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PubMed2001

Selective expression of electrical correlates of differential appetitive classical conditioning in a feeding network.

Electrical correlates of differential appetitive classical conditioning were recorded in the neural network that underlies feeding in the snail Lymnaea stagnalis. In spaced training (15 trials over 3 days), the lips and the tentacle were used as CS+ (reinforced conditioned stimulus) or CS- (nonreinforced conditioned stimulus) sites for behavioral tactile conditioning. In one group of experimental animals, touch to the lips (the CS+ site) was followed by sucrose (the unconditioned stimulus, US), but touch to the tentacle (the CS- site) was not reinforced. In a second experimental group the CS+/CS- sites were reversed. Semi-intact lip-tentacle-CNS preparations were made from both experimental groups and a naive control group. Intracellular recordings were made from the B3 motor neuron of the feeding network, which allowed the monitoring of activity in the feeding central pattern generator (CPG) interneurons as well as early synaptic inputs evoked by the touch stimulus. Following successful behavioral conditioning, the touch stimulus evoked CPG-driven fictive feeding activity at the CS+ but not the CS- sites in both experimental groups. Naive snails/preparations showed no touch responses. A weak asymmetrical stimulus generalization of conditioned feeding was not retained at the electrophysiological level. An early excitatory postsynaptic potential (EPSP) response to touch was only enhanced following conditioning in the Lip CS+/tentacle CS- group but not in the Tentacle CS+/lip CS- group. The results show that the main features of differential appetitive classical conditioning can be recorded at the electrophysiological level, but some characteristics of the conditioned response are selectively expressed in the reduced preparation.

Animals↗
PubMed2002

Distance-dependent Ni(2+)-sensitivity of synaptic plasticity in apical dendrites of hippocampal CA1 pyramidal cells.

Low concentration of Ni(2+), a T- and R-type voltage-dependent calcium channel (VDCC) blocker, is known to inhibit the induction of long-term potentiation (LTP) in the hippocampal CA1 pyramidal cells. These VDCCs are distributed more abundantly at the distal area of the apical dendrite than at the proximal dendritic area or soma. Therefore we investigated the relationship between the Ni(2+)-sensitivity of LTP induction and the synaptic location along the apical dendrite. Field potential recordings revealed that 25 microM Ni(2+) hardly influenced LTP at the proximal dendritic area (50 microM distant from the somata). In contrast, the same concentration of Ni(2+) inhibited the LTP induction mildly at the middle dendritic area (150 microM) and strongly at the distal dendritic area (250 microM). Ni(2+) did not significantly affect either the synaptic transmission at the distal dendrite or the burst-firing ability at the soma. However, synaptically evoked population spikes recorded near the somata were slightly reduced by Ni(2+) application, probably owing to occlusion of dendritic excitatory postsynaptic potential (EPSP) amplification. Even when the stimulating intensity was strengthened sufficiently to overcome such a reduction in spike generation during LTP induction, the magnitude of distal LTP was not significantly recovered from the Ni(2+)-dependent inhibition. These results suggest that Ni(2+) may inhibit the induction of distal LTP directly by blocking calcium influx through T- and/or R-type VDCCs. The differentially distributed calcium channels may play a critical role in the induction of LTP at dendritic synapses of the hippocampal pyramidal cells.

Animals↗
PubMed2004

Coexistence of gamma and high-frequency oscillations in rat medial entorhinal cortex in vitro.

High frequency oscillations (> 80-90 Hz) occur in neocortex and hippocampus in vivo where they are associated with specific behavioural states and more classical EEG frequency bands. In the hippocampus in vitro these oscillations can occur in the absence of pyramidal neuronal somatodendritic compartments and are temporally correlated with on-going, persistent gamma frequency oscillations. Their occurrence in the hippocampus is dependent on gap-junctional communication and it has been suggested that these high frequency oscillations originate as collective behaviour in populations of electrically coupled principal cell axonal compartments. Here we demonstrate that the superficial layers of medial entorhinal cortex can also generate high frequency oscillations associated with gamma rhythms. During persistent gamma frequency oscillations high frequency oscillations occur with a high bispectral coherence with the field gamma activity. Bursts of high frequency oscillations are temporally correlated with both the onset of compound excitatory postsynaptic potentials in fast-spiking interneurones and spikelet potentials in both pyramidal and stellate principal neurones. Both the gamma frequency and high frequency oscillations were attenuated by the gap junction blocker carbenoxolone. These data suggest that high frequency oscillations may represent the substrate for phasic drive to interneurones during persistent gamma oscillations in the medial entorhinal cortex.

