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PubMed1993

Interactions between excitatory amino acids and tachykinins in the rat spinal dorsal horn.

Whole-cell patch-clamp technique of freshly isolated rat spinal dorsal horn (DH) neurons, intracellular recording from DH neurons in a slice preparation, and high performance liquid chromatography with fluorimetric detection of release of endogenous glutamate and aspartate from spinal cord slice following activation of primary afferent fibers were employed to investigate interactions between excitatory amino acids (EAA) and tachykinins [substance P (SP) and neurokinin A (NKA)]. Potentiation of N-methyl-D-aspartate (NMDA)-, quisqualate (QA)- and alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA)-, but not kainate-induced currents by SP and NKA was found. Spantide II, a claimed novel nonselective tachykinin antagonist, effectively blocked the SP (2 nM)-induced potentiation of the responses of DH neurons to NMDA. In the presence of glycine (0.1 microM), the SP-evoked increase of the NMDA-induced current was prevented. However, 7-chlorokynurenic acid (2 microM), a competitive antagonist at the glycine allosteric site of the NMDA receptor, led to the reestablishment of the SP effect. Brief high frequency electrical stimulation of primary afferent fibers produced a long-lasting potentiation of presumed monosynaptic and polysynaptic excitatory postsynaptic potentials and sustained enhanced release of endogenous glutamate (218.3 +/- 66.1%) and aspartate (286.3 +/- 58.0%). Possible functional implications of the observed phenomena are discussed in relation to transmission and integration of sensory information, including pain.

Afferent Pathways↗
PubMed2002

Excitatory action of lead on rat sympathetic preganglionic neurons in vitro and in vivo.

Lead exposure elicited an increase in blood pressure and was considered to be a cardiovascular risk factor. The involvements of sympathetic nervous system and circulating catecholamines have been implicated in lead-induced hypertension. This study examined the effects of PbCl(2) on sympathetic preganglionic neurons (SPNs) in vitro and in vivo. In vitro electrophysiological study showed that superfusion of a low concentration (5 microM) of PbCl(2), which had no effects on membrane potential and spontaneous discharge rate, enhanced excitatory postsynaptic potentials (EPSPs) in some of the SPNs examined but inhibited inhibitory postsynaptic potentials (IPSPs) in other SPNs tested. A higher concentration (50 microM) of PbCl(2) inhibited both EPSPs and IPSPs in all SPNs examined. In vivo study showed that intrathecal injection of PbCl(2) (10 and 100 nmol) via an implanted cannula to the T7-T9 segments of urethane-anesthetized rats increased both the heart rate and mean arterial pressure. The pressor and tachycardic responses of intrathecal PbCl(2) (100 nmol) were attenuated by pretreatment with intravenous administration of hexamethonium (10 mg/kg) or intrathecal AP-5 (DL-2-amino-5-phosphonovaleric acid, 100 nmol), but were not significantly antagonized by prior intrathecal administration of CNQX (6-cyano-7-nitroquinoxaline-2,3-dione, 100 nmol). Taken together, these results demonstrated that lead may exert a stimulatory effect on SPNs, which may result from the enhancement of EPSPs and inhibition of IPSPs by low concentrations of lead.

2-Amino-5-phosphonovalerate↗
PubMed1998

Long-term changes of ionotropic glutamate and GABA receptors after unilateral permanent focal cerebral ischemia in the mouse brain.

