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PubMed1984

A mechanism for production of phase shifts in a pattern generator.

During motor activity of the pyloric system of the lobster stomatogastric ganglion, there are rhythmic alternations between activity in the pyloric dilator (PD) and pyloric (PY) motor neurons. We studied the phase relations between PD motor neuron activity and PY motor neuron activity in preparations cycling at a wide range of frequencies and after altering the activity of the PD neurons. The PY neurons fall into two classes, early (PE) and late (PL) (21), distinguished by the different phases in the pyloric cycle at which they fire. The phase at which PE neurons fired and the phase at which PL neurons fired was independent of pyloric cycle frequency over a range of frequencies from 0.5 to 2.25 Hz. The anterior burster (AB) interneuron is electrically coupled to the PD motor neurons. Together the AB and PD neurons form the pacemaker for the pyloric system. Synchronous depolarization of the AB and PD neurons evokes a complex inhibitory post-synaptic potential (IPSP) in PY neurons. This IPSP has two components: an early, AB neuron-derived component and a late, PD neuron-derived component. Deletion of the PD neurons from the pyloric circuit by photoinactivation removed the PD-evoked component of the pacemaker-evoked IPSP. This resulted in a decrease in the duration of the IPSP evoked by pacemaker depolarization and a significant advance in the firing phase of PY neurons. Bath application of dopamine was used to hyperpolarize and inhibit the PD neurons (30), causing them to release less neurotransmitter. As a consequence, the duration of the IPSP evoked by pacemaker depolarization was decreased and the firing phase of the PY neurons was significantly advanced. Stimulation of the inferior ventricular nerve (IVN) produces a slow excitation of the PD neurons (30), causing them to release more neurotransmitter. Consequently, the duration of the IPSP evoked by pacemaker depolarization was increased and the firing phase of the PY neurons was significantly retarded for several cycles of pyloric activity following IVN stimulation. Thus, modulation of the strength of PD-evoked inhibition in PY neurons is responsible for altering the firing phase of the PY neurons with respect to the pyloric pacemaker. We suggest that frequency of the pyloric output and the phase relations of the elements within the pyloric cycle can be regulated independently. The potential implications of these data for modulation of synaptic efficacy in other preparations are discussed.

Animals↗
PubMed1982

A dual effect of cobalt ions on the spontaneous release of transmitter at insect motor nerve terminals.

1. The effect of extracellular cobalt on the frequency of miniature excitatory post-synaptic potentials (MEPSPs) was studied in cockroach leg muscle fibres that had been depolarized with 20.8 mM-K saline. 2. Cobalt ions had a dual effect on the spontaneous release of transmitter, an inhibitory action being followed by an acceleratory. A reciprocal relationship between Ca2+ and Co2+ was found for both the inhibitory and acceleratory effects. 3. The equilibrium dissociation constant for Co2+ as a competitive antagonist of spontaneous release ranged from 0.4 to 0.65 mM. It is concluded that Co2+ is much more potent than Mg2+ in suppressing spontaneous transmitter release at the insect neuromuscular junction. The antagonism by extracellular Co2+ appears to occur only at the external surface site on the terminal membrane.

Acetylcholine↗
PubMedDate not supplied

[Nonspecific changes in the response of command neurons in Helix leucorum L. to a combination of 2 stimuli].

In a preparation of isolated nervous system of the snail (Helix leucorum L.) an analogue of conditioned food aversion reflex was reproduced using electrical stimulation of the chemoreceptive pathway as conditioned and stimulation of skin innervating nerves as unconditioned stimuli. In 65% of cases, pairing of these stimuli elicited a significant increase of synaptic potential amplitude evoked by the conditioned stimulus in command neurones of avoidance behaviour and/or appearance of action potentials. In 20% of cases in which reinforcement evoked less than 5 spikes, no increase of response to unconditioned stimuli was recorded. In 15% of cases in which no response of command neurones to stimulation of the chemoreceptive pathway was recorded, no changes were observed with any reinforcement. Nonassociative character of responsiveness changes was established in experiments with presentation of conditioned and unconditioned stimuli at random or of isolated unconditioned stimuli: these procedures evoked exactly the same changes as in experiments with temporal pairing of two stimuli.