Animals↗
PubMed2004

Slowly developing depression of N-methyl-D-aspartate receptor mediated responses in young rat hippocampi.

BACKGROUND: Activation of N-methyl-D-aspartate (NMDA) type glutamate receptors is essential in triggering various forms of synaptic plasticity. A critical issue is to what extent such plasticity involves persistent changes of glutamate receptor subtypes and many prior studies have suggested a main role for alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid (AMPA) receptors in mediating the effect. Our previous work in hippocampal slices revealed that, under pharmacological unblocking of NMDA receptors, both AMPA and NMDA receptor mediated responses undergo a slowly developing depression. In the present study we have further addressed this phenomenon, focusing on the contribution via NMDA receptors. Pharmacologically isolated NMDA receptor mediated excitatory postsynaptic potentials (EPSPs) were recorded for two independent synaptic pathways in CA1 area using perfusion with low Mg2+ (0.1 mM) to unblock NMDA receptors. RESULTS: Following unblocking of NMDA receptors, there was a gradual decline of NMDA receptor mediated EPSPs for 2-3 hours towards a stable level of ca. 60-70 % of the maximal size. If such an experimental session was repeated twice in the same pathway with a period of NMDA receptor blockade in between, the depression attained in the first session was still evident in the second one and no further decay occurred. The persistency of the depression was also validated by comparison between pathways. It was found that the responses of a control pathway, unstimulated in the first session of receptor unblocking, behaved as novel responses when tested in association with the depressed pathway under the second session. In similar experiments, but with AP5 present during the first session, there was no subsequent difference between NMDA EPSPs. CONCLUSIONS: Our findings show that merely evoking NMDA receptor mediated responses results in a depression which is input specific, induced via NMDA receptor activation, and is maintained for several hours through periods of receptor blockade. The similarity to key features of long-term depression and long-term potentiation suggests a possible relation to these phenomena. Additionally, a short term potentiation and decay (<5 min) were observed during sudden start of NMDA receptor activation supporting the idea that NMDA receptor mediated responses are highly plastic.

Animals↗
PubMed2000

Roles of ion channels in EPSP integration at neuronal dendrites.

Many different kinds of voltage-gated ion channels (Na+ channels, K+ channels, Ca2+ channels) exist at neuronal dendrites. Integration of dendritic electric signals (excitatory postsynaptic potentials (EPSPs), inhibitory postsynaptic potentials (IPSPs) and action potentials) and/or non-electric signals (Ca2+ and second messengers) occurs in restricted dendritic compartments consisting of spines and adjacent fine dendrites. Voltage-gated ion channels at neuronal dendrites play crucial roles in the integration of dendritic signals. Dendritic signals, in turn, play important roles in the modulation of local dendritic physiological functions (e.g. input-specific synaptic plasticity, long-term potentiation (LTP) and long term depression (LTD)). A combined experimental and theoretical approach is a good way to clarify the biophysical behaviors of dendritic ion channels. Analyses of dendritic ion channels can open the door to a new wave of discoveries about EPSP integration at neuronal dendrites.

Animals↗
PubMed1993

Long-term potentiation in hippocampal CA1: effects of afterdischarges, NMDA antagonists, and anticonvulsants.

