Biphasic Postsynaptic Potential Research Articles

Synaptic inputs to trigeminal primary afferent neurons cause firing and modulate intrinsic oscillatory activity.

In this paper, we investigated the influence of synapses on the cell bodies of trigeminal muscle spindle afferents that lie in the trigeminal mesencephalic nucleus (NVmes), using intracellular recordings in brain stem slices of young rats. Three types of synaptic responses could be evoked by electrical stimulation of the adjacent supratrigeminal, motor, and main sensory nuclei and the intertrigeminal area: monophasic depolarizing postsynaptic potentials (PSPs), biphasic PSPs, and all or none action potentials without underlying excitatory PSPs (EPSPs). Many PSPs and spikes were abolished by bath-application of 6,7-dinitroquinoxaline (DNQX) alone or combined with D,L-2-amino-5-phosphonovaleric acid (APV), suggesting that they are mediated by non-N-methyl-D-aspartate (NMDA) and NMDA glutamatergic receptors, while some action potentials were sensitive to bicuculline, indicating involvement of GABAA receptors. A number of cells showed spontaneous membrane potential oscillations, and stimulation of synaptic inputs increased the amplitude of the oscillations for several cycles, which often triggered repetitive firing. Furthermore, the oscillatory rhythm was reset by the stimulation. Our results show that synaptic inputs to muscle primary afferent neurons in NVmes from neighboring areas are mainly excitatory and that they cause firing. In addition, the inputs synchronize intrinsic oscillations, which may lead to sustained, synchronous firing in a subpopulation of afferents. This may be of importance during rapid biting and during the mastication of very hard or tough foods.

Two pharmacologically distinct receptors mediate two postsynaptic potential (PSP) compoments in the afferent synapse of the Plotosus electroreceptor

In the Plotosus electroreceptor, strong brief excitatory pulses to the ampulla induced bi-phasic postsynaptic potential (PSP), externally recorded in the afferent nerves, a fast PSP during the pulse and a later slow PSP. Both PSPs increased in size on increasing stimulus intensity, with a lower saturation level for the slow PSP. Time to peak for the fast PSP gradedly decreased to below 10 ms on stronger stimuli, while in contrast that for the slow PSP increased to over 100 ms. The two PSPs were readily distinguised pharmacologically. Some Glu antagonists, kynurenic acid ψ-DGG, supressed the slow PSP, but had litte effect on the fast PSP. The suppression was dose-dependent and reversible over the entire range of input-output relations. In addition, l-aspartate at 100–300 μM markedly prolonged the slow PSP pharmacology corresponding to a Glu receptor, and the other for the fast PSP of still unknwon receptors: one for the slow PSP pharmacologically corresponding to a Glu receptor, and the other for the fast PSP of still unknown property. The two PSPs, though discriminated under specified stimulus conditions, seem to be involved also in the synaptic responses of longer duration in general.

Integration of biphasic synaptic input by electrotonically coupled neuroendocrine caudodorsal cells in the pond snail.

The ovulation hormone-producing caudodorsal cells (CDCs) of the pond snail Lymnaea stagnalis form two clusters of electrotonically coupled cells, each containing a few specialized (ventral) cells that connect the clusters. The hormone is secreted during a pacemaker-driven discharge. The CDCs receive a biphasic cholinergic postsynaptic potential (PSP), consisting of a rapid excitatory postsynaptic potential (EPSP) and a slow inhibitory postsynaptic potential (IPSP) that is elicited by stimulation of nerves. The effect of the synaptic input on the discharge of the CDCs is described and the location of the synapse investigated by a combination of electrophysiological recordings and morphological techniques. The PSP interrupts the discharge and hastens its termination. In addition, it causes a reversal of the temporal order of the spikes of ventral cells (that normally lead) and dorsal cells (that lead only after the PSP). Ion-substitution experiments indicate that the ionic mechanism underlying the biphasic PSP is conventional, involving a conductance increase for Na+ (EPSP) and K+ (IPSP). Receptors mediating the inhibitory component occur only on the proximal axons of the ventral cells, both components are larger and reverse more readily in ventral cells. These findings suggest that the PSP is generated in the ventral cells. The biphasic PSP has no effect on electrical coupling, suggesting that it is not generated along the electrical pathways among the cells. Horseradish peroxidase (HRP) staining reveals that the lateral branches emerge from the proximal axons of the ventral cells only. In HRP-filled preparations processed for electron microscopy (EM) acetylcholinesterase is demonstrated at these branches where it occurs associated with synapses. The location on fine branches of the ventral cells explains the absence of an effect on electrotonic transmission, whereas the reluctance of components of the PSP to reverse at the expected potentials is due to the distribution of the synapses over more than one cell. It is concluded that the biphasic PSP is received only by the ventral cells and that it is conveyed electrotonically to the other cells.

