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PubMed2003

SNAP-25 Ser187 does not mediate phorbol ester enhancement of hippocampal synaptic transmission.

Phorbol esters, activators of protein kinase C (PKC), have been shown to enhance synaptic transmission. One potential downstream target of PKC in the presynaptic terminal is the soluble N-ethylmaleimide sensitive factor (NSF) attachment protein receptor (SNARE) SNAP-25, which has a PKC phosphorylation site in its C-terminal coil centered at serine 187 (S187/Ser187). We examined the role of S187 in hippocampal synaptic transmission. After proteolytic cleavage of native SNAP-25 by botulinum neurotoxin E (BoNT/E), synaptic transmission was restored in a subset of transfected CA3 pyramidal cells with a toxin-resistant form of SNAP-25 containing unaltered S187 (Swt), S187 mutated to alanine (SA) or S187 mutated to glutamate (SE). We observed that phorbol-12,13-diacetate (PDAc, 10 microM) induced potentiation of neurotransmission to a similar degree for both Swt and SA (2.4-fold and 3.1-fold increase, respectively). Furthermore, basal levels of transmission mediated by SE were reduced relative to that of Swt (failure rates of 72% and 41%, respectively). Together, these data suggest that phosphorylation of SNAP-25 S187 does not mediate the observed enhancement of neurotransmission by phorbol esters at hippocampal synapses.

Animals↗
PubMed1999

Analysing metabotropic glutamate group III receptor mediated modulation of synaptic transmission in the amygdala-kindled dentate gyrus of the rat.

Metabotropic glutamate receptors (mGluRs) provide a powerful control of synaptic transmission in the hippocampus and may serve as a target for drug development in human temporal lobe epilepsies. Agonists and antagonists at these receptors influence the development and propagation of seizures in some animal models of epilepsy. Experimental seizures can change the level of expression of mGluRs in the rat hippocampus. In the human dentate gyrus of patients suffering from temporal lobe epilepsy (TLE), group III mGluR mediated inhibition of synaptic transmission is almost lost in the sub-group with Ammon's horn sclerosis. We tested the modulation of synaptic transmission by the group III mGluR specific agonist L(+)-2-amino-4-phosphonobutyric acid (L-AP4) in the dentate gyrus outer molecular layer in control and amygdala-kindled rats, a common model for TLE. Extracellular field potential recordings upon subthreshold stimulation of lateral perforant path fibers were measured simultaneously in the outer molecular layer and granule cell layer. Analysis of 'paired-pulse' characteristics in the absence and presence of L-AP4 and group III mGluR mediated inhibition of synaptic transmission in the lateral perforant path revealed no significant alterations in fully kindled rats. Since there is no evidence of altered L-AP4 responses, a loss of group III mGluR function, particularly that of subtype mGluR8, seems not necessary for the kindling epilepsy.

Amygdala↗
PubMed2003

Cannabinoids decrease corticostriatal synaptic transmission via an effect on glutamate uptake.

Activation of cannabinoid CB1 receptors reduces glutamatergic synaptic transmission in the rodent striatum and is involved in the normal control of motor function by the basal ganglia. Here we investigated CB1 receptor regulation of glutamate release and uptake and synaptic transmission in the rat striatum. We show that CB1 receptor activation reduces both the release and uptake of [3H]glutamate in striatal slices. We also demonstrate that both activation of CB1 receptors and inhibition of glutamate uptake reduce corticostriatal synaptic transmission in a mutually occlusive manner and that both forms of depression are dependent on metabotropic glutamate receptor (mGluR) activation. We propose that CB1 receptor activation in the striatum decreases glutamate transporter activity and that the resulting increase in synaptic cleft glutamate concentration causes the activation of presynaptic mGluRs, which then decrease glutamate release.

Amino Acids↗
PubMed2006

Regulation of synaptic transmission by CRF receptors.

