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At least 685 records · Page 38Linked to original sources
PubMed2001

The effects of cooling and rewarming on the neuronal activity of pyramidal neurons in guinea pig hippocampal slices.

To investigate the reversibility of neuronal functions during deep and mild hypothermia, we have examined changes in membrane properties of pyramidal neurons of the CA3 region of hippocampal slices during cooling and rewarming (8 approximately 37 degrees C) of the perfusion medium. Hypothermia reduced the excitatory postsynaptic potential (EPSP) slope in a temperature dependent manner, but the EPSP amplitude was enhanced transiently between 30 and 25 degrees C. In observing spikes generated by either orthodromic stimulation or by direct intracellular current injection, the critical threshold for spike generation was decreased transiently at a temperature of 30 degrees C. In addition, the numbers of spikes were increased transiently regardless of the progressive prolongation of spike duration and latency with cooling. The resting membrane potential was stable from 37 to 20 degrees C. However, this potential showed a depolarizing shift at 15 degrees C. The neuronal activities, including membrane properties, recovered fully when the temperature was raised to 35 degrees C even from a low of 15 degrees C. In addition, field population spikes (PS) recorded in the pyramidal cell layer showed a complete reversibility after long-term severe hypothermia (8 degrees C). These results suggest that synaptic function, neuronal excitability and membrane properties maintain reversibility during deep hypothermia, as well as in mild hypothermia.

Action Potentials↗
PubMed1997

Induction of LTD in the dentate gyrus in vitro is NMDA receptor independent, but dependent on Ca2+ influx via low-voltage-activated Ca2+ channels and release of Ca2+ from intracellular stores.

The mechanisms of the induction of long-term depression (LTD) of field excitatory postsynaptic potentials (EPSPs) and whole cell patch-clamped excitatory postsynaptic currents (EPSCs) were studied in the dentate gyrus of the rat hippocampus. LTD of field EPSPs measuring 40% of control at 30 min poststimulation was induced by low-frequency stimulation consisting of 900 pulses at 1 Hz. LTD of EPSCs measuring 37% of control was induced by a pairing procedure consisting of 60 pulses at 1 Hz applied under voltage clamp at a holding potential of -40 mV. The induction of LTD of field EPSPs was dependent on an influx of extracellular calcium, being reduced in a low-Ca2+ (0.8 mM) medium. However, substantial LTD (26%) was still induced in such a medium, demonstrating the relatively low sensitivity of LTD induction to the level of extracellular Ca2+. A high concentration of the N-methyl-D-aspartate receptor antagonist D(-)-2-amino-5-phosphonopentanoic acid (D-AP5) (100 microM) did not significantly inhibit the induction of LTD of EPSCs evoked by the intracellular pairing procedure. D-AP5 partially reduced the magnitude of LTD of field EPSPs, but substantial LTD was still induced in the presence of AP5. The induction of LTD was strongly inhibited by Ni2+ (50 microM) but not by nifedipine (10 microM), indicating that Ca2+ influx via T-type, but not L-type, Ca2+ channels is required for the induction of LTD. The induction of LTD was strongly inhibited by thapsigargin, an agent known to deplete intracellular Ca2+ stores. The induction of LTD, but not long-term potentiation (LTP), was also strongly inhibited by ruthenium red, an agent known to block the ryanodine receptors located on intracellular Ca2+ stores. These results demonstrate that Ca2+ release from intracellular Ca2+ stores is required for the induction of LTD, but not LTP. The results of the present experiments suggest that the induction of LTD involves the entry of Ca2+ via low-voltage-activated voltage-gated Ca2+ channels followed by release of Ca2+ from intracellular ryanodine-receptor-sensitive Ca2+ stores.

Animals↗
PubMed2001

Mechanisms of frequency-specific responses of omega neuron 1 in crickets (Teleogryllus oceanicus): a polysynaptic pathway for song?