Long-term potentiation (LTP) of the basal dendritic population excitatory postsynaptic potential (EPSP) in hippocampal CA1 was readily elicited in behaving rats, without afterdischarges (ADs), by theta-frequency-patterned primed bursts (PBs) delivered to the contralateral CA1. A long-lasting postictal potentiation (PIP) was also elicited by high-frequency trains (1 s at 200 Hz), following an AD and a 5- to 10-min depression. The N-methyl-D-aspartate (NMDA) antagonist 2-amino-phosphonovalerate was effective in blocking both LTP and PIP. The noncompetitive NMDA antagonist MK801 (0.5 mg/kg ip) attenuated the PB-induced LTP but enhanced PIP. The anticonvulsants phenytoin (40 mg/kg ip) and U54494A (25 or 50 mg/kg ip) had no effects on the LTP induced by a PB but they, like MK801, enhanced PIP to various degrees. The apparent enhancement of PIP by anticonvulsants may be a direct result of shortening the hippocampal AD duration and alleviation of the postictal EPSP depression. It is inferred that the typical hippocampal AD did not induce potentiation, but rather a postictal depression of the EPSP or a suppression of LTP. The mechanism of the postictal depression is likely different from the NMDA receptor-mediated LTP and PIP and it may depend on the AD duration (and perhaps excessive CA2+ influx) but not critically on NMDA receptors.

2-Amino-5-phosphonovalerate↗
PubMed1976

Frequency facilitation and post-tetanic potentiation of a unitary synaptic potential in Aplysia californica are limited by different processes.

Post-tetanic potentiation (PTP) of the monosynaptic and unitary excitatory postsynaptic potential (EPSP) recorded in cell R15 of the abdominal ganglion of Aplysia californica was observed after repetitive stimulation of the right visceropleural connective. PTP at this synapse developed after a few pulses (about 20) and after trains of low frequency stimulation (1/2 sec) under normal physiological conditions of media and temperature. No phase of post-tetanic depression was observed. Evidence is presented that the PTP is due to an increase in transmitter release. The amplitude of the PTP was a function of the frequency and number of stimuli in the preceding train. The PTP was observed to decay, with a single exponential time course, to the size of an isolated EPSP. The rate constant of PTP decay depended upon both the frequency and number of stimuli in the preceding train. The magnitude of the various types of synaptic plasticities seen at this junction, i.e., synaptic depression, frequency facilitation and PTP, correlated with the size of an isolated EPSP as well as with each other. Based on the analysis of the data in terms of a flow model of transmitter release, it is concluded that: (a) during a train of repetitive stimulation the net rate of transmitter supply into the immediately available pool (net transmitter mobilization) increases, the efficiency of the release mechanism (fractional release) increases, and the pool of immediately available transmitter depletes; (b) upon the cessation of the train, as the peak amplitude of PTP is approached, the increased but diminishing rate of net transmitter mobilization refills the available pool to its equilibrium size, while the fractional release is still elevated; (c) during the PTP period after the peak potentiation, the elevated fractional release slowly decays with a single exponential time course; (d) the size of the facilitated EPSPs during the train is limited by the net rate of transmitter supply, although the efficiency of release is also increased; while the size of the EPSPs during the falling phase of the PTP period is determined solely by an increased efficiency of the release mechanism; and (e) the rising phase of the PTP observed in the period shortly after termination of the train is produced by the refilling of the depleted pool of available transmitter in the presence of an elevated release efficiency.

Animals↗
PubMed1987

Induction of long-term depression and potentiation by low- and high-frequency stimulation in the dentate area of the anesthetized rat: magnitude, time course and EEG.

We investigated the possible importance of stimulus train frequency for the induction and magnitude of long-term synaptic plasticity in the perforant path-granule cell pathway. Under the same experimental conditions, low- (15 Hz) or high-frequency (400 Hz) stimulation could elicit a profound long-term depression (LTD), or typical long-term potentiation (LTP), of the population spike amplitude, excitatory postsynaptic potential (EPSP) amplitude and spike onset latency. In addition, changes in the relationship between the EPSP and population spike amplitude indicated that granule cell excitability was enhanced during LTP and reduced during LTD. LTD occurred primarily after low-frequency stimulation (5 of 6 cases), and was always accompanied by striking changes in the EEG, most notably a biphasic slow potential. While the EEG changes were confined to the first 5 min after the tetanus, LTD lasted from 1 to 4 h. The nature of the EEG events is still unclear, it is suggested that they may represent a spreading depression-like episode. Finally, we found that LTP evoked by high-frequency stimulation was larger and generally reached peak magnitude faster than when it followed low-frequency stimulation. A possible mechanism and role for hippocampal LTD is proposed.

