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At least 1,585 records · Page 88Linked to original sources
PubMed1987

Presynaptic action of neuropeptide Y in area CA1 of the rat hippocampal slice.

1. Neuropeptide tyrosine (neuropeptide Y, NPY), a recently isolated endogenous brain peptide, reduces the extracellular population spike evoked by stimulation of stratum radiatum in area CA1 of the in vitro rat hippocampal slice, without reducing the antidromically evoked population spike. To test the hypothesis that NPY acts presynaptically, intracellular recordings were made of pyramidal neurones of area CA1 in vitro. 2. Bath application of 10(-6) M-NPY causes a long-lasting (1-1.5 h), reversible reduction of the orthodromically evoked excitatory post-synaptic potential (e.p.s.p.) recorded intracellularly from CA1 pyramidal neurones. This effect on the e.p.s.p. was dependent upon the concentration of NPY. 3. The resting membrane potential, slope input resistance, and action potential threshold, amplitude and duration of the CA1 pyramidal neurones were not affected by NPY. 4. The responses of CA1 pyramidal neurones to ionophoretic pulses of glutamate, applied to the dendrites during synaptic blockade, was also unaffected by NPY. 5. The evidence supports the hypothesis that NPY acts presynaptically in the CA1 region of hippocampus to reduce excitatory input to the pyramidal neurones.

Action Potentials↗
PubMed1991

Temperature sensitivity of graded synaptic transmission in the lobster stomatogastric ganglion.

We examined the temperature sensitivity of graded chemical synaptic strength within the pyloric circuit of the spiny lobster stomatogastric ganglion. Cooling from 20.4 degrees C to 11.3 degrees C reduced the graded synaptic potential (GSP) amplitude at all six pyloric synapses tested. Cooling appeared to reduce the slope of the linear part of the input-output curve at three of these synapses, and did not significantly alter the threshold for transmitter release at any synapses. Pairs of neurons with a presynaptic pyloric dilator (PD) cell showed reductions in graded synaptic strength at 16.5 degrees C but those with presynaptic lateral pyloric (LP) or ventral dilator (VD) cells did not. A generalized decrease in input resistance is not responsible for the reduced GSP amplitude upon cooling, as determined by input resistance, action potential amplitude and electrical coupling measurements. We conclude that cooling reduces graded chemical strength by a direct synaptic action. Since the PD and VD cells use the same transmitter and act on some of the same postsynaptic cells, their differential sensitivity to cooling further suggests a presynaptic site of action. The temperature range used in our experiments encompasses the range that the animal normally encounters in nature. Thus, the relative importance of graded synaptic interactions in generating the pyloric motor rhythm may vary with transient changes in temperature.

Action Potentials↗
PubMed1990

Dendritic action potentials activated by NMDA receptor-mediated EPSPs in CA1 hippocampal pyramidal cells.

Intradendritic recordings were obtained in rat CA1 hippocampal pyramidal cells. Repetitive stimulation produced substantial short-term potentiation of the dendritic excitatory postsynaptic potential (EPSP) which was partly attributable to activation of n-methyl-D-aspartate receptors. Accompanying the potentiated synaptic response were Na(+)-mediated spikes which appeared to originate at multiple sites in the dendritic arbor. These discrete dendritic action potentials are rarely distinguishable in somatic recordings, but may contribute to the subthreshold response at the pyramidal cell body. In addition, dendritic spikes may interact with other voltage-dependent dendritic conductances.

2-Amino-5-phosphonovalerate↗
PubMed2000

Effects of lead on long-term potentiation in hippocampal CA3 vary with age.

The effects of lead on long-term potentiation (LTP) in the hippocampal area CA3 were different in 30-day (P30) and 60-day-old (P60) rats upon either acute perfusion of lead to the isolated brain slice from controls or when recorded from slices from rats after chronic developmental exposure to lead. Lead caused a significant inhibition of LTP in 30-day CA3, and a significant potentiation in 60-day CA3 with either exposure paradigm. Consistent with the effects on LTP, lead inhibits phorbol ester-induced synaptic potentiation in 30-day rats and enhances phorbol ester-induced potentiation in 60-day rats. Protein kinase C (PKC) has been implicated in actions of lead but previous investigations have reported either a stimulation or a blockade of PKC by lead. Our results are consistent with the hypothesis that the effects of lead on LTP are mediated via an action on PKC, which varies with age.