Corticotropin-releasing factor (CRF or CRH) and its family of related peptides have long been recognized as hypothalamic-pituitary-adrenal (HPA) axis peptides that function to regulate the release of other hormones, e.g., ACTH. In addition, CRF acts outside the HPA axis not as a hormone, but as a regulator of synaptic transmission, pre- and post-synaptically, within specific CNS neuronal circuits. Synaptic transmission within the nervous system is today understood to be a more complex process compared to the concepts associated with the term 'synapse' introduced by Sherrington in 1897. Based on more than a century of progress with modern cellular and molecular experimental techniques, prior definitions and functions of synaptic molecules and their receptors need to be reconsidered (see Glossary and Fig. 1), especially in light of the important roles for CRF, its family of peptides and other potential endogenous regulators of neurotransmission, e.g., vasopressin, NPY, etc. (see Glossary). In addition, the property of 'constitutive activity' which is associated with G-protein coupled receptors (GPCRs) provides a persistent tonic mechanism to fine-tune synaptic transmission during both acute and chronic information transfer. We have applied the term 'regulator', adapted from the hormone literature, to CRF, as an example of a specific endogenous substance that functions to facilitate or depress the actions of neuromodulators on fast and slow synaptic responses. As such, synaptic neuroregulators provide a basic substrate to prime or initiate silently plastic processes underlying neurotransmitter-mediated information transfer at CNS synapses. Here we review the role of CRF to regulate CNS synaptic transmission and also suggest how under a variety of allostatic changes, e.g., associated with normal plasticity, or adaptations resulting from mental disorders, the synaptic regulatory role for CRF may be 'switched' in its polarity and/or magnitude in order to provide a coping mechanism to deal with daily and life-long stressors. Thus, a prominent role we assign to non-HPA axis CRF, its family of peptides, and their receptors, is to maintain both acute and chronic synaptic stability.

Animals↗
PubMed1997

Calcium channel types mediating synaptic transmission during aging.

The effects of omega-conotoxin (CTX) GVIA, omega-agatoxin (Aga) IVA, and the dihydropyridine nicardipine were studied on synaptic transmission in the hippocampus during aging. Field excitatory postsynaptic potentials (fEPSPs) were recorded in the CA1 region in slices from young and aged Fischer 344 rats. Peptide toxins reduced synaptic transmissions similarly in both age groups while nicardipine showed no effect. These results suggests that the well documented age-related changes in synaptic transmissions in the hippocampus cannot be explained by changes in the types of Ca2+ channel mediating synaptic transmission.

Agatoxins↗
PubMed2005

Sevoflurane blocks cholinergic synaptic transmission postsynaptically but does not affect short-term potentiation.

BACKGROUND: As compared with their effects on both inhibitory and excitatory synapses, little is known about the mechanisms by which general anesthetics affect synaptic plasticity that forms the basis for learning and memory at the cellular level. To test whether clinically relevant concentrations of sevoflurane affect short-term potentiation involving cholinergic synaptic transmission, the soma-soma synapses between identified, postsynaptic neurons were used. METHODS: Uniquely identifiable neurons visceral dorsal 4 (presynaptic) and left pedal dorsal 1 (postsynaptic) of the mollusk Lymnaea stagnalis were isolated from the intact ganglion and paired overnight in a soma-soma configuration. Simultaneous intracellular recordings coupled with fluorescent imaging of the FM1-43 dye were made in either the absence or the presence of sevoflurane. RESULTS: Cholinergic synapses, similar to those observed in vivo, developed between the neurons, and the synaptic transmission exhibited classic short-term, posttetanic potentiation. Action potential-induced (visceral dorsal 4), 1:1 excitatory postsynaptic potentials were reversibly and significantly suppressed by sevoflurane in a concentration-dependent manner. Fluorescent imaging with the dye FM1-43 revealed that sevoflurane did not affect presynaptic exocytosis or endocytosis; instead, postsynaptic nicotinic acetylcholine receptors were blocked in a concentration-dependent manner. To test the hypothesis that sevoflurane affects short-term potentiation, a posttetanic potentiation paradigm was used, and synaptic transmission was examined in either the presence or the absence of sevoflurane. Although 1.5% sevoflurane significantly reduced synaptic transmission between the paired cells, it did not affect the formation or retention of posttetanic potentiation at this synapse. CONCLUSIONS: This study demonstrates that sevoflurane blocks cholinergic synaptic transmission postsynaptically but does not affect short-term synaptic plasticity at the visceral dorsal 4-left pedal dorsal 1 synapse.