Long-term hyperexcitability was found after unilateral, permanent middle cerebral artery occlusion in exofocal neocortical areas of the adult mouse [Mittmann et al. (1998) Neuroscience 85, 15-27]. The aim of the present study was to test the hypothesis in an identical paradigm of ischemia. whether alterations in the densities of both excitatory and inhibitory amino acid receptors may underlie these pathophysiological changes. Alterations in densities of [3H]dizocilpine, [3H]D,L-amino-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid, [3H]kainate and [3H]muscimol binding sites were demonstrated with quantitative in vitro receptor autoradiography. All binding sites were severely reduced in the core of the ischemic lesion. A completely different reaction was found in the exofocal, histologically inconspicuous parts of the somatosensory cortex and the more remote neocortical areas of both hemispheres. The [3H]muscimol binding sites were significantly reduced four weeks after ischemia in the motor cortex, hindlimb representation area and exofocal parts of the primary and secondary somatosensory cortices of both hemispheres. The focus of the reduction in [3H]muscimol binding sites was found in lower layer V and upper layer VI. Contrastingly, the densities of [3H]dizocilpine binding sites were found to be increased in these areas, whereas those of [3H]D,L-alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid and [3H]kainate binding sites did not show significant changes. The [3H]dizocilpine binding site density increased predominantly in layers III and IV. All binding sites were also reduced in the retrogradely reacting, gliotic part of the ipsilateral ventroposterior thalamic nucleus, whereas the [3H]D,L-alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid binding sites were increased in the surround of the ipsilateral nucleus and no changes in binding sites were seen in the whole contralateral nucleus. We conclude that permanent local ischemia leads to a long-term and widespread impairment of the normal balance between binding sites of excitatory and inhibitory neurotransmitter receptors in neocortical areas far away from the focus of the post-ischemic tissue damage. The imbalance comprises an up-regulation of the [3H]dizocilpine binding sites in the ion channels of N-methyl-D-aspartate receptors and a down-regulation of [3H]muscimol binding sites of the GABA(A) receptors in the ipsi- and contralateral neocortex. These changes at the receptor level explain the previously observed hyperexcitability with the appearance of epileptiform field potentials and the long duration of excitatory postsynaptic potentials four weeks after ischemia.

Animals↗
PubMed2000

Three types of putative presympathetic neurons in the rostral ventrolateral medulla studied with rat brainstem-spinal cord preparation.

To study the electrophysiological properties of presympathetic neurons in the rostral ventrolateral medulla (RVLM), intracellular recordings were performed by the whole-cell patch-clamp technique. We utilized the neonatal rat brainstem-spinal cord preparation, in which the sympathetic neuronal network is thought to be preserved, unlike in slice preparation. In response to stimulation in the ipsilateral Th2 spinal segment including intermediolateral cell column (IML), 33 of 151 non-respiratory RVLM neurons showed antidromic action potentials with a constant latency of 45 ms, and can be considered as presympathetic neurons. We classified and characterized the RVLM presympathetic neurons into three types: 'regularly firing neurons (n=7)', which showed ramp depolarization and frequent action potentials (4.2+/-0.9 spikes/s) with rare excitatory postsynaptic potentials (EPSPs); 'irregularly firing neurons (n=21)', which exhibited many EPSPs that modulated the firing rate; and 'silent-type neurons (n=5)', which discharged action potentials only during current-induced depolarization. Lucifer-Yellow staining showed that the irregularly firing neurons were significantly larger and had more dendrites than the regularly firing neurons. All regularly firing neurons retained their discharges during low-Ca2+ -high-Mg2+ superfusion that blocks synaptic input, whereas the discharges in 11 of 16 irregularly firing neurons were abolished, suggesting that the regularly firing neurons discharged independently of synaptic input. Seven of 31 RVLM neurons were hyperpolarized by stimulation of vagal afferent nerves. In summary, three types of RVLM presympathetic neurons were characterized by the patch-clamp technique in the brainstem-spinal cord preparation, in which the connection was preserved from vagal afferent to the Th2 spinal segment through the RVLM. Since antidromic action potentials were demonstrated by stimulation in the Th2 spinal segment in 33 neurons of all three types, all types of RVLM neurons constitute a part of the sympathetic neuronal network.

Action Potentials↗
PubMed1992

Presynaptic histamine H1 and H3 receptors modulate sympathetic ganglionic synaptic transmission in the guinea-pig.