Age Factors↗
PubMed1982

Role of presynaptic calcium ions and channels in synaptic facilitation and depression at the squid giant synapse.

1. The roles of presynaptic calcium influx and calcium accumulation in synaptic facilitation and depression were explored at the giant synapse in the stellate ganglion of the squid. 2. Calcium currents were recorded in the presynaptic terminal, using a three-electrode voltage clamp and blocking sodium and potassium currents pharmacologically. The calcium influx was constant during pairs or trains of brief depolarizing pulses that elicited facilitating or depressing excitatory post-synaptic potentials (e.p.s.p.s). 3. The relationship between calcium influx and transmitter release during brief depolarizing pulses of varying amplitude resembled a power function with exponent of about 2. 4. Presynaptic calcium concentration transients were measured by injecting the dye arsenazo III and detecting absorbance changes microspectrophotometrically. Increments in intracellular free calcium accompanying single action potentials appeared constant for repeated action potentials that elicited facilitating e.p.s.p.s. 5. The presynaptic calcium concentration remains elevated for several seconds following action potentials. 6. Presynaptic injection of calcium ions by interbarrel ionophoresis evokes a postsynaptic depolarization, apparently reflecting a large increase in miniature e.p.s.p. frequency. Presynaptic action potentials remain unaffected by this treatment, but e.p.s.p.s triggered by them are facilitated for several seconds, and then depressed. 7. The results are consistent with the hypothesis that synaptic facilitation is due to the action of residual calcium or a calcium complex remaining in the presynaptic terminal after electrical activity. The late depression of release during calcium injection may be a result of the continual release of transmitter and consequent depletion of a presynaptic store.

Action Potentials↗
PubMed1983

Basic mechanisms of penicillin-induced epileptiform discharges.

A short survey is given of recent studies on epileptogenesis, concentrating on data obtained by adding penicillin to hippocampal slices in vitro. Epileptiform burst discharges, similar to the interictal responses of intact preparations, are elicited by synaptic activation. Neither the afferent fibres nor the synaptic transmission per se are changed. Excitatory synaptic potentials are, however, prolonged due to abolition of gamma-aminobutyric acid (GABA)-mediated inhibitory processes. The consequent increased membrane resistance allows the synaptic depolarization to trigger slow depolarizing waves, most likely in the dendrites. A possible explanation is that these waves are due to inward calcium currents, generated when the cell is in a special condition which facilitates such currents. The facilitatory factors are discussed.

Action Potentials↗
PubMed2000

Estradiol modulates long-term synaptic depression in female rat hippocampus.

Fluctuating estradiol levels in the adult, female rat modify the anatomical and functional organization of the hippocampal CA1 region. When systemic levels of estradiol are low, e.g., on estrus or in ovariectomized (OVX) rats, long-term synaptic potentiation is difficult to induce in vivo. However, little is known about the role of this ovarian hormone in long-term synaptic depression. Using multiple conditioning paradigms, we assess the magnitude of long-term depression (LTD) at CA3-CA1 synapses in vitro from adult, ovariectomized rats as a function of systemic estradiol replacement. In hippocampal slices from control OVX rats with low levels of estradiol, a low-frequency (2 Hz), asynchronous conditioning stimulation protocol does not produce LTD at 1 h postconditioning. However, this same protocol induces robust LTD in slices from estradiol-treated OVX rats. When the conditioning frequency is increased to 4 Hz, slices from both groups of rats show robust LTD in vitro. At an even higher conditioning frequency (10 Hz), the 2-Hz-based observations are reversed; no consistent changes in synaptic transmission are observed in slices from estradiol-treated OVX rats, but those from control rats (OVX + oil) show robust LTD. Thus estradiol reduces the frequency threshold for LTD induction at the CA3-CA1 synapses. Further, regardless of the conditioning frequency employed, where robust LTD is seen, its induction depends on normally functioning N-methyl-D-aspartate (NMDA) receptors during conditioning. The shift in conditioning frequency needed to elicit LTD is consistent with a decrease in NMDA receptor activation with decreasing estradiol levels.

