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PubMed1980

Rate-limiting step of inhibitory post-synaptic current decay in Aplysia buccal ganglia.

1. In neurones BL and BR 3, 6, 8, 9, 10 and 11 of Aplysia buccal ganglia, cholinergic inhibitory post-synaptic potentials are produced by activity in either of two presynaptic cells. In order to analyse the synaptic conductance change, neurones were voltage-clamped inhibitory post-synaptic currents (i.p.s.c.) recorded. 2. The synaptic conductance change rises to an average peak value of 0.65 micromho and decays exponentially with single time constant tau of 19 msec. 3. We have attempted to identify the rate-limiting step responsible for i.p.s.c. decay from among the following possibilities: (1) acetylcholine (ACh) supply, (2) ACh removal by diffusion, (3) ACh removal by hydrolysis or (4) a slow unbinding or conformational change closing open synaptic current channels. 4. Cooling prolongs tau, with Q10 of 5.2. Cooling and eserine treatment together produce greatly prolonged, exponentially decaying i.p.s.c.s with tau > 150 msec. These results suggest that ACh removal, either by diffusion or hydrolysis, is not the rate-limiting step. 5. Prolonging synaptic action potential time course with intracellular injection of tetraethylammonium broadens the i.p.s.c. peak but does not affect the decay tail, suggesting that the rate-limiting step is not ACh release. 6. The spectrum of ACh-induced current fluctuations is fitted by a double Lorentzian with cut-off frequencies of 7.8 and 47 Hz. The frequency of the slower component corresponds to the macroscopic i.p.s.c. decay tau. 7. We conclude that a slow conformational change closing open synaptic current channels is likely to determine i.p.s.c. decay. We cannot, however, exclude either delayed diffusion or a late tail of slow ACh release as possibilities.

Acetylcholine↗
PubMed1998

Neurophysiology of glutamatergic signalling and anthelmintic action in Ascaris suum: pharmacological evidence for a kainate receptor.

Electrophysiological and pharmacological techniques were used to study glutamatergic signalling in the parasitic nematode, Ascaris suum. Glutamate or kainate injections into whole worms produced a paralysed quasi-static posture similar to the waveform in behaving worms. The DE2 motorneuron class is a primary target. Several glutamatergic substances produced pronounced conductance increases and depolarization in DE2; domoate and kainate were the most potent agonists tested. Glutamate responses and spontaneous excitatory post-synaptic potentials in DE2 were reversibly blocked in sodium-free saline. DE2 sensitivity to exogenous glutamate was sustained during block of synaptic transmission suggesting that glutamatergic receptors are located on DE2 neurons. The glutamate-induced response was localized to the DE2 dendrite, coincident with the synapses responsible for spontaneous potentials in DE2. Steady-state potentials reached during glutamate superfusion were similar to the reversal potentials for both the spontaneous post-synaptic potentials and glutamate, also suggesting that these potentials may be glutamatergic. Non-N-methyl-D-aspartate receptor antagonists partially blocked spontaneous DE2 excitatory potentials and responses elicited by exogenous glutamate and kainate. This glutamatergic pathway may play a role in nematode locomotory behaviour and account for the paralysing anthelmintic action of excitatory amino acid analogues like kainate and domoate.

Animals↗
PubMed1991

Chronic exposure to alcohol during development alters the membrane properties of cerebellar Purkinje neurons in culture.

The active and passive membrane properties of developing Purkinje neurons in control cultures and cultures chronically treated with 20 or 40 mM ethanol for 1 or 2 weeks were examined using whole-cell current-clamp techniques. The membrane properties were characterized by the features of the voltage responses evoked by intracellular current injection of a series of depolarizing and hyperpolarizing current pulses. Analysis of these responses and background spontaneous activity showed several differences between the control and ethanol-treated Purkinje neurons: (1) membrane input resistance was significantly larger in the ethanol-treated neurons; (2) the percentage of neurons exhibiting immature firing patterns was significantly higher in the ethanol-treated neurons; (3) the afterhyperpolarization following a current-evoked train of action potentials was significantly larger in the ethanol-treated neurons; (4) spontaneous activity (synaptic potentials and synaptically evoked spike events) was significantly reduced in neurons treated with 40 mM ethanol for 1 week; spontaneous activity in neurons treated with 20 mM ethanol for 1 or 2 weeks was similar to that observed in the control group. These differences indicate that ethanol exposure during development directly alters the physiological properties of this CNS neuronal type. These neuronal actions of ethanol may contribute to the behavioral deficits observed in animals models of fetal alcohol syndrome. Similar target sites of ethanol action are likely to be present in the human CNS neurons and may be involved in human fetal alcohol syndrome.

