mean peak amplitude and area under the Ca2+ response were larger than during high-frequency stimulation. These results indicate that tetanization induces long-lasting synaptic plasticity in hippocampal inhibitory circuits. This plasticity involves an interaction between a Ca2(+)-mediated postsynaptic depression and an N-methyl-D-aspartate-mediated potentiation of GABAA and GABAB inhibition, and these processes are differentially sensitive to tetanization parameters.

Neurobehavioral profiles of children with neurofibromatosis 1 referred for learning disabilities are sex-specific.

We compared neurobehavioral profiles of 10 children with neurofibromatosis 1 (NF-1) referred for evaluation of learning disabilities (NF/LD) to those to learning disabled children without known genetic disease (LD), matched for age, sex, and estimated IQ. It was hypothesized that the NF/LD children would exhibit a neurobehavioral profile diagnostic of compromise of frontal/subcortical brain systems while those of the case controls would be heterogeneous. Records from a clinical data base were reviewed retrospectively for the neurological and neuropsychological components of an interdisciplinary learning disabilities evaluation. Neurological abnormalities were more frequent in the NF/LD group, involving gross and fine motor coordination, praxis, and megencephaly. As predicted, clinical neuropsychological diagnostic ratings and composite neurobehavioral observation scores were consistent with compromise of frontal systems in the NF/LD group. An unanticipated finding was that outcomes in the NF/LD group were sex dependent: Megencephaly was observed in females only; and the frontal/subcortical neurobehavioral profile was more consistently observed in females. Females with NF-1 with megencephaly may be at increased risk for a neurobehavioral syndrome contributing to LD that is consistent with compromise of frontal/subcortical brain systems.

Axons and synapses mediating startle-like responses evoked by electrical stimulation of the reticular formation in rats: symmetric and asymmetric collision effects.

A new method for determining the locations, directions of transmission and transmission times of synapses mediating electrically evoked responses is proposed here. Electrical stimulation of pontine or medullary reticular formation with one 0.1-ms pulse evokes a short-latency startle-like response. Two pulses were delivered to single sites at various interpulse intervals and the currents required to evoke a criterion startle response were measured. The results suggest that the startle-evoking substrates have absolute refractory periods that range from 0.25-0.6 ms. When one pulse was delivered to a caudal pontine site and a second pulse was delivered to a an ipsilateral medulla site, decreases in required current were observed as interpulse interval increased from +0.4 to +0.8 ms or as interpulse interval decreased from -0.4 to -0.8 ms. These collision-like effects, being symmetric around an interpulse interval of 0, suggest that electrically evoked startle is mediated by fast axons that pass longitudinally through medulla. When one pulse was delivered to the rostral pons and a second pulse to the ipsilateral medulla, however, required currents decreased sharply as interpulse intervals increased from +0.4 to 1.0 ms and as interpulse intervals decreased from +0.2 to -0.2 ms. These asymmetric collision-like effects suggest that strong synapses in the caudal pons, transmitting from pons to medulla, mediate electrically evoked startle. The 0.3-ms asymmetry suggests that the transmission time (i.e., from presynaptic stimulus to postsynaptic action potential) averaged 0.3 ms via monosynaptic connections. The short duration of collision (0.7 ms) suggests that only one postsynaptic action potential was produced with high probability for each presynaptic action potential. From the localization of these effects and the short refractory periods, we estimate that < 60 giant cells on each side of the ventral pontine reticular formation mediate the startle reflex in the rat.

Post-activation potentiation in the neocortex. III. Kindling-induced potentiation in the chronic preparation.