1. To study the effects of histamine on the efficacy of sympathetic ganglionic synaptic transmission, extracellular recordings of the postganglionic compound action potential (CAP) and intracellular recordings of excitatory postsynaptic potentials (EPSPs) elicited by preganglionic electrical stimulation were obtained from isolated guinea-pig superior cervical ganglia (SCG). 2. In different preparations, superfusion with histamine (0.1-100 microM) either potentiated or depressed the postganglionic CAP elicited by electrical stimulation of the cervical sympathetic trunk (0.2-3.0 Hz). The direction of response produced by histamine did not depend on stimulation frequency or histamine concentration; potentiation and depression both showed concentration dependence over the range of histamine concentrations tested. 3. Experiments employing a variety of histamine receptor agonists or antagonists revealed that histamine-induced potentiation of the postganglionic CAP could be attributed to histamine H1 receptor activation, and depression to H3 receptor activation. 4. Histamine similarly potentiated or depressed the intracellularly recorded EPSP. However, these opposite effects occurred at different synapses. In agreement with the studies on the postganglionic CAP, histamine H1 antagonists prevented histamine-induced potentiation of the EPSP and H3 receptor antagonists prevented histamine-induced depression. 5. Direct quantal analyses of histamine-induced synaptic potentiation and depression were implemented to determine the pre- and postsynaptic components of these effects. Quantal size was estimated by measuring the amplitude of spontaneous miniature EPSP amplitudes. Histamine-induced potentiation and depression of the evoked EPSP were found to be accompanied by increased or decreased quantal content respectively, and unchanged quantal size, providing evidence that presynaptic mechanisms were involved in mediating both effects. 6. Some guinea-pigs were actively sensitized to ovalbumin. Subsequent exposure of the isolated SCG from these animals to the sensitizing antigen produced changes in the EPSP amplitude that correlated significantly to the response produced by exogenously applied histamine at the same synapse. 7. The correspondence between the effects of specific antigen challenge and exogenous histamine on evoked EPSPs at a synapse provides evidence that endogenous histamine released during an immunological response to antigen challenge can activate histamine H1 and H3 receptors to modulate synaptic efficacy in sympathetic ganglia.

Action Potentials↗
PubMed1983

Posttetanic potentiation of group Ia EPSPs: possible mechanisms for differential distribution among medial gastrocnemius motoneurons.

We have reinvestigated the phenomenon of posttetanic potentiation (PTP) of group Ia monosynaptic excitatory postsynaptic potentials (EPSPs) in medial gastrocnemius (MG) alpha-motoneurons of pentobarbital-anesthetized cats. The results generally confirm earlier reports by Lüscher and colleagues (43, 44) of a negative correlation between the maximum percentage potentiation of Ia EPSP amplitude (Pmax) and 1) the mean amplitude of the pretetanic control EPSP in the same cell and 2) the input resistance of the postsynaptic motoneuron. These negative correlations, which we will refer to as "differential distribution of PTP" within the MG motor pool, were less strong in the present work than reported by Lüscher et al. (43, 44). We also found a relatively strong negative correlation between posttetanic EPSP depression, assessed by the amplitude of the first posttetanic EPSP, and the level of Pmax subsequently attained. We found no evidence that posttetanic depression is caused by failure of presynaptic action potentials. We investigated a second type of depression, referred to as "specific" synaptic depression, in which the second EPSP of paired responses (interval 250 ms) is, on average, smaller in peak amplitude than the first EPSP. This phenomenon appears to reflect decreases in the probability of transmitter release from previously activated synapses. Specific synaptic depression was consistently increased when paired responses were conditioned by a high-frequency tetanus. This is most easily explained by postulating that PTP results, at least in part, from an increase in the statistical probability of transmitter liberation from group Ia synapses that are activated (i.e., presumably invaded by action potentials) both before and after afferent tetanization. On the basis of the present results and other available evidence, we conclude that the differential distribution of PTP can be explained by two main factors: 1) the nonlinear relation between conductance and voltage changes inherent in all chemical synapses and 2) systematic variations in the properties of group Ia synapses that innervated different motoneurons, which remain to be clarified.

Animals↗
PubMed1990

Characteristics of background and evoked discharges of multireceptive neurons in lumbar spinal cord of cat.