Functional and structural correlates of cell size in paracerebral neurons of Pleurobranchaea californica.

1. The paracerebral neurons (PCNs) in the brain of the mollusk Pleurobranchaea are a population of 12-16 interneurons that send axons to the buccal ganglion and control cyclic feeding behavior (9). In the present study we show that the PCNs differ in size and that a number of functional and structural properties of the PCNs are closely correlated with cell size. 2. PCN soma diameter varies from about 30 to 120 micrometers. The diameters segregate into two distinct but overlapping populations, which correspond to independently assigned functional classifications of "tonic" and "phasic" PCNs. The mean soma diameters of two populations were 63 and 84 micrometers, respectively. 3. Two morphological features vary systematically with PCN soma size. First, soma diameter, axonal conduction velocity, and extracellular spike amplitude were positively correlated; therefore, PCN axon diameter presumably increases with soma diameter. Second, intrasomatic injection of lucifer yellow revealed that the small, tonic PCNs are multipolar, while the large, phasic PCNs are generally monopolar neurons. 4. Small PCNs discharge tonically in response to sustained current injection and have a weak effect on cyclic motor output recorded from nerves that innervate feeding muscles. In contrast, the large PCNs discharge phasically in bursts of action potentials that are coordinated with the cyclic motor output and have a comparatively strong effect on the rhythm. The motor effects of simultaneous tonic and phasic PCN stimulation are additive. 5. Tonic and phasic PCNs innervate different but partially overlapping populations of feeding motor neurons. Phasic PCNs typically inhibit motor neurons exiting buccal root 3, while tonic PCNs either have no effect or are weakly excitatory. 6. Tonic and phasic PCNs exhibit different intrinsic properties. In comparison with phasic PCNs, tonic PCNs have higher input resistances, higher spontaneous discharge rates at rest potential, lower firing thresholds to intrasomatically injected current, lower absolute voltage thresholds, greater pacemaker sensitivity, and greater total capacitance. 7. Tonic and phasic PCNs exhibit different input properties. Tonic PCNs are recruited before phasic ones during cycylic buccal motor output induced by stomatogastric nerve stimulation. Phasic PCNs receive powerful, cycylic inhibition that is not shared by tonic PCNs. In addition, extracellular stimulation of the large oral veil nerve of the brain excites tonic PCNs but causes a biphasic postsynaptic potential (PSP) in phasic PCNs that has a net inhibitory effect. Some excitatory synaptic input to phasic and tonic PCNs is unshared, while some is shared. 8. It is concluded that these command interneurons obey the size principle discovered earlier in motor neurons (4, 13-16). Cell size per se is not the causal variable, however; instead the underlying causes of the differences between small and large PCNs include different input and output organizations as well as different intrinsic functional and morphological properties.

Properties of synapses made by IVN command-interneurones in the stomatogastric ganglion of the spiny lobster Panulirus interruptus.

1. The IVN command interneurones synapse directly onto 11 identified neurones in the stomatogastric ganglion: the two pyloric dilators (PDs), the anterior burster (AB), ventricular dilator (VD), the four gastric mill neurones (GMs), the two lateral posterior gastric neurones (LPGNs), and Interneurone I (Int 1). 2. The IVN p.s.p.s in PD and AB are biphasic, and consist of a fast depolarizing component followed by a slower hyperpolarizing component. 3. The hyperpolarizing component of this biphasic postsynaptic potential is inhibitory, and appears to be the result of a conductance increase to K+ and Cl-. 4. The IVN p.s.p. in VD is excitatory and can drive VD one-for-one. 5. The IVN p.s.p.s in GM and LPGN are inhibitory. The amplitude of a single p.s.p. is small but, at high frequency, summation of p.s.p.s holds the postsynaptic membrane potential below threshold. 6. The facilitation characteristics of the p.s.p.s in each neurone are described. 7. The functional significance of these synaptic characteristics is discussed in terms of the modification of motor output caused by a burst of the IVN interneurones.

Peculiarities of orthodromic inhibition in pacemaker neurons in Helix pomatia

We used the intracellular recording method to study the effect of a group of nerves in the visceral complex on the activity of a pacemaking giantneuron located in the peripheral part of the visceral ganglion in a mollusk. Single excitations of the left and right pallial, the intestinal, and the anal nerves with electrical stimuli evoked similar responses, consisting of phases of rapid depolarization (duration 100 msec, amplitude 3–5 mV) and slower hyperpolarization (duration 400 msec, amplitude 5–8 mV). The excitation also had an aftereffect, which was expressed in inhibition of the background activity of the pacemaker for several seconds. The most interesting of the functional characteristics of that response was the effects of summation. With rhythmic excitation by stimuli of low frequency (0.5–1 c/sec) the result of summation was general hyperpolarization of the neuron and the appearance of giant inhibitory postsynaptic potentials (IPSP's) with an amplitude of 12–16 mV. With higher frequency of excitation (2–3 c/sec and upward) we observed depolarization replacing the hyperpolarization of the neuron, but IPSP's of large amplitude were absent. At the end of rhythmic excitation prolonged inhibition of the pacemaker's activity, lasting some minutes, occurred in all cases. This article discusses the possible mechanisms of that type of prolonged inhibition of the pacemaker's activity, the origin of the phases in biphasic responses, and the reasons for differences in the course of summation of biphasic postsynaptic potentials.