Previous experiments have shown the neocortex to be very resistant to the induction of long-term potentiation in chronic preparations. We show here that kindling-induced potentiation effects can be reliably produced in the neocortex of awake, freely moving rats. These effects develop rather slowly. In sites contralateral to the stimulation electrode, potentiation effects did not become clear until the animals had received about 5 days or more of stimulation. Ipsilateral sites required even longer (approximately 10 days), and both sites required more than 13 days to reach asymptotic levels of potentiation. Both monosynaptic and polysynaptic components were present in the neocortical field potentials. When population spikes were absent, the surface negative monosynaptic EPSP component tended to show a potentiation effect. If population spikes were present, they were generally enhanced while the monosynaptic population EPSP tended to be depressed. Consequently, the apparent depression may have been due to competing field currents. The later polysynaptic components (15-28 ms latency to peak) always showed a potentiation effect with 5 or more kindling stimulations and is presumed to result from activation of cortico-cortical associational fibers. All of these effects were long-lasting, showing little decay over a period of several weeks.

Post-activation potentiation in the neocortex. IV. Multiple sessions required for induction of long-term potentiation in the chronic preparation.

The neocortex in chronically prepared rats is very resistant to the induction of long-term potentiation (LTP). In the first of two experiments described in this paper, we tried unsuccessfully to induce neocortical LTP within one session by coactivating basal forebrain cholinergic and cortical inputs to our neocortical recording site. In the second experiment, we tested a new procedure which involved the application of repeated conditioning sessions over several days. This procedure was suggested by our finding that kindling-induced potentiation (KIP) of cortical field potentials could be reliably triggered but was slow to develop. We administered 30 high frequency trains per day to the corpus callosum for 25 days. LTP in callosal-neocortical field potentials became clear after about 5 days of stimulation and reached asymptotic levels by about 15 days. After the termination of treatment, LTP persisted for at least 4 weeks, the duration of our post-stimulation test period. As in previous experiments on kindling-induced potentiation, the potentiation effects were clear in both early population spike components and in a late (probably disynaptic) component. The monosynaptic EPSP component was often depressed, but this may have been due to competing field currents generated by the enhanced population spike activity. We discuss these results in the context of theories emphasizing slower but more permanent memory storage in neocortex compared to the hippocampus.

Crossed reticular formation connections that mediate the startle reflex in rats.

The startle response is a bilateral response even when elicited by unilateral acoustic or tactile stimuli. Similarly, unilateral electrical stimulation of the reticular formation also elicits a bilateral startle-like response. To examine whether crossed reticular formation connections can distribute the effects of unilateral stimulation across the midline, we delivered one pulse to the caudal pontine (RPC) or medullary reticular formation (MRF) and a second pulse to the opposite side of the brain, at various interpulse intervals. The symmetric collision effects suggest that axons which produce at least 37% (range 23-53%) of the startle response efficacy cross from RPC to RPC with a mean conduction velocity of 13 m/s. Similar collision effects were observed between RPC and MRF sites but at shorter conduction times. To examine which axons might cause these collision effect, the axonally transported label DiI was injected post mortem into 37 RPC sites. Many coarse axons were observed to cross in fascicles between bilateral RPC sites and then separate in the contralateral RPC. The fiber diameters and trajectories of these DiI-labelled axons are consistent with the conduction velocities and trajectories of the substrates mediating the startle-like response determined in collision tests.

Multiple central place foraging by spider monkeys: travel consequences of using many sleeping sites.

Central place foraging models assume that animals return to a single central place such as a nest, burrow, or sleeping site. Many animals, however choose between one of a limited number of central places. Such animals can be considered Multiple Central Place Foragers (MCPF), and such a strategy could reduce overall travel costs, if the forager selected a sleeping site close to current feeding areas. We examined the selection of sleeping sites (central places) by a community of spider monkeys (Ateles geoffroyi) in Santa Rosa National Park, Costa Rica in relation to the location of their feeding areas. Spider monkeys repeatedly used 11 sleeping trees, and they tended to choose the sleeping site closest to their current feeding area. A comparison of the observed travel distances with distances predicted for a MCPF strategy, a single central place strategy, and a strategy of randomly selecting sleeping sites demonstrated (1) that the MCPF strategy entailed the lowest travel costs, and (2) that the observed travel distance was best predicted by the MCPF strategy. Deviations between the observed distance travelled and the values predicted by the MCPF model increased after a feeding site had been used for several days. This appears to result from animals sampling their home range to locate new feeding sites.