Animals↗
PubMed1982

Electrophysiology and morphology of the developing hippocampus of fetal rabbits.

The pyramidal neurons of fetal rabbit hippocampus were studied using intracellular electrophysiological techniques in in vitro slice preparations. Correlative light and electron microscopic analyses were carried out on hippocampus during the 21st through the 29th day of fetal gestation. In intracellular experiments, neurons with all-or-none action potentials and near-adult level resting potentials were found even in the youngest preparations. Synaptic activity, however, was rare until about 24 days of gestation. CA1 neurons showed primarily excitatory synaptic potentials during fetal development, whereas CA3 neurons displayed both inhibitory and excitatory postsynaptic potentials at early stages. Anatomical studies suggested that pyramidal cell precursors were still dividing and migrating at 21 days; by 29 days, cellular migration was completed, and cellular intercommunication in the form of synapses was increasing. These experiments demonstrate that fetal central nervous system (CNS) material can be studied electrophysiologically without growing tissue in culture. Our results suggest that the newly differentiated hippocampal neurons have a limited repertoire of activities. Such data may provide a link between in vivo studies of postnatal CNS development and cell and tissue culture investigations of the properties of immature neurons.

Action Potentials↗
PubMed1977

The distribution of acetylcholine receptors on muscle fibres of regenerating salamander limbs.

1. Muscle fibres developing during limb regeneration were examined for responsiveness to acetylcholine (ACh) applied iontophoretically along the membrane. 2. Fibres which were uninnervated as well as those with non-transmitting synapses had high over-all sensitivities, with only minor variations along their length. 3. Functionally innervated fibres in which depolarization did not yet elicit action potentials had high over-all sensitivities, even when the synaptic potentials ahd amplitudes of 40-50 mV. In these the membrane in the vicinity of synapses tended to have sensitivities above the background level. 4. Upon the appearance of action potentials, several weeks after fibre innervation, the responsiveness to ACh began to decline in synapse free regions of the membrane. In mature muscle the sensitivity to ACh is restricted to sites of synaptic contact.

Acetylcholine↗
PubMed1981

Analysis of histamine actions by intra- and extracellular recording in hippocampal slices of the rat.

Extra- and intracellular recordings from CA1 pyramidal and dentate granule cells in hippocampal slices of the rat revealed a depressant effect of histamine which was usually accompanied by a hyperpolarization but no changes in conductance of the cell membrane. Synaptic potentials were unaffected. It is concluded that histamine has a post-synaptic action on ionic conductance in the dendrites, that allows a modulation of quick information transfer but no rapid synaptic transmission.

Action Potentials↗
PubMed1998

Plasticity in an electrosensory system. III. Contrasting properties of spatially segregated dendritic inputs.

Efferent neurons of the first-order electrosensory processing center of the brain, the electrosensory lateral line lobe (ELL), receive electroreceptor afferent input as well as feedback inputs descending from higher centers. These ELL efferents, pyramidal cells, adaptively filter predictable patterns of sensory input while preserving sensitivity to novel stimuli. The filter mechanism involves integration of centrally generated predictive inputs with the afferent inputs being canceled. The predictive inputs, referred to as "negative image" inputs, terminate on pyramidal cell apical dendrites and generate responses that are opposite those resulting from the predictable afference, hence integration of these signals results in attenuation of pyramidal cell responses. The system also shows a robust form of plasticity; the pyramidal cells learn, with a time course of a few minutes, to cancel new patterns of repetitive inputs. This is accomplished by adjusting the strength of excitatory and inhibitory apical dendritic inputs according to an anti-Hebbian learning rule. This study focuses on the properties of two separate pathways that convey descending information to pyramidal cell apical dendrites. One pathway terminates proximally, nearer to the pyramidal cell body, whereas the other terminates distally. Recordings of ELL evoked potentials, extracellular pyramidal cell spike responses, and intracellularly recorded synaptic potentials show that the pyramidal cells respond oppositely to moderate-frequency (> approximately 8 Hz) single pulse stimulation or repeated (1/s) tetanic activation of these two pathways. Repetitive activation of the proximally terminating pathway results in highly facilitating responses due to potentiation of pyramidal cell excitatory postsynaptic potentials (EPSPs). These same stimuli applied to the distally terminating pathway result in a reduction of pyramidal cell responses due to depression of EPSPs and potentiation of inhibitatory postsynaptic potentials (IPSPs). Anti-Hebbian plasticity was demonstrated by pairing tetanic stimulation of either pathway with changes in the postsynaptic cell's membrane potential. After stabilization of the response potentiation due to tetanic stimulation of the proximally terminating pathway, paired postsynaptic hyperpolarization resulted in further increases in spike responses and additional potentiation of pyramidal cell EPSPs. Paired postsynaptic depolarization reduced subsequent responses to the tetanus, depressed EPSP amplitudes, and, in many cases, potentiated IPSPs. The same pattern of plasticity was observed when postsynaptic hyper- or depolarization was paired with tetanic stimulation of the distally terminating pathway except that the plasticity was superimposed on the depressed pyramidal cell responses resulting from stimulating this pathway alone. Modulation of a postsynaptic form of synaptic depression is proposed to account for the anti-Hebbian plasticity associated with both pathways.