Animals↗
PubMed1986

[Effect of dimedrol on the function of the neuromuscular synapse and the generation of action potentials by motor nerve fibers].

Microelectrode registration of synaptic potentials in the frog cutaneous-pectoris muscle has shown dimedrol (7.9 X 10(-5) M) to act on synaptic transmission decreasing the quantal content, estimated by mean EPP amplitude to mean miniature EPP amplitude ratio, the quantal content calculated by variation coefficient of EPP amplitude being unaffected. The data suggest possible transmitter release and depletion of mediator stock. The experiments on isolated motor nerve fibers have demonstrated dimedrol to cause the increase in transmitter release probability by widening the action potentials in the terminals and thus enhancing Ca2+ influx.

Action Potentials↗
PubMed1993

In vivo tracing of pathways and spatio-temporal activity patterns in rat visual cortex using voltage sensitive dyes.

We monitored optical signals from cortex stained with a voltage sensitive dye to study activity evoked by intracortical electrical stimulation. The objectives were to study the spatial and temporal spread of activity from intrinsic connections near the stimulating electrode and to develop a new technique to study extrinsic projections from striate cortex to extrastriate target areas. Various measures were made of the time course of the optical signal (latency, rise time, decay time, temporal summation, facilitation versus depression, and presence or absence of a slow undershoot); in general, these measures were found to vary significantly across different response positions, different experiments, and even different runs within the same experiment. The spatial distribution of responses near the stimulating electrode in striate cortex was usually elliptical and was most often elongated along the anterior-posterior axis, with a typical size (full width at 75% max) of 1.3 mm (anterior-posterior axis) by 0.75 mm (medio-lateral axis). In some cases, complex spatio-temporal patterns were observed, in which the position of the maximum optical signal shifted with time or split into multiple peaks. In eight experiments, a response focus was found in extrastriate cortex at an expected location within the lateromedial area (LM). The response focus in LM was typically about half the size of that in striate cortex. In some experiments we observed additional focal responses in the anterolateral visual area (AL). The extrastriate responses showed a significant delay (3-10 ms) in onset and time to peak relative to the striate response. The validity of this technique for determining extrinsic projections was tested in two types of experiments. In the first, stimulation from two electrodes in striate cortex generated response foci consistent with the known topographic organization of area LM. In the second, the optically measured response focus was shown to correlate with the histologically reconstructed projection of a chemical tracer injected near the site of stimulation. We discuss the chain of neurophysiological events that occur during and after focal electrical stimulation and how they relate to the observed optical signal. We conclude that direct passive responses were a small component of our signal, that the component due to action potentials in directly stimulated neurons should have occurred in the first 1-2 ms post stimulus and is small compared to the peak signal, and that overall our signals were probably dominated by a combination of asynchronously occurring action potentials and excitatory and inhibitory synaptic potentials.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1992

Quantal analysis of suppressing action of baclofen on mossy fiber synapses in guinea pig hippocampus.

Baclofen, a selective agonist at the gamma-aminobutyric acidB (GABAB) receptor, has been considered to reduce the release of transmitter from nerve terminals by acting on presynaptic GABAB receptors, in addition to its postsynaptic action. The purpose of this study has been to re-examine quantitatively the action of baclofen in the hippocampus by a rigorous quantal analysis. (+/-)-Baclofen suppressed field potentials and intracellularly-recorded synaptic potentials induced in the subfield CA3 by mossy fiber stimulation in thin transverse sections of the guinea pig hippocampus. The amplitude distribution of excitatory postsynaptic potentials (EPSPs) induced monosynaptically by a granule cell could be described by the Pascal statistics. Suppression of the unitary EPSPs by baclofen (1 and 5 microM) was accompanied by decreases both in mean quantal content (m) and by mean quantal amplitude (q). The reduction in q was smaller than expected from a decrease in the input resistance of the postsynaptic neuron. It was suggested that the presynaptic and postsynaptic actions of baclofen contribute almost equally to suppression of the transmission at 1 microM, whereas the presynaptic action predominates at 5 microM.