In crickets (Teleogryllus oceanicus), the auditory interneuron omega neuron 1 (ON1) responds to sounds over a wide range of frequencies but is most sensitive to the frequency of conspecific songs (4.5 kHz). Response latency is longest for this same frequency. We investigate the mechanisms that might account for the longer latency of ON1 to cricket-like sounds. Intracellular recordings revealed no evidence for appropriately timed postsynaptic inhibition of ON1 that might increase its latency, nor was latency affected by picrotoxin. The onset of excitatory postsynaptic potentials (EPSPs) was delayed for 4.5 kHz stimuli compared with ultrasound stimuli, pointing to a presynaptic locus for the latency difference. When ON1 is stimulated with high frequencies, discrete, apparently unitary EPSPs can be recorded in its dendrite, and these are latency-locked to spikes recorded simultaneously in the auditory nerve. This suggests that input to ON1 from high-frequency-tuned auditory receptor neurons is monosynaptic. In agreement with this, brief ultrasound stimuli evoke a single, short-latency EPSP in ON1. In contrast, the EPSP evoked by a brief 4.5 kHz stimulus consists of an early component, similar in latency to that evoked by ultrasound and possibly evoked by ultrasound-tuned receptors, and a later, dominant component. We interpret the early peak as arising from a monosynaptic afferent pathway and the late peak from a polysynaptic afferent pathway. Multiple-peak EPSPs, with timing similar to those evoked by sound stimuli, were also evoked by electrical stimulation of the auditory nerve.

Acoustic Stimulation↗
PubMed1999

Age-dependent, steroid-specific effects of oestrogen on long-term potentiation in rat hippocampal slices.

1. Long-term potentiation (LTP) of hippocampal population spike responses and excitatory postsynaptic potentials (EPSPs) from area CA1 stratum pyramidale was induced in slices of rat hippocampus maintained in vitro following brief high-frequency stimulation (HFS) of the Schaffer collateral-commissural pathway. When administered to slices prior to HFS, 17beta-oestradiol (OE2), at a concentration as low as 0.1 nM, suppressed the magnitude of the resultant HFS-induced potentiation in slices from prepubertal animals (3 and 4 weeks old) of both sexes. 2. OE2 did not suppress the induction of LTP in slices taken from the hippocampus of adult animals of either sex. 3. There was no similar suppressant effect of 17alpha-oestradiol (OE1), progesterone (PRG) or testosterone (TST) on LTP in the young animals, even at a concentration 100 times greater than was effective for OE2. 4. The anti-oestrogen compound tamoxifen (TMX; 1.0 and 10.0 microM), which acts principally at intracellular binding sites within the nucleus, was without effect in diminishing the suppressant effect of OE2 on LTP in slices from young animals. 5. The LTP observed in slices from both 3-week-old and adult rats was AP5 sensitive and thus was shown to be dependent on activation of NMDA receptors. Results from whole-cell recording experiments suggested that OE2 caused the LTP-suppressant effect through an action on NMDA-mediated currents. 6. These data suggest an age-dependent and possibly a surface membrane receptor-mediated role for oestrogens in modulating the efficacy of input-output properties of CA1 neurones produced by HFS during a critical period in development.

Aging↗
PubMed2006

Mucosal stimulation activates secretomotor neurons via long myenteric pathways in guinea pig ileum.