Animals↗
PubMed2005

Different basal levels of CaMKII phosphorylated at Thr286/287 at nociceptive and low-threshold primary afferent synapses.

Postsynaptic autophosphorylation of Ca2+/calmodulin-dependent protein kinase II (CaMKII) at Thr286/287 is crucial for the induction of long-term potentiation at many glutamatergic synapses, and has also been implicated in the persistence of synaptic potentiation. However, the availability of CaMKII phosphorylated at Thr286/287 at individual glutamatergic synapses in vivo is unclear. We used post-embedding immunogold labelling to quantitatively analyse the ultrastructural localization of CaMKII phosphorylated at Thr286/287 (pCaMKII) at synapses formed by presumed nociceptive and low-threshold mechanosensitive primary afferent nerve endings in laminae I-IV of rat spinal cord. Immunogold labelling was enriched in the postsynaptic densities of such synapses, consistent with observations in pre-embedding immunoperoxidase-stained dorsal horn. Presynaptic axoplasm also exhibited sparse immunogold labelling, in peptidergic terminals partly associated with dense core vesicles. Analysis of single or serial pCaMKII-immunolabelled sections indicated that the large majority of synapses formed either by presumed peptidergic or non-peptidergic nociceptive primary afferent terminals in laminae I-II of the spinal cord, or by presumed low-threshold mechanosensitive primary afferent terminals in laminae IIi-IV, contained pCaMKII in their postsynaptic density. However, the postsynaptic levels of pCaMKII immunolabelling at low-threshold primary afferent synapses were only approximately 50% of those at nociceptive synapses. These results suggest that constitutively autophosphorylated CaMKII in the postsynaptic density is a common characteristic of glutamatergic synapses, thus potentially contributing to maintenance of synaptic efficacy. Furthermore, pCaMKII appears to be differentially regulated between high- and low-threshold primary afferent synapses, possibly reflecting different susceptibility to synaptic plasticity between these afferent pathways.

Animals↗
PubMed1981

Adenosine depression of hippocampal neurons in vitro: an intracellular study of dose-dependent actions on synaptic and membrane potentials.

In CA1 pyramidal neurons, 5 micrometer adenosine had no measurable effect on resting membrane potential or resistance, while excitatory and inhibitory postsynaptic potentials generated by orthodromic stimulation of the stratum radiatum were reduced by 20--60%. However, 10--20 micrometers adenosine not only markedly reduced (by 20--80%) the synaptic potentials, but also clearly hyperpolarized most pyramidal neurons. This effect was accompanied by a reduction in input resistance in about one-half of the cells and no measurable change in resistance in the rest. Monobutyryl cyclic AMP in concentrations of 50 micrometer or more also hyperpolarized neurons, usually no change in input resistance.

Adenosine↗
PubMed1999

Glutamate-triggered events inducing corticostriatal long-term depression.