Animals↗
PubMed1998

Post- and presynaptic effects of norepinephrine in guinea-pig colonic submucous plexus.

Intracellular recording techniques were used to investigate the effects of norepinephrine on submucous neurones in the guinea-pig distal colon. In 81% of the neurones, pressure microejection of norepinephrine produced a membrane hyperpolarization associated with a decrease in excitability and input resistance. Microejection of clonidine (1 microM) mimicked the norepinephrine-induced hyperpolarization, whereas both phentolamine (1 microM) and yohimbine (1 microM) reversibly suppressed it. Superfusion of norepinephrine (1 nM - 10 microM) hyperpolarized the cells in a concentration-dependent manner. Norepinephrine and clonidine (1 nM - 10 microM) caused a concentration-dependent presynaptic inhibition of stimulus-evoked cholinergic fast excitatory postsynaptic potential. Slow inhibitory post-synaptic potentials (sISPSs) were induced by focal electrical stimulation of the interganglionic fibre tracts in 43% of the neurones tested. Superfusion of both phentolamine (1 microM) and yohimbine (1 microM) reduced the sIPSPs while prazosin (1 microM) had no significant effect. We concluded that norepinephrine acted post- and presynaptically via alpha 2-adrenoreceptors to have an inhibitory effect on the guinea-pig colonic submucous. In addition, our study strongly supported the role of norepinephrine as a mediator of the sIPSPs. As a result, norepinephrine would primarily suppress information transfer within the neuronal circuits in guinea-pig colonic submucosal plexus.

Acetylcholine↗
PubMed1976

Centrifugal actions on amacrine and ganglion cells in the retina of the turtle.

1. An electrophysiological investigation of efferent synapses in the retina of the turtle was conducted by recording intracellularly from amacrine cells. These cells have been selected because in birds they have been shown to have direct anatomical connexions with centrifugal fibre terminals. 2. Amacrine cells could be easily distinguished from most other retinal cells, except ganglion cells, by their different photo-responses. Because both amacrine and ganglion cells may generate action potentials they were distinguished by their responses to optic nerve stimulation. 3. The response of ganglion cells to single shock stimulation of the optic nerve consists of an antidromic action potential followed by a late synaptic potential. 4. Cells which did not show antidromic responses but were electrically excitable, by passing direct current through the recording electrode, were considered to be amacrine cells. 5. Amacrine cells generate an e.p.s.p. in response to optic nerve stimulation. An analysis of the e.p.s.p. suggests that it may be due to a single afferent fibre terminating in the proximity of the cell soma. By analogy to the bird, it is concluded that the amacrine cells e.p.s.p.s result from the activation of centrifugal fibres.

Action Potentials↗
PubMed1978

Destruction of a single cell in the central nervous system of the leech as a means of analysing its connexions and functional role.

A method has been devised for killing an individual neurone in the C.N.S. of the leech by injecting it with Pronase. The technique has been used to examine the role of individual sensory and motor cells involved in producing reflex movements.1. After a neurone was injected with Pronase, either in an intact animal or an isolated ganglion, its cell body lost its resting and action potentials. Some hours later the injected cell's axons in the periphery failed to conduct impulses. In the intact animal the cell body could no longer be discerned after a few weeks.2. To test for destruction of processes within the neuropile, cells were injected first with the enzyme horseradish peroxidase (HRP) and then several hours later with Pronase. Absence of the characteristic HRP reaction product indicated that Pronase had spread throughout the arborization of the cell.3. Injection of Pronase into one cell did not produce overt electrophysiological or anatomical changes in other cells in the ganglion including neurones that were originally electrically coupled to the killed cell.4. Evidence that an individual cell was the only motoneurone supplying particular muscles was provided by destruction of that cell in otherwise intact animals, which resulted in a characteristic motor deficit in the area supplied by the killed cell. Over a period of months, functional recovery of the affected muscles occurred by way of homologous cells in adjacent ganglia.5. A further application of the technique was to trace the connexion that a particular sensory neurone makes onto two motoneurones that are electrically coupled. Normally, the sensory neurone gives rise to excitatory potentials in both post-synaptic cells. Synaptic potentials could still be recorded in one motor cell after the other had been destroyed by Pronase, indicating that synapses were made directly onto both of the motoneurones.