Anesthetics, Inhalation↗
PubMed2002

The target of Drosophila photoreceptor synaptic transmission is a histamine-gated chloride channel encoded by ort (hclA).

By screening Drosophila mutants that are potentially defective in synaptic transmission between photoreceptors and their target laminar neurons, L1/L2, (lack of electroretinogram on/off transients), we identified ort as a candidate gene encoding a histamine receptor subunit on L1/L2. We provide evidence that the ort gene corresponds to CG7411 (referred to as hclA), identified in the Drosophila genome data base, by P-element-mediated germ line rescue of the ort phenotype using cloned hclA cDNA and by showing that several ort mutants exhibit alterations in hclA regulatory or coding sequences and/or allele-dependent reductions in hclA transcript levels. Other workers have shown that hclA, when expressed in Xenopus oocytes, forms histamine-sensitive chloride channels. However, the connection between these chloride channels and photoreceptor synaptic transmission was not established. We show unequivocally that hclA-encoded channels are the channels required in photoreceptor synaptic transmission by 1) establishing the identity between hclA and ort and 2) showing that ort mutants are defective in photoreceptor synaptic transmission. Moreover, the present work shows that this function of the HCLA (ORT) protein is its native function in vivo.

Amino Acid Sequence↗
PubMed2006

Bilirubin potentiates inhibitory synaptic transmission in lateral superior olive neurons of the rat.

Bilirubin is a well-known neurotoxin that can result in multiple neurologic deficits. Previous studies have suggested that bilirubin affects aspects of synaptic transmission; however the acute effects of bilirubin on synaptic transmission have not been examined in real-time. In this study, using whole-cell voltage-clamp recordings, we observed the effect of bilirubin on inhibitory postsynaptic currents (IPSC) in postnatal 13-15-day-old neurons dissociated from lateral superior olive nuclei (LSO), one of the brainstem auditory nucleus that are highly vulnerable to bilirubin. The results showed that 10(-5)M bilirubin increased the frequency of spontaneous IPSC without causing change in their amplitudes or in the response to bath applied glycine, suggesting a presynaptic locus for the action. In the presence of tetrodotoxin, the frequency of miniature IPSC was also potentiated by 10(-5)M bilirubin. The facilitation by bilirubin was concentration dependent and increased with an increase in exposure time. Bicuculline only partially reduced the action of bilirubin. The action of bilirubin was observed in extracellular Ca(2+)-free ([Ca(2+)](o) free) solution but was fully occluded by pretreatment with BAPTA-AM in [Ca(2+)](o) free solution. Thus, in LSO neurons, bilirubin facilitates inhibitory synaptic transmission, in a manner independent of voltage-activated Na(+) and Ca(2+) channels but dependent on presynaptic [Ca(2+)](i). The increase of inhibitory synaptic transmission in response to acute bilirubin is a novel effect of bilirubin on the central nervous system and may have implications for neurotoxicity and the impairment of auditory transduction seen in hyperbilirubinemia.

Animals↗
PubMed2006

Depression of retinogeniculate synaptic transmission by presynaptic D(2)-like dopamine receptors in rat lateral geniculate nucleus.