Repetitive activation of corticostriatal fibers produces long-term depression (LTD) of excitatory synaptic potentials recorded from striatal spiny neurons. This form of synaptic plasticity might be considered the possible neural basis of some forms of motor learning and memory. In the present study, intracellular recordings were performed from rat corticostriatal slice preparations to study the role of glutamate and other critical factors underlying striatal LTD. In current-clamp, but not in voltage-clamp experiments, brief focal applications of glutamate, as well as high-frequency stimulation (HFS) of corticostriatal fibers, induced LTD. This pharmacological LTD and the HFS-induced LTD were mutually occlusive, suggesting that both forms of synaptic plasticity share common induction mechanisms. Isolated activation of either non-NMDA-ionotropic glutamate receptors (iGluRs) or metabotropic glutamate receptors (mGluRs), respectively by AMPA and t-ACPD failed to produce significant long-term changes of corticostriatal synaptic transmission. Conversely, LTD was obtained after the simultaneous application of AMPA plus t-ACPD. Moreover, also quisqualate, a compound that activates both iGluRs and group I mGluRs, was able to induce this form of pharmacological LTD. Electrical depolarization of the recorded neurons either alone or in the presence of t-ACPD and dopamine (DA) failed to mimic the effects of the activation of glutamate receptors in inducing LTD. However, electrical depolarization was able to induce LTD when preceded by coadministration of t-ACPD, DA, and a low dose of hydroxylamine, a compound generating nitric oxide (NO) in the tissue. None of these compounds alone produced LTD. Glutamate-induced LTD, as well as the HFS-induced LTD, was blocked by L-sulpiride, a D2 DA receptor antagonist, and by 7-nitroindazole monosodium salt, a NO synthase inhibitor. The present study indicates that four main factors are required to induce corticostriatal LTD: (1) membrane depolarization of the postsynaptic neuron; (2) activation of mGluRs; (3) activation of DA receptors; and (4) release of NO from striatal interneurons.

Animals↗
PubMed1957

Intracellular recording from the giant synapse of the squid.

1. Recording with glass micropipette electrodes inserted close to the synaptic region, in the presynaptic and in the postsynaptic fibers of the giant synapse in the stellate ganglion of the squid, has been accomplished. 2. The forms of the spike and of the synaptic potential are very much like those reported earlier (Bullock, 1948) from macroelectrodes. The crest time and the rate of fall are labile and depend on the state of fatigue, though the time of initiation of the postsynaptic potential does not. 3. It is concluded after examination of both intra- and extracellular recordings that there is a real synaptic delay of the order of 1 or 2 milliseconds at 15-20 degrees C. 4. There is sometimes a very small and sometimes no visible deflection in the intracellular postsynaptic record attributable to the presynaptic spike. It is concluded that transmission cannot be electrical. 5. The amplitude of the postsynaptic potential can be controlled over some range by the amplitude of the presynaptic potential. 6. Hyperpolarization of the postsynaptic membrane results in increase in amplitude of spikes up to 200 millivolts, in increase in the membrane potential level at which the spike flares up, but in no considerable change in the amplitude in postsynaptic potential. 7. The postsynaptic potential can add to the late falling phase and the undershoot of an antidromic spike in the postfiber but cannot add to the crest or early part of the falling phase. The earliest part of the antidromic spike during which the postsynaptic potential can add is probably a period of refractoriness to electrical shock by analogy with the properties of the axon.

Animals↗
PubMed1992

Postischemic alterations of complex spike cell discharges and evoked potentials in rat hippocampal CA1 region.

Postischemic alterations of spontaneous discharges of complex spike cells (CS cells) and evoked potential in the rat hippocampal CA1 region were studied. Following 5 min of ischemia, CS cell discharge reappeared approximately 5 min after reperfusion and the frequency remained low, reaching a final value of 66.1 +/- 16.0% (n = 11) of preischemic frequency 2 h later. However, only one of 7 CS cells subjected to 20 min of ischemia exhibited discharges 2 h later. In the group with 5 min of ischemia, we obtained CS cell discharges from all rats at both 1 and 2 days after ischemia, with cluster frequencies indistinguishable from preischemic levels. In the group with 20 min of ischemia, discharges were noted in 7 neurons of 11 rats after 1 day, and in only 2 neurons of 8 rats after 2 days: their mean frequencies were lower than preischemic levels. In experiments of evoked potentials, the mean percentages of amplitudes of the post-synaptic potential (psp) 2 h after 3, 5 and 20 min of ischemia were 98.0 +/- 10.7 (n = 8), 70.7 +/- 8.22 (n = 9) and 45.1 +/- 6.34% (n = 7) of preischemic amplitudes, respectively. These results suggest that the functional deterioration of spike generation, as well as synaptic transmission, starts during transient ischemia and/or at the early stage of reperfusion.