Anesthesia, General↗
PubMed1989

Comparison of opioid and GABA receptor control of excitability and membrane conductance in hippocampal CA1 pyramidal cells in rat.

Opioids are thought to increase the excitability of hippocampal pyramidal cells by decreasing release of neurotransmitter from inhibitory interneurons. This study compared the actions of the opioid agonist normorphine, and the GABA receptor antagonist bicuculline, on the responses of CA1 pyramidal cells to afferent stimulation. Both normorphine and bicuculline increased the sensitivity of pyramidal cells to presynaptic stimulation, increased the number of population spikes and action potentials elicited, increased the duration of the excitatory postsynaptic potential (EPSP) and reduced the change in input conductance during the early inhibitory postsynaptic potential (IPSP). Unlike bicuculline, normorphine also decreased the change in conductance during the late inhibitory postsynaptic potential. The decreased change in the conductance of pyramidal cells caused by normorphine during both early and late inhibitory postsynaptic potentials supports the hypothesis that opioids decrease the release of GABA from inhibitory interneurons. In addition to reducing GABA-mediated changes in conductance, both normorphine and bicuculline unmasked a D-APV-sensitive conductance, measured during the early inhibitory postsynaptic potential. These results demonstrate that activation of opioid receptors enhances the excitability of CA1 pyramidal cells by decreasing GABA-mediated early and late inhibitory postsynaptic potentials and by unmasking NMDA receptors.

2-Amino-5-phosphonovalerate↗
PubMed1987

Quantal analysis of potentiating action of phorbol ester on synaptic transmission in the hippocampus.

The mechanism of the potentiating action of phorbol diacetate on synaptic transmission in the hippocampus was studied by the quantal analysis technique. Thin transverse sections were prepared from guinea pig hippocampus and intracellular potentials were recorded from CA3 neurons. Unitary excitatory postsynaptic potentials (EPSPs) were induced in the impaled neurons by brief glutamate pulses administered to granule cells. The amplitude of the unitary EPSPs fluctuated according to Poisson distribution. From the mean and variance of the amplitude of the unitary EPSPs, the mean quantal content (m) and the mean quantal amplitude (q) were calculated. Before phorbol diacetate administration, the values of m and q were 9.7 +/- 1.4 and 1.1 +/- 0.28 mV (mean +/- S.D.), respectively. Potentiation of synaptic transmission by phorbol diacetate was accompanied by increases in the value of m. The value of q remained unchanged in most neurons and decreased in some. These results indicate that the phorbol ester causes an increase in release of neurotransmitter and thereby potentiates synaptic transmission.

Animals↗
PubMed1986

Slow cholinergic excitation of guinea pig hippocampal neurons is mediated by two muscarinic receptor subtypes.

Stimulation of cholinergic fibers or bath application of carbachol (0.1-10 microM) induced a slow excitability increase in CA3 neurons and dentate granule cells of hippocampal slices. This effect which was antagonized by atropine (1 microM) was mediated by two receptor subtypes: a pirenzepine (10 microM)-insensitive receptor, 'M2', and a pirenzepine (1 microM)-sensitive receptor, 'M1'. The M2-receptor activation led to a blockade of slow afterhyperpolarizations following trains of action potentials and to the occurrence of threshold-activated plateau-depolarizations associated with a conductance increase. The M1-receptor mediated a membrane depolarization sometimes associated with a conductance decrease which reversed its polarity at membrane potentials negative to -80 mV. The 'slow excitatory postsynaptic potential' which results from activation of cholinergic fibers is thus caused by the activation of two receptor subtypes.

Animals↗
PubMed1989

Serotonin acts in the synaptic region of sensory neurons in Aplysia to enhance transmitter release.

An important mechanism that contributes to sensitization in Aplysia is heterosynaptic facilitation of the synaptic connections between sensory neurons (SNs) and motor neurons (MNs). Heterosynaptic facilitation, in turn, is associated with broadening of the spike in the SN. Spike broadening is readily observed in recordings from somata of SNs, and from growth cones of SNs in culture, but broadening in synaptic terminals has only been inferred. Intracellular recordings were made from somata of SNs and from somata of follower MNs. Additional recordings were made from the axons of SNs as they enter the neuropil in the pedal ganglion. Serotonin (5-HT) broadened action potentials in axons of SNs and enhanced excitatory postsynaptic potentials (EPSPs) in the MNs, even after the axons of SNs were surgically separated from their somata. These results indicate that both heterosynaptic facilitation and spike broadening in the axon are due to the local action of 5-HT and can occur independently of modulation of membrane properties in the soma.