1. Intracellular recordings were made in laminae III-V of the dorsal horn of the cat spinal cord from a group of multireceptive neurons that exhibited similar physiological properties. The background discharge contained irregular and occasional clusters of action potentials, each arising from a complex excitatory postsynaptic potential (EPSP); brushing elicited more frequent clusters containing more action potentials, whereas noxious heating elicited more regular firing, with action potentials arising singly. The distribution of interspike intervals (ISIs) was measured for the background and heat-evoked discharges and revealed characteristic differences in pattern between the two states. 2. Statistical tests were applied to the point process of times of occurrence of spikes within a discharge to establish stationary, to identify renewal instants, and to describe the process between renewal instants. In each case, the statistical description of the discharge was related to the physiological state of the neuron as revealed by recording of synaptic potentials and analysis of the different activating inputs. 3. Background discharge was stationary, and spikes occurred singly or occasionally in clusters. The data were therefore analyzed as a series of "bursts," where a burst could be made up of one or more spikes. Examination of the pattern of serial dependence led to the conclusion that the point process renewed itself after each burst. This, together with the distribution of the intervals between bursts, suggested that bursts were triggered by single, distinct events, which occurred randomly at a slightly and randomly varying average rate. The variation in the number of spikes in a burst suggested random variation in the strength of the physiological trigger. 4. Clusters of action potentials arising from a complex EPSP could be produced by simultaneous stimulation of a number of fast-conducting A beta fibers in the periphery and gentle mechanical stimulation, whereas stimulation of slow C fibers and noxious heat evoked discrete EPSPs from which action potentials arose singly. It was, therefore, concluded that background activity was, at least in part, the result of random activity in a randomly varying number of A beta primary afferent fibers, which could arise from operative procedures. 5. The discharge evoked by heat was stationary, and the absence of serial dependence established that the point process renewed itself after every spike and was, therefore, a simple renewal process. The distribution of the ISIs suggested that each spike was triggered by a randomly occurring physiological event.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed2002

Serotonergic modulation of nonspiking local interneurones in the terminal abdominal ganglion of the crayfish.

The modulatory effect of serotonin on local circuit neurones forming the uropod motor control system of the crayfish Procambarus clarkii Girard was analysed electrophysiologically. Bath application of 10 micro mol l(-1) serotonin caused a decrease in the tonic spike activity of the exopodite reductor motor neurone. The inhibitory effect of serotonin on the motor neurone was dose-dependent and its spike discharge was completely suppressed for long periods by 1 mmol l(-1) serotonin perfusion. Nonspiking local interneurones in the terminal abdominal ganglion showed either a membrane depolarization (N=6) or hyperpolarization (N=9) of 10-30 mV in amplitude when 100 micro mol l(-1) serotonin was perfused for 3-5 min. By contrast, spiking local interneurones and intersegmental ascending interneurones showed no observable excitatory responses to the perfusion of serotonin but instead some showed a small membrane hyperpolarization of 2-5 mV. These results indicate that the nonspiking interneurones could contribute substantially to the level of tonic excitation of the uropod motor neurones. Sensory stimulation elicited depolarizing or hyperpolarizing potentials in the nonspiking interneurones and excitatory postsynaptic potentials (EPSPs) and spikes in the spiking interneurones. The sensory responses of spiking interneurones increased during bath application of serotonin and were reduced after 20-30 min of washing with normal saline. In the nonspiking interneurones, the amplitude of both depolarizing and hyperpolarizing potentials increased without any direct correlation with the serotonin-mediated potential change. This effect of serotonin was long-lasting and continued to enhance the responses of the nonspiking interneurones after washing. This postserotonin enhancement persisted for over 1 h.

Abdomen↗
PubMed1990

Monosynaptic connections between LPa7-LPa3 and LPa9-LPa3 neurons in the central nervous system of helix pomatia. Electrophysiological characteristics, monosynaptic plasticity, neurotransmission.

Monosynaptic inputs from LPa7 and LPa9 cells onto the LPa3 neuron were investigated in the isolated central neurons system (CNS) of snail Helix by means of simultaneous intracellular recording from pre- and post-synaptic neurons and electrical stimulation of the presynaptic neuron through the recording microelectrode. Each action potential of either presynaptic cell produced excitatory postsynaptic potential (EPSP) in the follower one with an amplitude of 0.6-5 mV. Repetitive suprathreshold stimuli, applied at frequencies higher than 1 per 5 min, induced depression of the monosynaptic response. The cholinergic antagonists, atropine and d-tubocurarine (10(-6)M- 10(-4)M), dose-dependently inhibited monosynaptic EPSP from either presynaptic cell. Cholinergic transmission is suggested between LPa7-LPa3 and LPa9-LPa3 cells.