Animals↗
PubMed2002

Postsynaptic application of a cAMP analogue reverses long-term potentiation in hippocampal CA1 pyramidal neurons.

The molecular mechanisms that underlie the maintenance of long-term potentiation (LTP) remain unclear. We have examined the influence of postsynaptic cAMP-dependent processes on LTP maintenance in CA1 hippocampal cells. After LTP induction, drugs affecting cAMP-dependent processes were perfused into the cell through a patch pipette. A cAMP analogue, Rp-cAMPS (4 mM), dramatically decreased the amplitude of potentiated synaptic responses. The amplitude of responses in the control pathway was also decreased but to a lesser extent, indicating a specific effect on the potentiation process. This specific effect was not due to the larger amplitude of potentiated responses, was not use-dependent and, unlike other factors that affect LTP maintenance, did not depend on the delay (2, 10, or 25 min) of drug application after LTP induction. Lower concentrations of Rp-cAMPS (1.0 and 0.4 mM) also produced an inhibitory effect but reduced the LTP and control pathways comparably. One possible action of Rp-cAMPS is competitive inhibition of protein kinase A (PKA). Surprisingly, a potent and noncompetitive PKA inhibitor, regulatory type II subunit of PKA, produced only a weak depression of potentiated and control responses indicating there must be other targets for Rp-cAMPS. Moreover, Sp-8-OH-cAMPS, which is an activator of PKA, and Rp-8-OH-cAMPS, which is a weak inhibitor of PKA, both produced effects similar to those of Rp-cAMPS. We conclude that there are postsynaptic cyclic nucleotide-dependent processes that can specifically alter the mechanisms that maintain LTP and that are not primarily dependent on PKA.

Animals↗
PubMedDate not supplied

Role of neurotrophins in synapse development and plasticity.

Neurotrophic factors are traditionally viewed as secretory proteins that regulate long-term survival and differentiation of neurons. The role of neurotrophic factors in the structural integrity of the nervous system makes them attractive candidates as therapeutic agents for neurodegenerative diseases. However, the fact that expression of many neurotrophic factors in the central nervous system is rapidly enhanced by neuronal activity suggests a new role for these factors in activity-dependent processes, such as synaptic development and plasticity. A series of recent studies has provided strong evidence for this novel function of neurotrophic factors. The neurotrophin family of proteins has been shown to acutely potentiate synaptic transmission at the neuromuscular junction and in the brain. These factors are also involved in the maturation of the neuromuscular synapses and in the development of synapses in the visual system. Gene targeting and physiological experiments demonstrate that brain-derived neurotrophic factor (BDNF) plays an important role in long-term potentiation (LTP), a cellular model for learning and memory. These findings have brought together two hotly pursued areas of neuroscience, namely, the function of neurotrophic factors and the mechanisms for synaptic plasticity. Continuous studies in this new field will help understand how synapses develop and function in the brain, and may have significant implications in treating learning disorders in both children and adults.

Adult↗
PubMed1977

Development of kitten hippocampal neurons.

Cells in the CA1 region of the hippocampus of kittens were studied using an in vitro slice preparation. Good quality intracellular records were obtained from over 100 cells from kittens 2 days to 4 weeks of age. Cell resistance was high in 2-day-old animals and decreased over the following 4 weeks. Both excitatory and inhibitory synaptic potentials were seen in all animals. EPSPs were only weakly effective in triggering spikes in the youngest kittens, but were greatly potentiated by repetitive stimulation at 3-10/sec; IPSPs caused a potent blockade of cell discharge in even the youngest preparations. Stimulation of the orthodromic input pathway led to a complex series of excitatory and inhibitory synaptic events which was not seen in the adult. In the 2- and 4-week-old kittens, a cell type with physiological properties different from the predominant pyramidal cell began to appear in recordings from the CA1 region. Technical difficulties inherent in in vivo recordings from neonatal animals were considerably less with the in vitro technique. Careful developmental studies may now be pursued in the slice at the single cell synaptic level.