Animals↗
PubMed1996

Electrotonic architecture of hippocampal CA1 pyramidal neurons based on three-dimensional reconstructions.

1. The spread of electrical signals in pyramidal neurons from the CA1 field of rat hippocampus was investigated through multicompartmental modeling based on three-dimensional morphometric reconstructions of four of these cells. These models were used to dissect the electrotonic architecture of these neurons, and to evaluate the equivalent cylinder approach that this laboratory and others have previously applied to them. Robustness of results was verified by the use of wide ranges of values of specific membrane resistance (Rm) and cytoplasmic resistivity. 2. The anatomy exhibited extreme departures from a key assumption of the equivalent cylinder model, the so-called "3/2 power law." 3. The compartmental models showed that the frequency distribution of steady-state electrotonic distances between the soma and the dendritic terminations was multimodal, with a large range and a sizeable coefficient of variation. This violated another central assumption of the equivalent cylinder model, namely, that all terminations are electronically equidistant from the soma. This finding, which was observed both for "centrifugal" (away from the soma) and "centripetal" (toward the soma) spread of electrical signals, indicates that the concept of an equivalent electrotonic length for the whole dendritic tree is not appropriate for these neurons. 4. The multiple peaks in the electrotonic distance distributions, whether for centrifugal or centripetal voltage transfer, were clearly related to the laminar organization of synaptic afferents in the CA1 region. 5. The results in the three preceding paragraphs reveal how little of the electrotonic architecture of these neurons is captured by a simple equivalent cylinder model. The multicompartmental model is more appropriate for exploring synaptic signaling and transient events in CA1 pyramidal neurons. 6. There was significant attenuation of synaptic potential, current, and charge as they spread from the dendritic tree to the soma. Charge suffered the least and voltage suffered the most attenuation. Attenuation depended weakly on Rm and strongly on synaptic location. Delay of time to peak was more distorted for voltage than for current and was more affected by Rm. 7. Adequate space clamp is not possible for most of the synapses on these cells. Application of a somatic voltage clamp had no significant effect on voltage transients in the subsynaptic membrane. 8. The possible existence of steep voltage gradients within the dendritic tree is consistent with the idea that there can be some degree of local processing and that different regions of the neuron may function semiautonomously. These spatial gradients are potentially relevant to synaptic plasticity in the hippocampus, and they also suggest caution in interpreting some neurophysiological results.

Animals↗
PubMed2007

Reducing the variability of neural responses: a computational theory of spike-timing-dependent plasticity.

Experimental studies have observed synaptic potentiation when a presynaptic neuron fires shortly before a postsynaptic neuron and synaptic depression when the presynaptic neuron fires shortly after. The dependence of synaptic modulation on the precise timing of the two action potentials is known as spike-timing dependent plasticity (STDP). We derive STDP from a simple computational principle: synapses adapt so as to minimize the postsynaptic neuron's response variability to a given presynaptic input, causing the neuron's output to become more reliable in the face of noise. Using an objective function that minimizes response variability and the biophysically realistic spike-response model of Gerstner (2001), we simulate neurophysiological experiments and obtain the characteristic STDP curve along with other phenomena, including the reduction in synaptic plasticity as synaptic efficacy increases. We compare our account to other efforts to derive STDP from computational principles and argue that our account provides the most comprehensive coverage of the phenomena. Thus, reliability of neural response in the face of noise may be a key goal of unsupervised cortical adaptation.

Action Potentials↗
PubMed1993

Electrophysiology of dopamine-denervated striatal neurons. Implications for Parkinson's disease.