Action Potentials↗
PubMed1982

Multiple actions of acetylcholine on hippocampal pyramidal cells in organotypic explant cultures.

Hippocampal cultures were prepared from 7- to 10-day-old rats by means of the roller-type technique. The preservation of the characteristic hippocampal cytoarchitecture allowed, after many weeks in vitro, impalement of pyramidal cells by microelectrodes under visual control. Application of 10(-7) to 10(-5) M acetylcholine to the bath depolarized hippocampal pyramidal cells, strongly increased their rate of firing and induced paroxysmal depolarization shifts. This depolarizing action was accompanied by a reduction in the amplitude of evoked postsynaptic potentials. Whereas it was not clear whether the decrease in the amplitude of the excitatory postsynaptic potentials was only a result of membrane depolarization, acetylcholine clearly and reversibly reduced the potency of evoked inhibitory postsynaptic potentials. Iontophoresis of acetylcholine to the perisomatic region of pyramidal neurons, like acetylcholine applied to the bath, increased their firing rate and powerfully decreased the amplitude and duration of spontaneous and evoked inhibitory postsynaptic potentials. In contrast, iontophoresis of acetylcholine in the pyramidal cell layer at a distance from the recorded neuron generated a hyperpolarizing response associated with a reduction in firing rate. At high current strength, the initial hyperpolarization was (often) followed by a paroxysmal depolarization shift. High frequency electrical stimulation with electrodes located close to the acetylcholine pipette in the pyramidal cell layer (i.e. about 1 mm away from the recorded neuron) mimicked the acetylcholine effect. Resistance measurements indicated that membrane input resistance was decreased in the majority of cells during application of acetylcholine. This decrease in membrane resistance may result from a direct action of acetylcholine or from an increased synaptic activity. Synaptic alterations induced by acetylcholine were quick in onset and in recovery, while the increase in the rate of firing occurred somewhat later. Atropine (10(-5) M), which had no significant action by itself, completely abolished the action of acetylcholine applied to the bath or by iontophoresis. In contradistinction, naloxone did not influence the acetylcholine effects, although opiates and opioid peptides produce paroxysmal depolarization shifts in pyramidal cells which resemble those induced by acetylcholine. Addition of 8-16 mM magnesium to the bathing solution or exposure of the cultures to a calcium-free solution containing 1 mM cobalt abolished the effects of acetylcholine. In the presence of 10(-6) g/ml tetrodotoxin, 10(-5) M acetylcholine decreased the membrane input resistance of pyramidal cells, reduced their threshold for the generation of tetrodotoxin-resistant spikes and generated paroxysmal depolarization shifts in a proportion of pyramidal cells...

Acetylcholine↗
PubMed2000

Decreased ability of rat temporal hippocampal CA1 region to produce long-term potentiation.

Tetanic stimulation of Schaffer collaterals in the CA1 region of transverse slices, taken from the septal (dorsal) part of young rat hippocampus, produced N-Methyl-D-aspartate-dependent long-term potentiation (LTP) of the rising slope of excitatory postsynaptic potential (mean 38%). Under identical conditions of stimulation (100 Hz, 1 s) slices taken from the temporal (ventral) third of hippocampus presented a substantially reduced ability for LTP (mean 5%). The defect appeared to lie with the induction rather than the maintenance phase of LTP. These results suggest that a significant functional differentiation at the local synaptic plasticity level occurs between the two poles of hippocampus, which together with the substantial differences in their extrinsic connections, may help explain the reported differential participation of neurons in these parts of hippocampus during animal memory tests.

Animals↗
PubMed1980

Peptidergic transmitters in synaptic boutons of sympathetic ganglia.