Action Potentials↗
PubMed1992

Receptor changes and LTP: an analysis using aniracetam, a drug that reversibly modifies glutamate (AMPA) receptors.

The hypothesis that long-term potentiation (LTP) involves receptor modifications was tested with aniracetam, a nootropic drug that selectively increases currents mediated by the AMPA subclass of glutamate receptors. Aniracetam had different effects on the waveform of synaptic potentials in hippocampus before and after induction of LTP: (1) the drug caused a slight reduction (or delay) of the initial segment of the response after LTP; and (2) the facilitatory effects of aniracetam occurred at a later time point in the response after LTP than before. The interactions between LTP and aniracetam were still present when synaptic responses were greatly reduced by partial blockade of postsynaptic receptors and were not reproduced by increasing release or the number of stimulated synapses. A mathematical treatment of synaptic currents produced the following results: (1) if aniracetam facilitates AMPA receptor currents simply by reducing desensitization, then its complex interaction with LTP emerges when potentiation changes the kinetic and conductance properties of receptor channels; (2) if aniracetam also significantly increases conductance, then the experimental data can be reproduced by modeling LTP as an increase in channel conductance alone.

Animals↗
PubMed2000

Differential modulation of auditory thalamocortical and intracortical synaptic transmission by cholinergic agonist.

To investigate synaptic mechanisms underlying information processing in auditory cortex, we examined cholinergic modulation of synaptic transmission in a novel slice preparation containing thalamocortical and intracortical inputs to mouse auditory cortex. Extracellular and intracellular recordings were made in cortical layer IV while alternately stimulating thalamocortical afferents (via medial geniculate or downstream subcortical stimulation) and intracortical afferents. Either subcortical or intracortical stimulation elicited a fast, 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX)-sensitive, monosynaptic EPSP followed by long-duration, polysynaptic activity. The cholinergic agonist carbachol suppressed each of the synaptic potentials to different degrees. At low concentrations (5 microM) carbachol strongly reduced (>60%) the polysynaptic slow potentials for both pathways but did not affect the monosynaptic fast potentials. At higher doses (10-50 microM), carbachol also reduced the fast potentials, but reduced the intracortically-elicited fast potential significantly more than the thalamocortically-elicited fast potential, which at times was actually enhanced. Atropine (0.5 microM) blocked the effects of carbachol, indicating muscarinic receptor involvement. We conclude that muscarinic modulation can strongly suppress intracortical synaptic activity while exerting less suppression, or actually enhancing, thalamocortical inputs. Such differential actions imply that auditory information processing may favor sensory information relayed through the thalamus over ongoing cortical activity during periods of increased acetylcholine (ACh) release.

2-Amino-5-phosphonovalerate↗
PubMed1998

Dendritic properties of hippocampal CA1 pyramidal neurons in the rat: intracellular staining in vivo and in vitro.

Dendritic morphology and passive cable properties determine many aspects of synaptic integration in complex neurons, together with voltage-dependent membrane conductances. We investigated dendritic properties of CA1 pyramidal neurons intracellularly labeled during in vivo and in vitro physiologic recordings, by using similar intracellular staining and three-dimensional reconstruction techniques. Total dendritic length of the in vivo neurons was similar to that of the in vitro cells. After correction for shrinkage, cell extent in three-dimensional representation was not different between the two groups. Both in vivo and in vitro neurons demonstrated a variable degree of symmetry, with some neurons showing more cylindrical symmetry around the main apical axis, whereas other neurons were more elliptical, with the variation likely due to preparation and preservation conditions. Branch order analysis revealed no difference in the number of branch orders or dendritic complexity. Passive conduction of dendritic signals to the soma in these neurons shows considerable attenuation, particularly with higher frequency signals (such as synaptic potentials compared with steady-state signals), despite a relatively short electrotonic length. Essential aspects of morphometric appearance and complex dendritic integration critical to CA1 pyramidal cell functioning are preserved across neurons defined from the two different hippocampal preparations used in this study.