Animals↗
PubMed1985

Long-term changes in hippocampal physiology and learning ability of rats after intrahippocampal tetanus toxin.

A chronic epileptic syndrome can be induced by injecting minute doses of tetanus toxin into rat hippocampi. This causes intermittent epileptic fits over a period of 2-4 weeks, after which the fits cease, and the electroencephalogram (e.e.g.) appears to return to normal over the following 2-3 weeks. However, once they have recovered from the seizures, the rats exhibit a remarkably persistent impairment of learning and memory, which is the subject of the present study. Learning ability was assessed using a radial arm maze task, in which the rats had to visit each of eight arms for a food reward. The toxin-injected rats learnt this task more slowly than control-injected. Evoked potentials from the CA3 pyramidal cells were recorded in terminal experiments under halothane anaesthesia. Long term potentiation of the post-synaptic response to the commissural pathway from the contralateral hippocampus appeared to be unaffected by the previous toxin treatment, at least over periods of up to 5 h. The toxin-injected group differed from the control in having consistently smaller post-synaptic population spikes in their evoked responses, so that stimuli were less effective in exciting the post-synaptic neurones. This applied both to the contralateral commissural input, and to the ipsilateral mossy fibre input. No differences were found between the toxin and control groups in the size of the antidromic population spike in the commissural response, or in the population excitatory post-synaptic potential (e.p.s.p.) for either input. Thus the depressed output from CA3 pyramidal cells cannot be explained either by a loss of these neurones (confirming earlier neuropathological observations), or by a loss of excitatory afferents. While its precise cause remains unknown, the depressed output from the CA3 region was statistically correlated with the learning impairment, and we believe provides a reasonable explanation of this behavioural deficit.

Action Potentials↗
PubMed1987

Actions of gamma-aminobutyric acid on rat supraoptic nucleus neurosecretory neurones in vitro.

1. Intracellular recordings were obtained from thirty-eight rat supraoptic nucleus (s.o.n.) neurosecretory neurones in perfused hypothalamic explants. Changes in membrane potential and conductance were monitored following application of gamma-aminobutyric acid (GABA), and related agonists and antagonists. 2. GABA depressed action potential discharge of all of thirty-five s.o.n. neurones tested and induced either membrane hyperpolarization or depolarization. Neurones that displayed membrane hyperpolarization in response to lower GABA concentrations (30-300 microM) demonstrated a biphasic membrane voltage change with a later depolarizing phase as a response to higher concentrations (up to 3000 microM). 3. GABA (10-3000 microM) induced a prominent concentration-dependent increase in membrane conductance in all neurones. The critical slope for the log-log plot of [GABA] vs. GABA-induced membrane conductance was 1.7, indicating co-operativity in the GABA receptor-induced conductance change. 4. Muscimol (0.3-30 microM) potently mimicked all the effects of GABA. Bicuculline (1-100 microM) antagonized the effects of GABA and muscimol in a competitive manner. 5. Glycine and taurine (1-10 mM) had weak effects, although comparatively similar to those of GABA. These actions were blocked both by bicuculline (100 microM) and by strychnine (1 microM). At higher concentrations (greater than 10 microM), strychnine also antagonized the actions of GABA. 6. In recordings with potassium-acetate-filled micropipettes, the reversal potential of hyperpolarizing membrane voltage responses to GABA was -72.5 +/- 1.5 mV in close agreement (+/- 5 mV) with the reversal potential of inhibitory post-synaptic potentials (i.p.s.p.s) recorded in the same neurones. Depolarizing responses to GABA reversed polarity at -50 +/- 1.6 mV. In recordings with KCl-filled micropipettes, voltage responses to GABA were always depolarizing and reversed near -40.0 +/- 4.3 mV. Similarly, reduction of the concentration of chloride ions in the perfusion medium from 134 to 10.4 mM induced a positive shift of the GABA reversal potential by 40-50 mV. 7. From measurements of input resistance (Rin) and cell time constant (tau O), input capacitance (Cin; representing total membrane capacitance) was calculated as 78.9 +/- 2.1 pF. During responses to GABA or muscimol, decreased Rin was accompanied by a linearly related decrease in tau o indicating that these substances had no effect on the membrane capacitance of s.o.n. neurones.(ABSTRACT TRUNCATED AT 400 WORDS)