This study examined whether mucosal stimulation activates long secretomotor neural reflexes and, if so, how they are organized. The submucosa of in vitro full thickness guinea pig ileal preparations was exposed in the distal portion and intracellular recordings were obtained from electrophysiologically identified secretomotor neurons. Axons in the intact mucosa of the oral segment were stimulated by a large bipolar stimulating electrode. In control preparations, a single stimulus pulse evoked a fast excitatory postsynaptic potential (EPSP) in 86% of neurons located 0.7-1.0 cm anal to the stimulus site. A stimulus train evoked multiple fast EPSPs, but slow EPSPs were not observed. To examine whether mucosal stimulation specifically activated mucosal sensory nerve terminals, the mucosa/submucosa was severed from the underlying layers and repositioned. In these preparations, fast EPSPs could not be elicited in 89% of cells. Superfusion with phorbol dibutyrate enhanced excitability of sensory neurons and pressure-pulse application of serotonin to the mucosa increased the fast EPSPs evoked by mucosal stimulation, providing further evidence that sensory neurons were involved. To determine whether these reflexes projected through the myenteric plexus, this plexus was surgically lesioned between the stimulus site and the impaled neuron. No fast EPSPs were recorded in these preparations following mucosal stimulation whereas lesioning the submucosal plexus had no effect. These results demonstrate that mucosal stimulation triggers a long myenteric pathway that activates submucosal secretomotor neurons. This pathway projects in parallel with motor and vasodilator reflexes, and this common pathway may enable coordination of intestinal secretion, blood flow, and motility.

Action Potentials↗
PubMed2000

Tetrodotoxin-sensitive persistent current boosts the depolarization of retinal amacrine cells in goldfish.

To light illumination retinal amacrine cells respond with graded depolarization accompanied by a spike discharge. It has been assumed that the graded depolarization is produced solely by the excitatory synaptic inputs from bipolar cells. Here we demonstrate that a tetrodotoxin (TTX)-sensitive persistent current also contributes to the graded depolarization. This current was isolated in amacrine cells of the goldfish retinal slice preparations by the whole-cell patch clamp technique. The activation threshold of the persistent current was about -50 mV, approximately 10 mV more positive than the membrane potential in the dark. Therefore, it is highly likely that the TTX-sensitive persistent current is a booster of the excitatory postsynaptic potential in amacrine cells.

Action Potentials↗
PubMed2005

Intracellular analysis of reflex pathways underlying the stumbling corrective reaction during fictive locomotion in the cat.

In cat and humans, contact between an obstacle and the dorsum of the foot evokes the stumbling corrective reaction (reflex) that lifts the foot to avoid falling. This reflex can also be evoked by short trains of stimuli to the cutaneous superficial peroneal (SP) nerve in decerebrate cats during the flexion phase of fictive locomotion. Here we examine intracellular events in hindlimb motoneurons accompanying stumbling correction. SP stimulation delivered during the flexion phase excites knee flexor motoneurons at short latency [minimum excitatory postsynaptic potential (EPSP) latency 1.8 ms; mean 2.7 ms]. Although a similar short latency excitation occurs in ankle extensors (mean latency, 2.8 ms), recruitment is delayed until successive shocks in the stimulus train overcome the locomotor-related hyperpolarization of ankle extensors. In ankle flexor motoneurons, SP stimulation evokes an inhibition (mean latency, 2.7 ms) that briefly reduces or stops their firing during the flexion phase. There is a phase-dependent modulation of SP-evoked EPSP amplitude as well as latency during locomotion. However, the more obvious change in SP reflex pathways with the onset of fictive locomotion is the reduced inhibition of ankle extensor motoneurons and the increased inhibition of ankle flexors. These results show that the characteristic pattern of hindlimb motoneuron activation during SP nerve-evoked stumbling correction results from 1) di- and trisynaptic excitation of knee flexor and ankle extensor motoneurons; 2) increased inhibitory postsynaptic potentials in ankle flexors and a suppression of inhibition in extensors, 3) sculpting of the short-latency SP postsynaptic effects by motoneuron membrane potential, and 4) longer latency excitatory effects that are likely evoked by lumbar interneurons involved in the generation of fictive locomotion.

Animals↗
PubMed2005

Recurrent networks of submucous neurons controlling intestinal secretion: a modeling study.