Acetylcholine↗
PubMed1994

Conserved spatial learning in cooled rats in spite of slowing of dentate field potentials.

Behaviorally induced brain temperature changes have significant effects on field potentials recorded in the hippocampal formation. All components of the field potential are slowed during cooling. Field excitatory postsynaptic potentials (f-EPSPs) are often reduced, while the population spike is increased in this state. To investigate whether such synaptic alterations affect hippocampus-dependent learning, we have compared the effects of reduced brain temperature on dentate field potentials and spatial learning in a Morris water maze. Rats were implanted with thermistors in the brain. A subset of the rats received electrodes for field potential recording in the perforant path-granule cell synapses of the dentate gyrus. After recovery, the rats were cooled by swimming in a pool of water. This invariably led to a brain temperature reduction of several degrees centigrade and a delay of the extracellular response. In addition, the field potential changed as described above. The effect of these changes on spatial learning in a second pool, the water maze, was determined by first cooling and then reheating each rat to a given level of brain temperature prior to each spatial training session. In spite of marked changes in dentate field potentials, all rats trained at brain temperatures above 30 degrees C learned to find the submerged platform similarly well. The speed of acquisition and the final precision of search behavior were also similar in these rats. Only rats that had been cooled below 30 degrees C failed to locate the hidden target. These animals also showed clear evidence of motor impairment.(ABSTRACT TRUNCATED AT 250 WORDS)

Action Potentials↗
PubMedDate not supplied

[Spontaneous potentiation of the focal potentials of field CA1 in rat hippocampal slices surviving long term in the absence of electrical stimulation].

Changes of synaptic efficiency after the long-term deprivation of afferent inputs were studied in the pathway from Schaffer collaterals to CA1 neurons in rat hippocampal slices. The long-term deprivation was obtained by a cessation of stimulation of the tested input for up to 4 hours short series of stimuli (5-10 tests) being applied every hour. Control afferent inputs were stimulated during all the experiment with 0.05 cps pulses. Evoked field potentials, i.e. population spikes (PS) and excitatory postsynaptic potentials (pEPSP) were recorded. The long-term absence of stimulation resulted in an enhancement (in comparison with the control, p < 0.001) of the PS amplitude up to 208% of the base level. This phenomenon was specific to deprived inputs and had the properties of the EPSP-Spike-potentiation, but the paired-pulse test showed rather an increase than a decrease of feedback inhibition. It is suggested that common mechanisms underly "deprivation-induced potentiation" and the late phase of the post-tetanic long-term potentiation.

Animals↗
PubMed2002

Synaptic connections and small circuits involving excitatory and inhibitory neurons in layers 2-5 of adult rat and cat neocortex: triple intracellular recordings and biocytin labelling in vitro.

Dual and triple intracellular recordings with biocytin labelling in slices of adult neocortex explored small circuits of synaptically connected neurons. 679 paired recordings in rat and 319 in cat yielded 135 and 42 excitatory postsynaptic potentials (EPSPs) and 37 and 26 inhibitory postsynaptic potentials (IPSPs), respectively. Patterns of connectivity and synaptic properties were similar in the two species, although differences of scale and in the range of morphologies were observed. Excitatory 'forward' projections from layer 4 to 3, like those from layer 3 to 5, targeted pyramidal cells and a small proportion of interneurons, while excitatory 'back' projections from layer 3 to 4 selected interneurons, including parvalbumin immuno-positive basket cells. Layer 4 interneurons that inhibited layer 3 pyramidal cells included both basket cells and dendrite-targeting cells. Large interneurons, resembling cells previously described as large basket cells, in layers 4 and 3 (cat), with long myelinated horizontal axon collaterals received frequent excitatory inputs from both layers. A very high rate of connectivity was observed between pairs of interneurons, often with quite different morphologies, and the resultant IPSPs, like the EPSPs recorded in interneurons, were brief compared with those recorded in pyramidal and spiny stellate cells.

Animals↗
PubMed2003

Presynaptic group I metabotropic glutamate receptors modulate synaptic transmission in the rat superior colliculus via 4-AP sensitive K(+) channels.