Action Potentials↗
PubMed1988

Effects of putative neurotransmitters on sympathetic preganglionic neurons.

Epinephrine, substance P, and glutamate have all been hypothesized as primary chemical mediators in the descending pathway from the brain stem "vasomotor center" to SPNs. Interestingly, lesions of or antagonists to epinephrine, substance P, glutamate, and 5-HT neurons all abolish sympathetic activity and reduce blood pressure to a level similar to that in a spinal-transected animal. However, it is unlikely that all these substances are primary mediators of sympathetic information carried from the brain stem to the spinal cord. How then do we resolve these findings? A plausible explanation is that monoamines and neuropeptides act in the IML, as in other areas of the central nervous system, as neuromodulators, setting the level of excitability of SPNs rather than relaying sympathetic information over a functionally specific pathway from brain stem sympathetic neurons to the IML. For example, the time course of the norepinephrine-mediated slow EPSPs and IPSPs in SPNs is consistent with a gain-setting function. Likewise, the depolarization of SPNs by 5-HT is similar to the depolarization elicited in myenteric and celiac ganglion cells. In these ganglia, 5-HT appears to mediate a slow excitatory potential that enhances incoming fast synaptic potentials. A similar gain-enhancing effect of 5-HT has been demonstrated in facial motoneurons. By analogy, epinephrine is likely to act as a neuromodulator in the IML rather than to serve as the primary mediator of sympathetic information descending from the brain stem. Similarly, it is difficult to imagine that an agent with such a long duration of excitatory action as substance P could serve as the primary descending transmitter in a system where moment to moment changes in activity are essential. It is more likely that substance P aids in setting the excitability of SPNs. Pharmacological antagonism of any of the excitatory neuromodulators (i.e. gain setters) might act to decrease, at least temporarily, the excitability of SPNs to the point where primary sympathetic activity from the brain stem could not excite SPNs. This accounts for the wide variety of pharmacological agents that act to eliminate sympathetic activity and drastically reduce blood pressure. On the basis of the above arguments, the most logical candidate for a transmitter mediating primary excitatory sympathetic information from brain stem "vasomotor centers" would be an excitatory amino acid. Fast EPSPs in SPNs appear to be mediated by glutamate and excitatory amino acid antagonists markedly inhibit sympathetic activity.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1986

Distribution of activity in the spinal terminations of single hair follicle afferent fibers to somatotopically identified regions of the cat spinal cord.

