ENDOGENOUS CANNABINOIDS AND SYNAPTIC TRANSMISSION; IS THE GRASS ALWAYS GREENER ON THE OTHER SIDE?

Neuroreport ◽  
2001 ◽  
Vol 12 (9) ◽  
pp. A64
Author(s):  
Guido Mannaioni
2004 ◽  
Vol 2 (1) ◽  
pp. 49-57 ◽  
Author(s):  
M. Kano ◽  
T. Ohno-Shosaku ◽  
T. Maejima ◽  
T. Yoshida ◽  
K. Hashimoto

2008 ◽  
Vol 100 (2) ◽  
pp. 1113-1126 ◽  
Author(s):  
Sun Hee Cho Lee ◽  
Karen Taylor ◽  
Franklin B. Krasne

Serotonin can produce multiple, contradictory modulatory effects on strength of synaptic transmission in both vertebrate and invertebrate nerve circuits. In crayfish, serotonin (5-HT) can both facilitate and depress transmission to lateral giant escape command neurons; however, which effect is manifest during application, as well as the sign and duration of effects that may continue long after 5-HT washout, may depend on history of application as well as on concentration. We report that protein kinase A (PKA) signaling is essential to the production of facilitation but depression is mediated by non-cAMP/PKA signaling pathways. However, we unexpectedly found that PKA activity is essential for the decay of depression when serotonin is washed out. This, and evidence from the effects of a variety of serotonin application regimens, suggest that facilitatory and depressive states coexist and compete and that the decay of each is dependent on stimulation by the other. A computational model that incorporates these assumptions can account for and rationalize the varied effects of a wide range of serotonin application regimens.


Evoked transmitter release is abnormal at the larval neuromuscular junctions of two Drosophila mutants. Following a single nerve impulse, the increased calcium conductance at the nerve terminal, which lasts for 1 ms in normal larvae, lasts for at least 60 ms in one mutant and several seconds in the other. Both mutations appear to affect the same gene on the X-chromosome. Normal larvae treated with 4-aminopyridine, a potassium channel blocking agent, mimic the abnormal synaptic transmission of one mutant. Normal larvae treated with tetraethylammonium, another potassium channel blocking agent, mimic the abnormal synaptic transmission of the other mutant. From these and other experiments, we suggest that the abnormal neuromuscular transmission in these mutants may be caused by defective potassium channels in the nerve terminal membrane.


1989 ◽  
Vol 236 (1284) ◽  
pp. 253-268 ◽  

Experiments have been made to follow the development of chemical and electrical transmission between pairs of leech neurons in culture. 1. The cell bodies of identified neurons were isolated from the CNS by suction after mild enzyme treatment, together with a length of the initial segment (or ‘stump’). The neurons tested were Retzius cells (R), annulus erector motoneurons (AE), Anterior pagoda cells (AP) and pressure sensory cells (P). Pairs of cells were placed together in various configurations, with different sites on their surfaces making contact. 2. When pairs of Retzius cells were apposed with their stumps touching, serotonergic, chemically mediated synaptic transmission became apparent before electrical transmission. By 2.5 h impulses in either of the two Retzius cells produced hyperpolarizing inhibitory potentials in the other. These potentials were reversed by raised intracellular CI and showed clear facilitation. The strength of chemical transmission between Retzius cells increased over the next 72 h. 3. After chemical transmission had been established, weak non-recti­fying electrical transmission became apparent between Retzius cells at about 24–72 h. By 4 days coupling became stronger and tended to obscure chemically evoked synaptic potentials. 4. When pairs of Retzius cells were aligned in culture with the tip of one cell stump touching the soma of the other, chemical transmission also developed rapidly. Transmission was, however, in one direction, from stump to soma. At later stages non-rectifying electrical coupling devel­oped as with stump-stump configuration. With the cell bodies of two Retzius cells apposed, electrical coupling developed after several days, before chemical transmission could be observed. 5. When Retzius and P cells were cultured with their stumps in con­tact, inhibitory chemical synaptic transmission developed within 24 h. Transmission was always in one direction, from Retzius to P cell. Electrical coupling of Retzius and P cells never occurred whatever the spatial relations of the cells to one another. 6. Annulus erector motoneurons, which contain ACh and a peptide resembling FMRFamide, first developed electrical coupling when the two stumps were in contact and then, later, bi-directional chemical transmission. Anterior Pagoda pairs placed stump-to-stump showed electrical connections. 7. Electronmicrographs revealed the presence of synaptic structures within24 h after Retzius-Retzius, Retzius-P or AE–AE stumps were apposed. 8. The specificity of connections between cultured cells was similar to that observed in earlier experiments. A marked difference was in the speed and reliability with which chemical synapses developed when stumps were in contact. The results show that the tip of a neuron represents a preferential site for the formation of chemical synapses.