1. Group I metabotropic glutamate receptors (mGluRs) are thought to be important modulators of neuronal function in the superior colliculus (SC). Here, we investigated the pharmacology and signalling mechanisms underlying group I mGluR-mediated inhibition of neuronal excitability and synaptic transmission in the rat SC slice. 2. The group I agonist (RS)-3,5-dihydroxyphenylglycine (DHPG) potently depressed synaptically evoked excitatory postsynaptic potentials (EPSPs), currents (EPSCs), and action potentials in a dose-dependent manner (IC50: 6.3 microm). This was strongly reduced by the broad-spectrum antagonist (+)-alpha-methyl-4-carboxyphenylglycine (MCPG, 1 mm, approximately 95% reduction), by the mGluR1 antagonist LY367385 (100 microm, approximately 80% reduction) but not by the mGluR5 antagonist 6-methyl-2-(phenylethynyl)-pyridine (MPEP, 1-100 microm). 3. The putative mGluR5-specific agonist (RS)-2-chloro-5-hydroxyphenylglycine (CHPG, 500 microm) also inhibited EPSPs. Interestingly, CHPG's actions were not blocked by MPEP, but LY367385 (100 microm) reduced the effect of CHPG by 50%. 4. Inhibition induced by DHPG was independent of phospholipase C (PLC)/protein kinase C pathways, and did not require intact intracellular Ca2+ stores. It was not abolished but enhanced by the GABAA antagonist bicuculline (5 microm), suggesting that DHPG's action was not due to facilitated inhibition or changes in neuronal network activity. 5. The K+ channel antagonist 4-aminopyridine (4-AP, 50-100 microm) converted the inhibitory effect of DHPG into facilitation. Paired-pulse depression was strongly reduced by DHPG, an effect that was also prevented by 4-AP. 6. Our data indicate that group I agonists regulate transmitter release, presumably via an autoreceptor in the SC. This receptor may be involved in adaptation to repetitive stimulation via a non-PLC mediated pathway.

4-Aminopyridine↗
PubMed2003

Impaired long-term potentiation in obese zucker rats: possible involvement of presynaptic mechanism.

Electrophysiological investigation of basal synaptic transmission and synaptic plasticity in the CA1 region of the hippocampus was carried out in anesthetized obese Zucker rats (OZR). Comparison of the input/output curves of basal field excitatory postsynaptic potential indicates that these are similar in both the OZR and its lean counterpart suggesting that basal synaptic transmission is intact in the OZR. However, high frequency stimulation evokes long-term potentiation (LTP) in the lean rat but not in the OZR. Since post-tetanic potentiation and paired pulse facilitation, forms of short-term potentiation of presynaptic origin, are also severely impaired in the OZR, the results imply that impairment of CA1 hippocampal LTP in these obese rats may be due, in part, to impaired presynaptic function. The results emphasize the potential deleterious effect of obesity on learning and memory functions of the CNS.

Animals↗
PubMed1999

Developmental exposure to a commercial PCB mixture (Aroclor 1254) produces a persistent impairment in long-term potentiation in the rat dentate gyrus in vivo.

Developmental exposure to polycholorinated biphenyls (PCBs) has been associated with cognitive deficits in humans and laboratory animals. The present study sought to examine synaptic plasticity in the hippocampus, a brain region critical for some types of memory function, in animals exposed to PCBs early in development. Pregnant Long-Evans rats were administered either corn oil (control) or 6 mg/kg/day of a commercial PCB mixture, Aroclor 1254 (A1254) by gavage from gestational day (GD) 6 until pups were weaned on postnatal day (PND) 21. In adult male offspring (3-6 months of age), field potentials evoked by perforant path stimulation were recorded in the dentate gyrus under urethane anesthesia. Input/output (I/O) functions were assessed by averaging the response evoked in the dentate gyrus to stimulus pulses delivered to the perforant path in an ascending intensity series. Long-term potentiation (LTP) was induced by delivering a series of brief high frequency (400 Hz) train bursts to the perforant path at a moderate stimulus intensity and I/O functions were reassessed 1 h later. No differences in baseline synaptic population spike (PS) and minor effects on excitatory postsynaptic potential (EPSP) slope amplitudes were discerned between the groups prior to train delivery. Post-train I/O functions, however, revealed a 50% decrement in the magnitude of LTP in PCB-exposed animals. These data are the first to demonstrate persistent decrements in hippocampal synaptic plasticity in the intact animal following developmental exposure to PCBs. Disruption of early brain ontogeny due to developmental PCB exposure may underlie perturbations in the neurological substrates that support synaptic plasticity and contribute to deficits in LTP and learning that persist into adulthood.