Single-unit spike-triggered averaging has been used to study the distribution of activity in the central processes of 11 single hair follicle afferent (HFA) fibers in relation to the somatotopic organization of dorsal horn neurons (DHNs). Central responses could be recorded from all but one HFA, and the waveforms of these responses were similar to the biphasic, monophasic positive and compound terminal potentials (TPs), the triphasic, positive-negative-positive axonal (preterminal) potentials (APs), and the focal synaptic potentials (FSPs) described by other workers in different preparations. No central responses could be recorded from one HFA even though this axon was shown to be intact throughout the experiment and noise levels in the averaged records were below 3.1 microV. The spatial organization of TPs and APs mirrored the anatomical organization determined using intraaxonal staining only in that the region containing these potentials was a longitudinally orientated narrow (mean width = 405 microns) strip of dorsal horn. Within this strip large TPs, APs, and FSPs were usually found only in those regions in which the receptive field (RF) of the HFA was relatively central to the RFs of DHNs. The region in which the RFs of DHNs encompassed the RF of the HFA, the somatotopically appropriate region, was also organized into a longitudinally orientated strip of dorsal horn of approximately the same width as the strip containing TPs and APs. In any single experiment the strips formed by the somatotopically appropriate region and the TP-AP region occupied the same mediolateral position, but in contrast, the rostral and/or caudal boundaries of these strips often occurred at different levels along the dorsal horn. In some cases the TP-AP strip extended rostrally and/or caudally beyond the somatotopically appropriate region or ended at the same rostrocaudal level. In other cases the somatotopically appropriate region extended rostrally and/or caudally beyond the TP-AP strip. These results are discussed in relation to the rostrocaudal spread of the dendritic trees and the RF organization of DHNs. The results show clearly that in intact cats, anesthetized with alpha-chloralose, some HFAs give rise to collaterals in somatotopically inappropriate regions of the dorsal horn and that at least some parts of these collaterals are invaded by incoming action potentials. The question of whether some HFAs give rise to collaterals that are either infrequently invaded or not invaded at all is discussed.

Animals↗
PubMed1996

Laminar localization, morphology, and physiological properties of pyramidal neurons that have the low-threshold calcium current in the guinea-pig medial frontal cortex.

One of the several types of ionic currents present in central neurons is the low-threshold, or T-type calcium current (LTCC). This current is responsible for the firing of low-threshold calcium spikes (LTS) and participates in the generation of rhythmic activity and bursts of action potentials in several brain nuclei. We have studied the distribution and properties of pyramidal neurons recorded from the guinea-pig medial frontal cortex that have this calcium current. Pyramidal neurons were recorded in an in vitro slice preparation using either current clamp or single-electrode voltage-clamp recording. Pyramidal neurons that generated LTS or had the LTCC were found only between 500 mm from the pial surface and the white matter (approximately layers V/VI) and were absent in more superficial layers. All pyramidal neurons that fired LTS or had the LTCC were characterized as regular spiking and had some important morphological and physiological differences from the rest of the pyramidal neurons studied. This group of neurons had shorter and less complex apical dendritic arbors, fired action potentials of lower amplitude and longer duration, and were the only type of pyramidal neurons able to generate bursts of action potentials. In addition, the inhibitory synaptic potentials elicited by stimulation of layer I were more powerful in this group of neurons. This research provides new evidence for the presence of the LTCC in subsets of cortical pyramidal neurons, which have specific and well defined morphological and physiological properties.

Animals↗
PubMed2005

Ubiquitin C-terminal hydrolase L3 (Uchl3) is involved in working memory.

Regulated proteolysis by the ubiquitin pathway has been implicated in control of the cell cycle, transcriptional activation, cell fate and growth, and synaptogenesis. The ubiquitin-proteasome system is involved in synaptic plasticity and is proposed to be part of a molecular switch that converts short-term synaptic potentiation to long-term changes in synaptic strength. In Aplysia, a component of the ubiquitin system termed ubiquitin C-terminal hydrolase (Ap-Uch) has been shown to be essential for long-term facilitation. To examine whether Uch plays a role in learning, memory, and synaptic plasticity in mammals, we have analyzed mice homozygous for a targeted mutation in ubiquitin C-terminal hydrolase L3 (Uchl3), an orthologue of Ap-Uch. Mice homozygous for the mutation in Uchl3 are viable, with no obvious developmental, histological, or fertility abnormalities. We demonstrate that Uchl3-/- mice have a significant learning deficit relative to wild type littermates in the spatial version of the Morris water maze and the 8-arm radial maze. Further, the impaired performance in the 8-arm radial maze of Uchl3-/- mice is due to significantly increased working memory errors. Examination of hippocampal long-term potentiation (LTP), a form of synaptic plasticity thought to underlie memory storage, revealed no significant differences in LTP in hippocampal slices from Uchl3-/- mice. Our results suggest a novel role for ubiquitin C-terminal hydrolase enzymes in mammals in spatial learning and working memory.

Animals↗
PubMed2006

What do dendrites and their synapses tell the neuron?