1977 ◽  
Vol 55 (6) ◽  
pp. 1391-1393 ◽  
Author(s):  
D. Lekić

The action of AMP (adenosine 5′-monophosphate) on synaptic transmission of Renshaw cells has been studied in cats under Dial anaesthesia. AMP applied iontophoretically reversibly reduced synaptic responses of Renshaw cells evoked by stimulation of ventral roots, as well as their spontaneous firing; however, there were no marked effects on discharges of these cells caused by iontophoretic application of acetylcholine, aspartate, and glutamate. On the other hand, AMP had no comparable effect on synaptic responses of dorsal horn interneurones evoked by stimulation of dorsal roots or their spontaneous discharges.


Genetics ◽  
1989 ◽  
Vol 121 (4) ◽  
pp. 703-721 ◽  
Author(s):  
C Desai ◽  
H R Horvitz

Abstract We have isolated and characterized 45 Caenorhabditis elegans mutants presumed to be defective in the functioning of the hermaphrodite-specific neurons (HSNs). Like hermaphrodites that lack the HSN motor neurons, these mutants are egg-laying defective and do not lay eggs in response to exogenous imipramine but do lay eggs in response to exogenous serotonin. Twenty of the 45 mutations define 10 new egl genes; the other 25 mutations are alleles of five previously defined genes, four of which are known to affect the HSNs. Seven mutations in three genes cause the HSNs to die in hermaphrodites, as they normally do in males. These genes appear to be involved in the determination of the sexual phenotype of the HSNs, and one of them (egl-41) is a newly identified gene that may function generally in sex determination. Five of the 15 genes are defined only by mutations that have dominant effects on egg laying. One gene egl(n1108), is defined by a temperature-sensitive allele that has a temperature-sensitive period after HSN development is complete, suggesting that egl(n1108) may be involved in HSN synaptic transmission. Four of the genes are defined by single alleles, which suggests that other such genes remain to be discovered. Mutations in no more than 4 of the 15 genes specifically affect the HSNs, indicating that there are few genes with functions needed only in this single type of nerve cell.