Secretomotor neurons, immunoreactive for vasoactive intestinal peptide (VIP), are important in controlling chloride secretion in the small intestine. These neurons form functional synapses with other submucosal VIP neurons and transmit via slow excitatory postsynaptic potentials (EPSPs). Thus they form a recurrent network with positive feedback. Intrinsic sensory neurons within the submucosa are also likely to form recurrent networks with positive feedback, provide substantial output to VIP neurons, and receive input from VIP neurons. If positive feedback within recurrent networks is sufficiently large, then neurons in the network respond to even small stimuli by firing at their maximum possible rate, even after the stimulus is removed. However, it is not clear whether such a mechanism operates within the recurrent networks of submucous neurons. We investigated this question by performing computer simulations of realistic models of VIP and intrinsic sensory neuron networks. In the expected range of electrophysiological properties, we found that activity in the VIP neuron network decayed slowly after cessation of a stimulus, indicating that positive feedback is not strong enough to support the uncontrolled firing state. The addition of intrinsic sensory neurons produced a low stable firing rate consistent with the common finding that basal secretory activity is, in part, neurogenic. Changing electrophysiological properties enables these recurrent networks to support the uncontrolled firing state, which may have implications with hypersecretion in the presence of enterotoxins such as cholera-toxin.

Action Potentials↗
PubMed2006

Dopamine presynaptically depresses fast inhibitory synaptic transmission via D4 receptor-protein kinase A pathway in the rat dorsolateral septal nucleus.

The lateral septal nucleus receives a diffuse dopaminergic input originating from the ventral tegmental area of the brain stem. We examined whether dopamine (DA) modulates synaptic transmission in the slice preparation of the rat dorsolateral septal nucleus (DLSN). Bath application (10-15 min) of DA (30 muM) markedly depressed the amplitude of fast and slow inhibitory postsynaptic potentials (IPSPs) in DLSN neurons, while it produced only a minor depression of the amplitude of excitatory postsynaptic potentials (EPSPs) obtained in the presence of bicuculline. DA (30 muM) depressed the monosynaptic fast IPSP to approximately 50% of control, but did not depress the inward current (I(GABA)) induced by exogenous gamma-aminobutyric acid (GABA). DA decreased the frequency of miniature fast IPSPs (m-fIPSPs) without significantly changing their amplitude. PD 168077, a selective D4 receptor agonist, depressed the fast and slow IPSPs but not the EPSP and decreased the frequency of m-fIPSPs. Both DA and PD 168077 increased the paired-pulse ratio of the monosynaptic fast IPSP. The inhibitory effect of DA on the fast IPSP was significantly attenuated by L-741,742, an antagonist at D4 receptors, but not by SCH 23390 and sulpiride, a D1-like and a D2-like receptor antagonist, respectively. N-ethylmaleimide, a blocker of pertussis toxin (PTX)-sensitive G protein (G(i/o)), attenuated the DA-induced depression of the fast IPSP. N-[2-((p-bromocinnamyl) amino)ethyl]-5-isoquinoline sulfonamide, a protein kinase A (PKA) inhibitor, attenuated the DA-induced depression of the fast IPSP. These results suggest that DA inhibits spontaneous and evoked release of GABA via the D4 receptor-G(i)-protein-PKA system in DLSN neurons.

Animals↗
PubMed2003

Changes in the readily releasable pool of transmitter and in efficacy of release induced by high-frequency firing at Aplysia sensorimotor synapses in culture.

Synaptic transmission at the sensory neuron-motor neuron synapses of Aplysia, like transmission at many synapses of both vertebrates and invertebrates, is increased after a short burst of high-frequency stimulation (HFS), a phenomenon known as posttetanic potentiation (PTP). PTP is generally attributable to an increase in transmitter release from presynaptic neurons. We investigated whether changes in the readily releasable pool of transmitter (RRP) contribute to the potentiation that follows HFS. We compared the changes in excitatory postsynaptic potentials (EPSPs) evoked with action potentials to changes in the RRP as estimated from the asynchronous transmitter release elicited by a hypertonic solution. The changes in the EPSP were correlated with changes in the RRP, but the changes matched quantitatively only at connections whose initial synaptic strength was greater than the median for all experiments. At weaker connections, the increase in the RRP was insufficient to account for PTP. Weaker connections initially released a smaller fraction of the RRP with each EPSP than stronger ones, and this fraction increased at weaker connections after HFS. Moreover, the initial transmitter release in response to the hypertonic solution was accelerated after HFS, indicating that the increase in the efficacy of release was not restricted to excitation-secretion coupling. Modulation of the RRP and of the efficacy of release thus both contribute to the enhancement of transmitter release by HFS.