Extraretinal projections onto neurons in the dorsal lateral geniculate nucleus (dLGN) play an important role in modifying sensory information as it is relayed from the visual thalamus to neocortex. The dLGN receives dopaminergic innervation from the ventral tegmental area; however, the role of dopamine in synaptic transmission in dLGN has not been explored. In the present study, whole cell recordings were obtained to examine the actions of dopamine on glutamatergic synaptic transmission. Dopamine (2-100 microm) strongly suppressed excitatory synaptic transmission in dLGN relay neurons that was evoked by optic tract stimulation and mediated by both N-methyl-d-aspartate and non-N-methyl-d-aspartate glutamate receptors. In contrast, dopamine did not alter inhibitory synaptic transmission arising from either dLGN interneurons or thalamic reticular nucleus neurons. The suppressive action of dopamine on excitatory synaptic transmission was mimicked by the D(2)-like dopamine receptor agonist bromocriptine (2-25 microm) but not by the D(1)-like receptor agonist SKF38393 (10-25 microm). In addition, the dopamine-mediated suppression was antagonized by the D(2)-like receptor antagonist sulpiride (10-20 microm) but not by the D(1)-like receptor antagonist SCH23390 (5-25 microm). The dopamine-mediated decrease in evoked excitatory postsynaptic current amplitude was accompanied by an increase in the magnitude of paired-pulse depression. Furthermore, dopamine also reduced the frequency but not the amplitude of miniature excitatory postsynaptic currents. Taken together, these data suggest that dopamine may act presynaptically to regulate the release of glutamate at the retinogeniculate synapse and modify transmission of visual information in the dLGN.

Anesthetics, Local↗
PubMed1980

Strontium supports synaptic transmission and long-lasting potentiation in the hippocampus.

(1) Synaptic transmission was studied in isolated transverse hippocampal slices from guinea pigs. Extracellular evoked potentials were recorded in the region CA1. (2) Changing the normal perfusion solution (containing 2 mM Ca2+) to calcium-free Ringer abolished synaptic transmission which was again restored by adding strontium. A synaptic efficacy of 25--50% ofn normal was obtained for 10 mM Sr2+. (3) Two different synaptic inputs to CA1 pyramidal cells were tested with respect to their ability to produce long-lasting synaptic potentiation after tetanization in strontium Ringer. Following a brief tetanus the field EPSP and, especially, the population spike were greatly enhanced. (4) The potentiation so produced was similar to the long-lasting potentiation seen in the normal slice, because it (i) had a very long duration (hours), (ii) was specific for the tetanized pathway, (iii) showed potentiation of both 'volley-EPSP' and 'EPSP-spike' relations, and (iv) was accompanied by short-lasting (less than 5 min) generalized depression.

Animals↗
PubMed1996

Muscarinic receptor regulation of synaptic transmission in airway parasympathetic ganglia.

Muscarinic receptor regulation of synaptic transmission in guinea pig bronchial parasympathetic ganglia was evaluated with the use of intracellular recording of the intrinsic ganglion neurons. Methacholine (1 microM) decreased the amplitude of vagus nerve-stimulated fast excitatory postsynaptic potentials (fEPSP) by 33 and 46% (at 0.8 and 8.0 Hz, respectively) but had no effect on the amplitude of the depolarizations evoked by a bath-applied nicotinic receptor agonist. Methoctramine (1 microM) inhibited methacholine's effect on fEPSP but alone did not influence the magnitude of the fEPSP evoked by vagus nerve stimulation. Methacholine (10 microM) depolarized a subpopulation of neurons (approximately 4 mV), which was blocked by pirenzepine (0.1 microM). In other neurons, either no effect or a small (1-5 mV) hyperpolarization was noted. Cholinergic contractions of bronchial smooth muscle elicited by electrical field stimulation were potentiated by methoctramine to the same extent as those evoked by vagus nerve (preganglionic) stimulation. The data indicate that M2 receptor activation can lead to inhibition of presynaptic acetylcholine release and consequently a significant inhibition of synaptic transmission in bronchial parasympathetic ganglia. The physiological role of this neuromodulatory effect appears limited, however, when studied in the in vitro setting.

Animals↗
PubMed1993

A model of graded synaptic transmission for use in dynamic network simulations.