This essay looks at the historical significance of four APS classic papers that are freely available online: Rall W. Distinguishing theoretical synaptic potentials computed for different soma-dendritic distributions of synaptic input. J Neurophysiol 30: 1138-1168, 1967 (http://jn.physiology.org/cgi/reprint/30/5/1138). Rall W, Burke RE, Smith TG, Nelson PG, and Frank K. Dendritic location of synapses and possible mechanisms for the monosynaptic EPSP in motoneurons. J Neurophysiol 30: 1169-1193, 1967 (http://jn.physiology.org/cgi/reprint/30/5/1169). Rall W and Shepherd GM. Theoretical reconstruction of field potentials and dendrodendritic synaptic interactions in olfactory bulb. J Neurophysiol 31: 884-915, 1968 (http://jn.physiology.org/cgi/reprint/31/6/884). Segev I and Rall W. Computational study of an excitable dendritic spine. J Neurophysiol 60: 499-523, 1988 (http://jn.physiology.org/cgi/reprint/60/2/499).

Dendrites↗
PubMed2005

A model of bidirectional synaptic plasticity: from signaling network to channel conductance.

In many regions of the brain, including the mammalian cortex, the strength of synaptic transmission can be bidirectionally regulated by cortical activity (synaptic plasticity). One line of evidence indicates that long-term synaptic potentiation (LTP) and long-term synaptic depression (LTD), correlate with the phosphorylation/dephosphorylation of sites on the alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptor subunit protein GluR1. Bidirectional synaptic plasticity can be induced by different frequencies of presynaptic stimulation, but there is considerable evidence indicating that the key variable is calcium influx through postsynaptic N-methyl-d-aspartate (NMDA) receptors. Here, we present a biophysical model of bidirectional synaptic plasticity based on [Ca2+]-dependent phospho/dephosphorylation of the GluR1 subunit of the AMPA receptor. The primary assumption of the model, for which there is wide experimental support, is that the postsynaptic calcium concentration, and consequent activation of calcium-dependent protein kinases and phosphatases, is the trigger for phosphorylation/dephosphorylation at GluR1 and consequent induction of LTP/LTD. We explore several different mathematical approaches, all of them based on mass-action assumptions. First, we use a first order approach, in which transition rates are functions of an activator, in this case calcium. Second, we adopt the Michaelis-Menten approach with different assumptions about the signal transduction cascades, ranging from abstract to more detailed and biologically plausible models. Despite the different assumptions made in each model, in each case, LTD is induced by a moderate increase in postsynaptic calcium and LTP is induced by high Ca2+ concentration.

Animals↗
PubMed2004

Synaptic strengthening mediated by bone morphogenetic protein-dependent retrograde signaling in the Drosophila CNS.

Retrograde signaling is an essential component of synaptic development and physiology. Previous studies show that bone morphogenetic protein (BMP)-dependent retrograde signaling is required for the proper development of the neuromuscular junction (NMJ) in Drosophila. These studies, moreover, raised the significant possibility that the development of central motor circuitry might similarly be reliant on such signaling. To test this hypothesis, retrograde signaling between postsynaptic motoneurons and their presynaptic interneurons is examined. Postsynaptic expression of an adenylate cyclase encoded by rutabaga (rut), is sufficient to strengthen synaptic transmission at these identified central synapses. Results are presented to show that the underlying mechanism is dependent on BMP retrograde signaling. Thus, presynaptic expression of an activated TGF-beta receptor, thickvien (tkv), or postsynaptic expression of a TGF-beta ligand, glass-bottom boat (gbb), is sufficient to phenocopy strengthening of synaptic transmission. In the absence of gbb, endogenous synaptic transmission is significantly weakened and, moreover, postsynaptic overexpression of rut is unable to potentiate synaptic function. Potentiation of presynaptic neurotransmitter release, mediated by increased postsynaptic expression of gbb, is dependent on normal cholinergic activity, indicative that either the secretion of this retrograde signal, or its transduction, is activity dependent. Thus, in addition to the development of the NMJ and expression of myoactive FMRFamide-like peptides in specific central neurons, the results of the present study indicate that this retrograde signaling cascade also integrates the development and function of central motor circuitry that controls movement in Drosophila larvae.

Adenylyl Cyclases↗