Action Potentials↗
PubMed1988

Release of neuroactive substances: homocysteic acid as an endogenous agonist of the NMDA receptor.

Sulfur containing amino acids such as homocysteic acid (HCA), cysteinsulfinic acid, homocysteinsulfinic acid are released by depolarization of slices from various rat brain regions in a Ca++-dependent manner. L-HCA excites caudate neurons through their N-methyl-D-aspartic acid (NMDA) receptor and potentiates their cortically evoked excitatory postsynaptic potentials. 35S-methionine can label the releasable pool of HCA, and thus appears as a precursor of HCA. Thus HCA is a transmitter candidate which acts predominantly on the NMDA receptor.

Animals↗
PubMed1988

The role of calcium in short-term potentiation in the rat hippocampal slice.

Short-term potentiation of extracellular field excitatory postsynaptic potentials (EPSP's) was investigated in the stratum radiatum of CA1 of the rat hippocampal slice in vitro. A presynaptic tetanus consisting of a single train of stimuli at 250 Hz evoked short-term potentiation (STP), but not long-term potentiation (LTP) of small amplitude, just suprathreshold, EPSP's in a medium containing 2 mM Ca and 2 mM Mg. Increasing the number of stimuli in the tetanus enhanced the initial amplitude of the STP to a maximum of 40-70% with 30-40 stimuli, and enhanced the decay time constant of STP to a maximum of 60-80 s. Increasing the Ca influx by raising external Ca, lowering Mg or adding the agent 4-aminopyridine caused a large increase in the initial amplitude of STP but only a very slight increase in the decay time of STP. LTP was frequently evoked in high Ca/Mg ratios of 2.0 or 4.0, but not in 1.0 or 0.5.

Action Potentials↗
PubMed1988

Selective long-term potentiation in the pyriform cortex.

Electrical stimulation of the olfactory bulb (OB) produces an evoked potential in the pyriform cortex (PC) characterized by an initial surface-negative wave (period 1) representing activation of PC pyramidal cells via the lateral olfactory tract, followed by a surface-positive wave (period 2) which is temporally associated with recurrent and feed-forward inhibition. The experiment reported here examined the changes that occur in the PC evoked potential following a pattern of stimulation that has been found to produce short- and long-term potentiation (LTP) in other areas of the forebrain. Male Long-Evans rats with electrodes in the OB and PC were divided into two groups. LTP animals received high-frequency stimulation of the OB (30 trains of 10 pulses each at a frequency of 100 Hz). Control animals received the same number of pulses at a lower frequency (1 Hz). This procedure was repeated 6 times at 2-day intervals. Neither high- nor low-frequency stimulation altered period 1 of the PC evoked potential, indicating that synaptic input arriving via the lateral olfactory tract was unaffected. However, LTP animals exhibited a marked increase in the amplitude and duration of period 2 which appeared to reflect two separate processes: a short-term change that peaked within 30 min of the trains; and a long-term change that accumulated across the 6 treatments. LTP of period 2 persisted in latent form for at least 32 days after the last treatment. Control animals exhibited only small changes that were attributed to the paired-pulse stimulation used for testing rather than the 1 Hz Control trains. These results suggest that repeated high-frequency stimulation of the OB causes a persistent alteration in the way information is processed within the PC. The form of LTP demonstrated here is markedly different from that found in the hippocampal formation, where potentiation of the monosynaptic excitatory postsynaptic potential is a prominent effect. The functional significance of this change cannot be determined with certainty from the present experiment, but available evidence suggests that it represents an enhancement of inhibitory processes within the PC.