1. The heartbeat central pattern-generating network of the medicinal leech contains elemental neural oscillators, comprising reciprocally inhibitory pairs of segmental heart interneurons, that use graded as well as spike-mediated synaptic transmission. We are in the process of developing a general computer model of this pattern generator. Our modeling goal is to explore the interaction of membrane currents and synaptic transmission that promote oscillation in heart interneurons. As a first step toward this goal, we have developed a computer model of graded synaptic transmission between reciprocally inhibitory heart interneurons. Previously gathered voltage-clamp data of presynaptic Ca2+ currents and simultaneous postsynaptic currents and potentials (5 mM external [Ca2+]) were used as the bases of the model. 2. We assumed that presynaptic Ca2+ current was composed of distinct fast (ICaF) and slow (Icas) components because there are two distinct time courses of inactivation for this current. We fitted standard Hodgkin-Huxley equations (Eq. 1 and 2, APPENDIX) to these components using first-order activation and inactivation kinetics. 3. Graded synaptic transfer in the model is based on calculation of a dimensionless variable [P]. A portion of both IcaF and ICaS determined by a factor A contributes to [P], and a removal factor B decreases [P] (Eq. 4, APPENDIX). [P] can be roughly equated to the [Ca2+] in an unspecified volume that is effective in causing transmitter release. Transmitter release, and thus postsynaptic conductance, is related to [P]3 (Eq. 3, APPENDIX). 4. We adapted our model to voltage-clamp data gathered at physiological external [Ca2+] (2.0 mM) and tested it for shorter presynaptic voltage steps. Presynaptic Ca2+ currents and synaptic transfer were well simulated under all conditions. 5. The graded synaptic transfer model could be used in a network simulation to reproduce the oscillatory activity of a reciprocally inhibitory pair of heart interneurons. Because synaptic transmission in the model is an explicit function of presynaptic Ca2+ current, the model should prove useful to explore the interaction between membrane currents and synaptic transmission that promote and modulate oscillation in reciprocally inhibitory heart interneurons.

Adaptation, Physiological↗
PubMed1998

Adenosine A2 receptors modulate hippocampal synaptic transmission via a cyclic-AMP-dependent pathway.

Blockade of adenosine A2 receptors has been shown to significantly reduce the level of tetanus-induced long-term potentiation in area CA1 of rat hippocampus [Kessey K. et al. (1997) Brain Res. 756, 184-190; Sekino Y. et al. (1991) Biochem. biophys. Res. Commun. 181, 1010-1014]. In the present study, the effects of A2 receptor activation and blockade on the modulation of normal synaptic transmission and tetanus-induced long-term potentiation were examined at the Schaffer-CA1 synapse in rat hippocampal slices. A2 receptor activation reversibly enhanced synaptic transmission evoked by low-frequency test pulses as measured by the dendritic field excitatory postsynaptic potential. In the presence of A1 receptor blockade, A2 activation further enhanced the excitatory postsynaptic potential, while A2 receptor blockade resulted in a reversible decrease of the excitatory postsynaptic potential. The A2a receptor agonist, CGS21680, had no effect on the excitatory postsynaptic potential, suggesting that tonic activation of A2b receptors contributes to synaptic transmission under normal physiological conditions. Furthermore, we investigated the contribution of A2 receptors to the level of tetanus-induced long-term potentiation. Under control conditions, a single tetanus potentiated the excitatory postsynaptic potential by 63.5% relative to baseline 30 min post-tetanus. In contrast, tetanus-induced long-term potentiation during A2 blockade was 21.3%. A2 receptor activation increased the level of tetanus-induced long-term potentiation to 90.2%. Because A2 receptors are known to stimulate cyclic-AMP accumulation, the possible involvement of cyclic-AMP was examined. Forskolin, a direct adenylate cyclase activator, and 8-bromo-cyclic-AMP, a membrane-permeable analog of cyclic-AMP, were able to reconstitute tetanus-induced long-term potentiation during A2 receptor blockade; however, the inactive analog 1,9-dideoxyforskolin had no effect, indicating that the effects of A2 activation on synaptic transmission were mediated largely through the regulation of intracellular cyclic-AMP. Because A1 receptors exert an opposing effect on synaptic transmission relative to A2 receptors, these results suggest that the stoichiometry of A1 versus A2 receptor activation appears to play an important role in the modulation of normal synaptic transmission and long-term potentiation in the CA1 region of the hippocampus.

Animals↗
PubMed1987

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

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

Animals↗
PubMed1997

Regional differences in glial cell modulation of synaptic transmission.