1996 ◽  
Vol 76 (3) ◽  
pp. 1942-1957 ◽  
Author(s):  
J. M. Goldberg

1. The vestibular type I hair cell and its calyx ending can communicate in three ways. 1) In conventional synaptic transmission an excitatory neurotransmitter is released in multimolecular packets from the hair cell and depolarizes the ending. 2) Ephaptic transmission occurs because currents originating in one structure change the membrane potential of the other structure. 3) Potassium is released from the hair cell during transduction, accumulates in the intercellular space, and can depolarize both the hair cell and the ending. 2. A system of steady-state cable equations was used to analyze conventional and ephaptic transmission. The equations describe the membrane potentials of the hair cell's basolateral surface and of the ending's inner and outer faces. A terminal resistor represents the apical pole of the hair cell and a second terminal resistor represents the parent fiber and other processes connected to the ending. Transducer currents are delivered to the hair cell at its apex and synaptic currents are delivered to the inner or outer faces of the ending at its base. 3. The presence of a calyx ending can reduce conventional synaptic transmission by lowering the postsynaptic input impedance and by introducing an intercellular component into the postsynaptic depolarization of the inner face. Transmission is expressed as a percentage of the synaptic depolarization that would occur in the absence of the ending. Increasing the specific resistance of the inner and outer faces from 150 to 15,000 omega.cm2 improves transmission almost tenfold, from 10% to > 90%. Selectively increasing the impedance of one or the other face results in only a twofold improvement. Under all conditions, transmission is similar for inner- and outer-face synaptic inputs. 4. Hair cell transducer currents cause an ephaptic hyperpolarization of the calyx inner face and a depolarization of the outer face. Excitatory postsynaptic currents originating in the calyx inner face hyperpolarize the apical part of the hair cell and depolarize its base. Outer-face excitatory currents depolarize the hair cell apex and hyperpolarize the base. On the basis of plausible assumptions about the magnitudes of input currents and about the electrical properties of the elements, it was estimated that ephaptic transmission to or from the inner face results in voltages of 0.5-2 mV in the target structure. Transmission to or from the outer face is 10-25 times less effective. 5. During transduction, K+ ions leave the hair cell's basolateral surface and accumulate in the intercellular space separating it from the calyx inner face. The accumulation was analyzed by combining cable and electrodiffusion theories. To make the theories consistent, the resistance of the intercellular space was derived from the Nernst-Planck equation. It was found that the steady-state intercellular current consisted of a diffusional and an electrical component. The diffusional component was 50-100 times larger than the electrical component. 6. Delta x[K+], the steady-state increase in intercellular K+ concentration from a baseline concentration of 4 mM, is proportional to IA, the magnitude of the transducer current, and is only slightly affected by the basolateral impedance. For a uniform distribution of basolateral currents, the proportionality constant, delta x[K+]/IA, is 0.07 mM/pA at the base and declines to 0 at the apex. A transducer current of 100 pA can result in a delta x[K+] of 7 mM at the base and a possible 25-mV depolarization of the hair cell and the ending. 7. Intercellular K+ accumulation has kinetics with a dominant rate constant of 12 s-1, corresponding to a first-order low-pass filter with a corner frequency of 2 Hz. Kinetics is sufficiently fast for accumulation to participate in the transduction of normally occurring head movements. (ABSTRACT TRUNCATED)


2021 ◽  
Vol 55 (4) ◽  
pp. 73-77
Author(s):  
Vik.V. Yasnetsov ◽  
◽  
Yu.V. Ivanov ◽  
S.K. Karsanova ◽  
V.V. Yasnetsov ◽  
...  

Experiments on hippocampal slices in rats showed that, in contrast to piracetam (100 µM to 10 mM), two new tripeptides, i.e. H-asparagil-glutamyl-proline-OH and H-asparagil-glutamyl-arginin-OH (concentrations 500 µM, 1 and 2.5 mM respectively), strengthened the orthodrome population responses in field СА1. In all three concentrations the effect of H-asparagil-glutamyl-proline-OH was stronger than of the other tripeptide. That is both tripeptides facilitate synaptic transmission within the Schaffer collaterals-pyramidal neurons system in hippocumpal field CA1. Similarly to piracetam (100 µM, within 15 minutes) these tripeptides supported short-term potentiation of the hippocampal synaptic transfer by N-methyl-D-aspartate (NMDA). Specific NMDA-receptors antagonist D-AP5 cancelled the NMDA effect fully which infers that the observed effect is achieved through activation of NMDA-receptors. Effect from H-asparagil-glutamyl-proline-OH excelled equally piracetam and H-asparagil-glutamyl-arginin-OH; H-asparagil-glutamyl-arginin-OH excelled piracetam only.


2021 ◽  
Author(s):  
Margot Wohl ◽  
Kenta Asahina

Neuropeptides influence animal behaviors through complex molecular and cellular mechanisms, many of which are difficult to predict solely from synaptic connectivity. Here, we uncovered two separate downstream targets that are differentially modulated by the neuropeptide tachykinin, which promotes Drosophila aggression. Tachykinin from a single sexually dimorphic group of neurons recruits two separate downstream groups of neurons. One downstream group, synaptically connected to the tachykinergic neurons, expresses the receptor TkR86C and is necessary for aggression. Tachykinin supports the strength of cholinergic excitatory synaptic transmission between the tachykinergic and TkR86C downstream neurons. The other downstream group expresses the TkR99D receptor and is recruited primarily when tachykinin is over-expressed in the source neurons. This circuit reconfiguration correlates with the quantitative and qualitative enhancement of aggression observed when tachykinin is present in excess. Our data highlight how the amount of neuropeptide released from a small number of neurons can reshape the activity patterns of multiple downstream neural populations.


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