Animals↗
PubMed1990

Dendritic action potentials activated by NMDA receptor-mediated EPSPs in CA1 hippocampal pyramidal cells.

Intradendritic recordings were obtained in rat CA1 hippocampal pyramidal cells. Repetitive stimulation produced substantial short-term potentiation of the dendritic excitatory postsynaptic potential (EPSP) which was partly attributable to activation of n-methyl-D-aspartate receptors. Accompanying the potentiated synaptic response were Na(+)-mediated spikes which appeared to originate at multiple sites in the dendritic arbor. These discrete dendritic action potentials are rarely distinguishable in somatic recordings, but may contribute to the subthreshold response at the pyramidal cell body. In addition, dendritic spikes may interact with other voltage-dependent dendritic conductances.

2-Amino-5-phosphonovalerate↗
PubMed1991

Synaptic potentiation in the hippocampal CA1 region induced by application of N-methyl-D-aspartate.

The effect of local pressure application of N-methyl-D-aspartate (NMDA) in the synaptic layer of CA1 pyramidal cells was investigated in the guinea pig hippocampal slice preparation using extracellular recording technique. Application of NMDA produced a transient depression and a subsequent 30-60 min potentiation of the field excitatory postsynaptic potential (EPSP) seen as an increase of the initial slope and amplitude of the EPSP. The increase in amplitude was consistently greater than that of the initial slope. Prior tetanization that caused saturation of long-term potentiation prevented the generation of an NMDA-induced potentiation of the initial slope for more than 1-2 h, but not the generation of an increase of the amplitude.

Animals↗
PubMed1982

Metoclopramide mimics a D-1 type of dopamine action in rabbit superior cervical ganglion.

Metoclopramide (MCP) in a sufficiently high concentration (100 microM) induced a large and persisting potentiation of slow-excitatory postsynaptic potentials (s-epsp) and slow-inhibitory postsynaptic potentials (s-epsp) but depressed in fast epsp. This modulatory action of metoclopramide was markedly suppressed by (+)-butaclamol (7 microM) and, to a lesser extent, by spiroperidol (2.5-4 microM). Metoclopramide also possessed weak anti-acetylcholinesterase activity(I50% = 245 microM; measured by Dr N. Inestrosa), but this was shown not to account for the potentiating actions of metoclopramide. Thus, although metoclopramide is a D-2 antagonist, it appears to mimic the D-1 action of dopamine in modulating the slow psps.

Action Potentials↗
PubMed1991

Intracellular recordings from canine intracardiac ganglion cells.

Stable transmembrane potentials were recorded from 60 canine intracardiac ganglion cells taken from 10 dogs, which had intact synaptic connections: mean resting membrane potential, input resistance and time constant were 61.5 mV, 70 M omega and 3.3 ms. Action potentials could be evoked by intrasomal current injection and by orthodromic and antidromic stimulation of interganglionic nerves. Orthodromic action potentials were initiated by excitatory postsynaptic potentials and mediated by nicotinic receptors. All action potentials could be blocked by tetrodotoxin. Intracellular labeling revealed large cell bodies and long dendritic and axonal processes. Thus, the functional and anatomical properties of canine cardiac ganglion cells and their synaptic connections can be elucidated using this preparation.

Action Potentials↗
PubMed1986

Prenatal protein malnutrition affects synaptic potentiation in the dentate gyrus of rats in adulthood.

Long-term potentiation (LTP) was studied in the dentate gyrus of anesthetized normal and prenatally protein malnourished rats in adulthood. LTP was initiated by high-frequency stimulation of the perforant path. Potentiation of both population excitatory postsynaptic potential (EPSP) slope and population spike was studied at various times after conditioning out to 5 h. The results indicate that prenatal protein malnutrition has a differential effect on LTP. Although potentiation of the population spike was relatively unaffected, prenatal protein malnutrition did lead to a significant reduction in potentiation of the population EPSP. Several possibilities are proposed as to the cause of the differential effect.

Animals↗