Metabolic integrity of glial cells in field CA1 of the guinea pig hippocampus is critical to maintenance of synaptic transmission (Keyser and Pellmar [1994] Glia 10:237-243). To determine if this tight glial-neuronal coupling is equally important in other brain regions, we compared the effect of fluoroacetate (FAC), a glial specific metabolic blocker, on synaptic transmission in field CA1 to synaptic transmission in area dentata (DG). FAC was significantly more effective in decreasing synaptic potentials in CA1 than in DG. A similar regional disparity in the FAC-induced decrease in ATP levels was evident. Isocitrate, a glial specific metabolic substrate, prevented the FAC-induced synaptic depression in both CA1 and DG. The results suggest that glia of CA1 and dentate respond differently to metabolic challenge. Modulation of this glial-neuronal coupling could provide a regionally specific mechanism for synaptic plasticity. Additionally, site-specific glial-neuronal interactions can impact on a variety of physiological and pathophysiological conditions.

Animals↗
PubMed1998

Capsaicin facilitates excitatory but not inhibitory synaptic transmission in substantia gelatinosa of the rat spinal cord.

Actions of capsaicin were examined on synaptic transmissions in the substantia gelatinosa (SG) of adult rat spinal cord slices using the whole-cell patch-recording technique. Bath-applied capsaicin at a concentration of 2 microM activated a slow inward current (having an amplitude of 33 pA at -70 mV), which was accompanied by an increase in the frequency of glutamatergic spontaneous excitatory postsynaptic currents (sEPSCs; by 234%); these actions were blocked by a capsaicin-receptor antagonist, capsazepine (10 microM). The capsaicin-induced increase in sEPSC frequency was resistant to tetrodotoxin (0.5-1 microM). On the other hand, capsaicin (2 microM) did not affect either glycine- or gamma-aminobutyric acid-mediated spontaneous synaptic transmission. The results indicate that capsaicin enhances excitatory but not inhibitory synaptic transmission, possibly through a direct action on primary afferent terminals in the SG. As the SG has been thought to participate in nociceptive pathway, it is suggested that such a presynaptic action of capsaicin contributes to nociceptive transmissions.

Animals↗
PubMed2002

NMDA-receptor trafficking and targeting: implications for synaptic transmission and plasticity.

Dynamic regulation of synaptic efficacy is thought to play a crucial role in formation of neuronal connections and in experience-dependent modification of neural circuitry. The molecular and cellular mechanisms by which synaptic changes are triggered and expressed are the focus of intense interest. This articles reviews recent evidence that NMDA receptors undergo dynamically regulated targeting and trafficking, and that the physical transport of NMDA receptors in and out of the synaptic membrane contributes to several forms of long-lasting synaptic plasticity. The identification of targeting and internalization sequences in NMDA-receptor subunits has begun the unraveling of some mechanisms that underlie activity-dependent redistribution of NMDA receptors. Given that NMDA receptors are widely expressed throughout the CNS, regulation of NMDA-receptor trafficking provides a potentially important way to modulate efficacy of synaptic transmission.

Animals↗
PubMed1988

Calcium-sensitive recovery of extracellular potassium and synaptic transmission in rat hippocampal slices exposed to brief anoxia.

We examined the possibility that Ca2+-sensitive inhibition of synaptic transmission following anoxia involves compromise of ion transport activity. Rat hippocampal slices were superfused with artificial cerebrospinal fluids containing different concentrations of CaCl2, and subjected to short anoxia. Durations of anoxia were sufficient to provoke anoxic depolarization, indicated by a sudden rise in extracellular K+ (K+o). Following anoxia, apparent K+ transport was assessed by measuring the magnitude of subnormal K+o (the K+o undershoot) in hippocampal region CA1. Recovery of synaptic transmission 1 h after anoxia was determined by evaluation of the magnitudes of the orthodromically stimulated population spike recorded from CA1 pyramidal cells. K+o undershoots and recovery of synaptic transmission decreased as CaCl2 or the duration of anoxic depolarization increased. These data suggest: (1) that increased artificial cerebrospinal fluid CaCl2 compromised K+ reaccumulation after anoxia; and (2) that ion transport dysfunction may inhibit recovery of synaptic transmission.

Action Potentials↗