Unilateral 6-hydroxydopamine-induced lesions of the substantia nigra have been used as an experimental model for Parkinson's disease. Although the biochemical and the behavioural effects of striatal denervation have been widely characterized, the physiological and pharmacological changes caused by dopamine depletion at the cellular level are still unknown. We studied the electrical activity of single rat striatal neurons recorded intracellularly in vitro from a brain slice preparation. Recordings were obtained at different periods after the denervation (4, 6, 8 months). In dopamine-denervated slices, unlike naive slices, most of the neurons showed spontaneous depolarizing postsynaptic potentials. The percentage of cells showing spontaneous depolarizing postsynaptic potentials was maximal 4 months after the denervation. In most of the dopamine-denervated neurons (60%) spontaneous depolarizing postsynaptic potentials were reversibly blocked by 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX, 10 microM), an antagonist of non-N-methyl-D-aspartate glutamate receptors. In some neurons, however, the amplitude of spontaneous depolarizing postsynaptic potentials was reduced by bicuculline (30 microM) suggesting that they were mediated by the release of endogenous gamma-aminobutyric acid (GABA). Intrinsic membrane properties (membrane potential, input resistance and firing pattern) and postsynaptic responses to different agonists of excitatory amino acid receptors were not altered in neurons recorded from dopamine-depleted slices. In dopamine-depleted slices, unlike in naive slices, LY 171555 (0.1-10 microM), a D2 dopamine receptor agonist, reduced the frequency and the amplitude of CNQX-sensitive spontaneous depolarizing postsynaptic potentials and reduced the amplitude of glutamate-mediated synaptic potentials evoked by cortical stimulation. LY 171555 did not affect the membrane responses to exogenous glutamate. SKF 38393 (3 microM), a D1 dopamine receptor agonist, decreased postsynaptic excitability of striatal neurons recorded from naive animals. On the contrary, this agonist was ineffective in most of the cells obtained from dopamine-depleted slices. These results suggest that dopamine-denervation augments neuronal excitability in the striatum. Abnormal excitability of striatal neurons is not caused by changes of the intrinsic membrane properties of these cells, but is the result of increased glutamatergic cortical inputs to the striatum. Dopamine-denervation also alters the physiological responses to dopamine receptor stimulation. Nigral lesions induce supersensitivity of D2 dopamine receptors controlling the release of glutamate and reduce the inhibitory influence of D1 receptors at postsynaptic level. These functional changes of the striatal neurons may alter the output signals from the striatum to the other structures of the basal ganglia and then produce most of the physiopathological changes observed in Parkinson's disease.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗
PubMed1995

A role for calcium/calmodulin-dependent protein kinase in mediating synaptic modulation by a neuropeptide.

The crayfish neuropeptide DRNFLRFamide (DF2) has previously been shown to increase the amplitude of excitatory post-synaptic potentials (EPSPs) in crayfish muscles by enhancing transmitter release from synaptic terminals [18]. This effect involves at least two types of kinase enzyme: one or more kinases which mediate the initial rise in EPSP amplitude, and protein kinase C (PKC) which prolongs the elevation in EPSP amplitude for several minutes [6,7]. The present investigation was aimed at identifying kinases that participate in the initial response. KN-62, an inhibitor of Ca2+/calmodulin-dependent protein kinase, delayed the rise in EPSP amplitude induced by DF2. The maximal response to the peptide occurred in about 40 min when KN-62 was present and in 15 min when the inhibitor was absent. KN-62 did not significantly alter EPSP amplitude by itself. KN-04, a structural analog of KN-62 which does not block Ca2+/CaM kinase activity, did not alter EPSP amplitude or the response to the neuropeptide. These data strongly suggest that Ca2+/CaM kinase participates in the initial increase in transmitter release.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗
PubMed2000

Properties of solitary tract neurons receiving inputs from the sub-diaphragmatic vagus nerve.