Action Potentials↗
PubMed2000

Enhancement of persistent Na+ current by sea anemone toxin (ATX II) exerts dual action on hippocampal excitability.

We used anemone toxin II (ATX II) to study how a selective enhancement of persistent Na+ current (INaP) would affect the excitability of CA1 pyramidal neurons in the hippocampal slice. In whole-cell recordings from CA1 cell somata, local application of ATX II (10 microM) into the stratum pyramidale invariably depolarized the neurons and produced sustained burst discharges with depolarizing plateau potentials of variable amplitude and length. However, the strong excitatory action of ATX II, observed on the single cell level, was not mirrored in field potential recordings from the same hippocampal subfield. The amplitude of the electrically evoked population spike declined, reflecting the decreased availability of fast Na+ channels, and the intracellulary recorded burst discharges were not detected by the field electrode. The lacking synchronization of cellular bursting activity was seen during both local and bath application of ATX II, suggesting that the toxin, in addition to promoting burst discharges of individual neurons, simultaneously dampens network excitability. In fact, ATX II reduced afferent fibre volleys (reflecting axonal excitability) and field excitatory postsynaptic potentials (EPSPs) in a similar fashion. As the expression of different Na+ channel subtypes appears to be compartmentalized within hippocampal neurons, we propose that point mutations leading to pathologically enhanced INaP might exert quite opposite effects, depending on the type and location of the Na+ channel affected. Whereas alterations of somatodendritic Na+ channels would give rise to bursting activity, alterations of axonal Na+ channels would primarily decrease network excitability.

Action Potentials↗
PubMed1998

Intracellular responses of the rat anteroventral cochlear nucleus to intracochlear electrical stimulation.

The anteroventral cochlear nucleus (AVCN) is the first central processing site for acoustic information. The influence and extent of convergent auditory nerve input to AVCN neurons was investigated using brief (<0.2 ms) intracochlear electrical activation of spiral ganglion cells. In 40 neurons recorded in vivo, the major intracellular response to stimulation was an excitatory postsynaptic potential (EPSP) with short latency (approximately 1 ms) and fast rise time (<1 ms). Graduated EPSP amplitude increases were also seen with increasing stimulation strength resulting in spike generation. Hyperpolarization followed excitation in most neurons, its extent distinguished three response types: Type I showed no hyperpolarization; Type II and Type III displayed short (<10 ms) and long (>19 ms) duration hyperpolarization, respectively. Hyperpolarization was attributed to an inhibitory postsynaptic potential (IPSP) in addition to spike after hyperpolarization. Neurobiotin filling identified Type I and II neurons as stellate and Type III as bushy cells. These results suggests that AVCN neurons receive direct, possibly convergent, excitatory input from auditory nerves emanating from spiral ganglion cells with hyperpolarization resulting from polysynaptic inhibitory input.

Animals↗
PubMed1998

Regeneration of phasic motor axons on a crayfish tonic muscle: neuron specifies synapses.

Motor neurons are matched to their target muscles, often forming separate phasic and tonic systems as in the abdomen of crayfish where they are used for rapid escape and slow postural movements, respectively. To assess the role of motor neuron and muscle fiber in forming synapses we attempted a mismatch experiment by allotransplanting a phasic nerve attached to its ganglion to a denervated tonic muscle. Regenerating motor axons sprouted 10-30 branches (typical of phasic motor neurons, as tonic ones sprout far fewer branches) to reinnervate muscle fibers and form synapses that produced large excitatory postsynaptic potentials (typical of phasic motor neurons, as tonic synapses give small potentials). Therefore motor neurons, not muscle fibers, appear to specify one of the major properties of regenerating neuromuscular synapses.

Animals↗