Dendritic synapses and reversal potentials: Theoretical implications of the view from the soma

The dendritic location of synapses, and the usual intrasomatic location of the recording and stimulating microelectrode, will cause the postsynaptic potential (PSP) to be relatively insensitive to changes in the somatic resting potential. When reversal of a PSP is attained, this same decoupling effect causes the measured reversal (“equilibrium”) potential to be in error by a large factor. When the synapse is located one-half space constant away, the reversal potential will appear to be 65% further away from the resting potential than it is at the subsynaptic site. At one space constant, the error is 171%. Other experimental design considerations in CNS synaptic physiology are: (a) The height-voltage (P-V) curve for a composite PSP may be predicted, showing that nearby PSP will mask more distant contributions. (b) If a large distant EPSP and a smaller nearby IPSP are mixed together, giving the appearance of a somewhat smaller EPSP, a steep P-V curve will result which could be misinterpreted as implying a somatic EPSP. (c) Biphasic PSP may result from spatially distributed synapses or from IPSP contamination. It is concluded that these problems may be avoided by the use of single-bouton PSP, which eliminate the possibility of spatial summation, temporal dispersion, and IPSP contamination. The demonstration of the conductance increase model for EPSP, as opposed to electrical synapses and electrogenic pumps, depends strongly upon such design considerations.

Polyphasic Synaptic Activity

This chapter describes polyphasic synaptic activity. In chemical synapses, the transmitter released by a presynaptic neuron combines with specific receptor molecules in the postsynaptic neuronal membrane. This combination produces permeability changes for specific ions; thus, electric currents are created in the postsynaptic neuron that either depolarizes and excites it or hyperpolarizes and inhibits it. The measurable potential changes are called “postsynaptic potentials.” The inhibition comprises a short depolarizing phase followed by a long-duration hyperpolarizing inhibitory phase. Another type of inhibition of long duration comprises a fast hyperpolarizing phase followed by a slow hyperpolarizing phase. The neuronal interaction produces a complex response in the postsynaptic neuron. The electrical synapse responsible for the biphasic postsynaptic potential (BPSP) is based on the plurality of different postsynaptic receptors to the same transmitter substance. Thus, BPSP represents a rare case of electrically transmitted inhibition.

A direct synaptic connexion between the left and right giant cells in Aplysia.

1. In Aplysia fasciata, intrasomatic stimulation of the giant cell (RGC) of the right upper quadrant of the abdominal ganglia is followed after a constant delay by the appearance of a synaptic potential recorded in the giant cell (LGC) of the left pleural ganglion.2. The synaptic potential recorded in the LGC soma has a biphasic form (hence biphasic post-synaptic potential or BPSP) consisting of a fast depolarizing phase of about 200-800 muV amplitude and 0.15-0.25 sec duration, followed by a slow hyperpolarizing phase of about 200-800 muV amplitude and 1-3 sec duration.3. During repetitive stimulation summation results in an over-all hyperpolarization at low frequencies (less than 5/sec) and an over-all depolarization for higher frequencies. Very high frequencies (25/sec) of stimulation of the RGC may elicit a spike in the LGC.4. Stimulation with two shocks showed increasing effects with shorter intervals on both the depolarizing and hyperpolarizing phase. These effects were progressive and there was no falling out of one of the two phases as might be expected if the BPSP was a composite of an inhibitory post-synaptic potential (IPSP) and an excitatory post-synaptic potential (EPSP).5. The effects of artificially imposed polarization of the LGC through a second micro-electrode suggest that the BPSP results from a chemical transmission mechanism for both its depolarizing and hyperpolarizing phases but electrical transmission cannot be excluded.6. Curare has no effect on the BPSP and thus excludes a cholinergic transmission mechanism. Chloride ions injected into the LGC soma do not appear to modify the BPSP and hence it is concluded that the hyperpolarizing phase is different from IPSPs of the same cell.7. No synaptic potential is recorded in the RGC following stimulation of the LGC, except in a single preparation in which the RGC soma was situated in the right pleural ganglion. In this case the synaptic potential recorded in both giant cells following stimulation of the other, was biphasic in form.8. It is concluded that the BPSP is a unitary monosynaptic potential which is a characteristic feature of the organization of these two giant cells.