Chemical synaptic transmission

About: Chemical synaptic transmission is a research topic. Over the lifetime, 268 publications have been published within this topic receiving 17634 citations.

Short-Term Synaptic Plasticity

Abstract: ▪ Abstract Synaptic transmission is a dynamic process. Postsynaptic responses wax and wane as presynaptic activity evolves. This prominent characteristic of chemical synaptic transmission is a crucial determinant of the response properties of synapses and, in turn, of the stimulus properties selected by neural networks and of the patterns of activity generated by those networks. This review focuses on synaptic changes that result from prior activity in the synapse under study, and is restricted to short-term effects that last for at most a few minutes. Forms of synaptic enhancement, such as facilitation, augmentation, and post-tetanic potentiation, are usually attributed to effects of a residual elevation in presynaptic [Ca2+]i, acting on one or more molecular targets that appear to be distinct from the secretory trigger responsible for fast exocytosis and phasic release of transmitter to single action potentials. We discuss the evidence for this hypothesis, and the origins of the different kinetic phases...

Electrical coupling underlies high-frequency oscillations in the hippocampus in vitro

Abstract: Coherent oscillations, in which ensembles of neurons fire in a repeated and synchronous manner, are thought to be important in higher brain functions. In the hippocampus, these discharges are categorized according to their frequency as theta (4-10Hz), gamma (20-80 Hz) and high-frequency (approximately 200 Hz) discharges, and they occur in relation to different behavioural states. The synaptic bases of theta and gamma rhythms have been extensively studied but the cellular bases for high-frequency oscillations are not understood. Here we report that high-frequency network oscillations are present in rat brain slices in vitro, occurring as a brief series of repetitive population spikes at 150-200 Hz in all hippocampal principal cell layers. Moreover, this synchronous activity is not mediated through the more commonly studied modes of chemical synaptic transmission, but is in fact a result of direct electrotonic coupling of neurons, most likely through gap-junctional connections. Thus high-frequency oscillations synchronize the activity of electrically coupled subsets of principal neurons within the well-documented synaptic network of the hippocampus.

Use-dependent increases in glutamate concentration activate presynaptic metabotropic glutamate receptors.

Abstract: The classical view of fast chemical synaptic transmission is that released neurotransmitter acts locally on postsynaptic receptors and is cleared from the synaptic cleft within a few milliseconds by diffusion and by specific reuptake mechanisms. This rapid clearance restricts the spread of neurotransmitter and, combined with the low affinities of many ionotropic receptors, ensures that synaptic transmission occurs in a point-to-point fashion. We now show, however, that when transmitter release is enhanced at hippocampal mossy fibre synapses, the concentration of glutamate increases and its clearance is delayed; this allows it to spread away from the synapse and to activate presynaptic inhibitory metabotropic glutamate receptors (mGluRs). At normal levels of glutamate release during low-frequency activity, these presynaptic receptors are not activated. When glutamate concentration is increased by higher-frequency activity or by blocking glutamate uptake, however, these receptors become activated, leading to a rapid inhibition of transmitter release. This effect may be related to the long-term depression of mossy fibre synaptic responses that has recently been shown after prolonged activation of presynaptic mGluRs (refs 2, 3). The use-dependent activation of presynaptic mGluRs that we describe here thus represents a negative feedback mechanism for controlling the strength of synaptic transmission.

Synchronized bursting of CA1 hippocampal pyramidal cells in the absence of synaptic transmission

Abstract: The synchronization of neuronal firing, seen at its most dramatic in the epilepsies, has generally been attributed to synaptic interactions1–5. We have now discovered a rhythmic spontaneous bursting activity produced by non-synaptic mechanisms. It develops in rat hippocampal slices after chemical synaptic transmission has been blocked by incubation in low Ca2+, increased Mg2+ solutions, and persists with almost clockwork regularity for several hours. We report here that spontaneous firing of all the neurones recorded in the slice increased, consistent with the known effects of Ca2+ on membrane properties and synaptic transmission6–10, but the synchronous ‘field bursts’, and presumably their underlying mechanisms, were restricted to the population of pyramidal neurones in the hippocampal CA1 region. Thus, these low Ca2+ field bursts are different from the Ca2+-dependent synchronous bursts induced in slices by penicillin which originate in the population of pyramidal cells of the CA3 region1–3.

G Protein Regulation of Potassium Ion Channels

Abstract: Upon stimulation of vagal nerves, acetylcholine (ACh)c is released from axonal terminals and decelerates the heart beat. This historic discovery by Otto Loewi in the 1920s established the concept of chemical synaptic transmission ([Loewi, 1921][1]; [Loewi and Navaratil, 1926][2]). Since then, many