Vagal afferents ascending from the gastrointestinal tract synapse on neurons in the nucleus of the solitary tract. Although these neurons constitute a significant proportion of solitary tract cells their firing behaviour and synaptic properties are not documented. Since gastrointestinal tract afferent termination sites overlap with regions mediating cardiorespiratory reflexes the possibility of convergence with afferents mediating cardiovascular and respiratory reflexes was proposed. Here we describe some electrophysiological and morphological properties of solitary tract neurons orthodromically driven from the subdiaphragmatic vagus nerves and assess possible convergent inputs from cardiorespiratory afferents. Whole-cell recordings of solitary tract neurons responding to electrical stimulation of the sub-diaphragmatic vagus nerves (0.1-1 ms; 1-10 V; 2-20 Hz) were made in a working heart-brainstem preparation of rat. Baroreceptors were stimulated by raising pressure in the aorta or carotid sinus, whereas aortic injection of sodium cyanide (0.05% solution 25-50 microl) was used to activate peripheral chemoreceptors. Phrenic nerve activity and heart rate were monitored continuously. Of 88 solitary tract neurons tested, 39 responded with an evoked excitatory synaptic potential following stimulation of the sub-diaphragmatic vagus nerves. Resting membrane potential and input resistance of sub-diaphragmatic vagus nerve driven solitary tract neurons were 53.2 +/- 0.5 mV and 291 +/- 17 Mohms, respectively (mean +/- S.E.M.). Response latencies to sub-diaphragmatic vagus nerve stimulation were divided into two groups: <20 ms (16.0 +/- 2 ms, n = 7; mean +/- S.E.M.) and >20 ms (77.3 +/- 5 ms, n = 32). One additional neuron displayed an evoked inhibitory postsynaptic potential (latency 175 ms). Nineteen neurons showed ongoing activity which consisted of either irregular single action potential firing (0.5-10 Hz; n = 12) or burst discharge (n = 7). Of 33 neurons tested, 17 showed spike frequency adaptation during injection of positive current, whereas 19 of 38 cells displayed rebound excitation following release from hyperpolarized potentials. There was no correlation between these properties and synaptic latencies. Ninety-one per cent of neurons tested displayed synaptic depression following paired pulse stimulation of the sub-diaphragmatic vagus nerve over intervals up to 500 ms. Stimulation of either baroreceptors (n = 31) or chemoreceptors (n = 36) failed to elicit a synaptic response in all sub-diaphragmatic vagus nerve-driven solitary tract neurons. Neurobiotin-labelled solitary tract neurons (n = 10) were from both latency groups and were located medial to the solitary tract at the level of area postrema, -0.3 mm to +1 mm from the obex. One cell was located in commissural subnucleus at midline, seven cells dorsal to the tractus solitarius and three ventral and medial to it. Soma sizes were 23 +/- 9.6 x 14 +/- 4.9 microm (range: 50 x 16 microm to 15 x 7 microm). The number of primary dendrites varied from three to five, secondary from one to eight and tertiary zero to four. Labelled axons were found in seven cells which ramified extensively in the solitary tract nucleus (n = 3) and/or branched extensively in the dorsal vagal motonucleus (n = 3) and/or projected towards the ventrolateral medulla (n = 3). We conclude that solitary tract neurons receiving signals from the sub-diaphragmatic vagus nerves (most likely from gastrointestinal tract structures) appear to be a distinct pool of neurons. There was a heterogeneity in terms of both their ongoing activity and projection targets but despite this, there were three consistent properties. First, sub-diaphragmatic vagus nerve evoked predominantly excitatory synaptic responses in solitary tract neurons; second, neurons exhibited lasting paired pulse depression following activation of sub-diaphragmatic vagus nerves; and third, sub-diaphragmatic vagus nerve-driven solitary tract neurons were

Afferent Pathways↗
PubMed1994

Alpha subunit of calcium/calmodulin-dependent protein kinase enhances excitatory amino acid and synaptic responses of rat spinal dorsal horn neurons.

1. Here we report that in acutely isolated rat spinal dorsal horn (DH) neurons, the alpha-amino-3-hydroxy-5-methyl-4-isoxazole-propionic acid (AMPA)/kainate and N-methyl-D-aspartate (NMDA) receptors can be regulated by endogenous and exogenous calcium/calmodulin-dependent protein kinase II (CaM-KII). Intracellularly applied, the alpha-subunit of CaM-KII enhanced AMPA/kainate and NMDA currents recorded with the use of the whole cell patch-clamp technique. 2. Microcystin, a nonselective phosphatases inhibitor, also enhances AMPA and NMDA responses. 3. Conventional intracellular recordings were made from substantia gelatinosa neurons in spinal cord slices to determine the effect of intracellular application of CaM-KII on excitatory synaptic potentials evoked by electrical stimulation of primary afferent fibers. Excitatory synaptic transmission was enhanced by CaM-KII, which is consistent with the importance of phosphorylation of the postsynaptic AMPA/kainate and NMDA receptor-ion complexes in the short- and long-term changes in synaptic transmission.

Animals↗