In sympathetic ganglia of the bullfrog, a slow synaptic potential lasting for minutes--the late slow excitatory postsynaptic potential (e.p.s.p.)--was discovered. This slow response, unlike other previously known synaptic potentials in the autonomic nervous system, is not mediated by acetylcholine or monoamines. Similar non-cholinergic, non-adrenergic slow synaptic potentials have since been found in several other vertebrate autonomic ganglia. We found that the late slow e.p.s.p. is probably mediated by a peptide that is identical to, or closely resembles, mammalian luteinizing hormone releasing hormone (LHRH), because (1) when applied directly to sympathetic neurones, LHRH and its agonists elicit a slow depolarization, associated with similar changes in membrane conductance and excitability as those occurring during the late slow e.p.s.p. Furthermore, both peptide-induced and nerve-evoked responses are blocked by antagonists of LHRH; and (2) radioimmunoassays indicate that a chain of sympathetic ganglia contains 100-800 pg of a LHRH-like peptide. Its distribution among spinal nerves, the great reduction of this substance following denervation, and its release from ganglia following isotonic KCl treatment or nerve stimulation suggest that the LHRH-like material is contained in preganglionic nerve fibres. Here we report that immunohistochemical staining of sympathetic ganglia shows that LHRH-like immunoreactivity is indeed present in synaptic boutons. We also show that the two types of ganglion cells (B cells and C cells) receive strikingly different patterns of peptidergic innervation.

Animals↗
PubMed1990

Long-term potentiation of electrotonic coupling at mixed synapses.

Long-term potentiation of chemical synapses is closely related to memory and learning. Studies of this process have concentrated on chemically mediated excitatory synapses. By contrast, activity-dependent modification of gap junctions, which also widely exist in higher structures such as hippocampus and neocortex, has not been described. Here we report that at mixed synapses between sensory afferents and an identified reticulospinal neuron, the electrotonic coupling potential can be potentiated, as well as the chemically mediated excitatory postsynaptic potential, for a prolonged time period using a stimulation paradigm like that which produces long-term potentiation in hippocampus. The effect on coupling is due to an increase in gap-junctional conductance. Our data indicate that the potentiation of both synaptic components requires an increase in intracellular calcium, involves activation of NMDA (N-methyl-D-aspartate) receptors, and is specific to the tetanized pathway.

Afferent Pathways↗
PubMed1987

Newly identified 'glutamate interneurons' and their role in locomotion in the lamprey spinal cord.

A new class of excitatory premotor interneurons that are important in the generation of locomotion in the lamprey has now been described. In the isolated spinal cord, these neurons act simultaneously with their postsynaptic motoneurons during fictive swimming. They are small and numerous, and they monosynaptically excite both motoneurons and inhibitory premotor interneurons. The excitatory postsynaptic potentials are depressed by an antagonist of excitatory amino acids. These interneurons receive reticulospinal input from the brain stem and polysynaptic input form skin afferents. A model of the network underlying locomotion based on the synaptic interactions of these neurons can now be proposed for the lamprey.

Animals↗
PubMed1998

Cortical plasticity: from synapses to maps.

It has been clear for almost two decades that cortical representations in adult animals are not fixed entities, but rather, are dynamic and are continuously modified by experience. The cortex can preferentially allocate area to represent the particular peripheral input sources that are proportionally most used. Alterations in cortical representations appear to underlie learning tasks dependent on the use of the behaviorally important peripheral inputs that they represent. The rules governing this cortical representational plasticity following manipulations of inputs, including learning, are increasingly well understood. In parallel with developments in the field of cortical map plasticity, studies of synaptic plasticity have characterized specific elementary forms of plasticity, including associative long-term potentiation and long-term depression of excitatory postsynaptic potentials. Investigators have made many important strides toward understanding the molecular underpinnings of these fundamental plasticity processes and toward defining the learning rules that govern their induction. The fields of cortical synaptic plasticity and cortical map plasticity have been implicitly linked by the hypothesis that synaptic plasticity underlies cortical map reorganization. Recent experimental and theoretical work has provided increasingly stronger support for this hypothesis. The goal of the current paper is to review the fields of both synaptic and cortical map plasticity with an emphasis on the work that attempts to unite both fields. A second objective is to highlight the gaps in our understanding of synaptic and cellular mechanisms underlying cortical representational plasticity.

Animals↗