Animals↗
PubMed1991

Simulations of a phase comparing neuron of the electric fish Eigenmannia.

1. Investigations of the jamming avoidance response in the weakly electric fish Eigenmannia have shown that the 'small cell', an identified cell type in lamina 6 of the torus semicircularis, can distinguish a brief time difference between the phase of externally applied sinusoidally varying electrical fields. Computer simulations were performed to determine what physiological and anatomical features of the small cell could permit this. 2. The small cell shows apparent inhibition despite having no identified inhibitory synaptic input. This effect was produced in the model using voltage-sensitive membrane channels. These permit an initial sub-threshold excitatory post-synaptic potential (EPSP) to increase the threshold to firing, preventing a subsequent EPSP from firing the cell. 3. Noise and conduction failure appeared to improve the range of cell responsivity. The addition of noise permitted a gradual change in cell firing with change in time disparity, allowing the cell to signal more subtle changes in disparity at the expense of decreased selectivity for a specific absolute time disparity. 4. The cell's multiple dendrites permit a 47% reduction in jitter for incoming signals. Other aspects of dendrite organization did not appear to contribute to the cell's precision.

Animals↗
PubMed1976

Regulation of neuronal properties by afferent connections. I. Functional changes in snail neurons following section of presysnaptic nerve fibers.

The left cerebral connective of snail ganglia containing afferent inputs to a particular neuron was sectioned. One week after the operation synaptic potentials were not obtained when the connective was stimulated, and they had not reappeared after 60 days. The current-voltage relationship of denervated cells showed a rectification in the hyperpolarizing direction, whereas that of control cells had an ohmic behavior. Depolarization or conductance changes produced by ACh or carbachol showed a supersensitivity in denervated cells, evidenced by a shift to the left of the dose-response curve and an increase of the maximal responses obtained. The reversal potential of ACh shifted from--22 mV in the control to--8 mV in denervated cells. Depolarization produced by serotonin was similar in control and denervated cells.

Acetylcholine↗
PubMed1983

Evidence of slow IPSP in mammalian prevertebral ganglia.

A short train of nerve stimulation evoked in a portion of neurons of the guinea pig inferior mesenteric ganglia a slow hyperpolarization (slow IPSP) which persisted when the preceding orthodromic spikes were reduced to subthreshold EPSPs by curare, was reversibly abolished in a low Ca solution, and was not blocked by atropine; furthermore, the post-tetanic hyperpolarization induced by direct intracellular stimulation was generally smaller than the slow IPSP evoked by nerve stimulation. The slow IPSP was often associated with a fall in membrane resistance and its amplitude decreased with membrane hyperpolarization. The results indicate that the slow hyperpolarization is a synaptic potential, and differs from the slow IPSP observed in mammalian and amphibian paravertebral ganglionic neurons in that it is atropine insensitive.

Animals↗
PubMed1988

Pertussis toxin pretreatment discriminates between pre- and postsynaptic actions of baclofen in rat dorsal raphe nucleus in vitro.

Intracellular recordings were made from rat dorsal raphe neurons in vitro. Baclofen (30 microM) and 5-carboxamidotryptamine (5-CT, 300 nM to 1 microM) hyperpolarized these neurons by 10 and 13 mV, respectively. Depolarizing synaptic potentials (DSPs) were evoked by single shocks: baclofen reduced the amplitude of the DSP by 81%, but 5-CT reduced it by only 23%. The somatic response to iontophoretically applied glutamate pulses was reduced by 12% by baclofen, and 23% by 5-CT. In slices from rats pretreated with intracerebroventricular pertussis toxin (PTX), the ability of baclofen to reduce the DSP was almost unchanged, although the hyperpolarizing action of baclofen, and both actions of 5-CT were virtually eliminated. We conclude that it is possible to distinguish the pre- and postsynaptic actions of baclofen with PTX, and that the actions of 5-CT are both blocked.

Animals↗
PubMed1983

Influence of the medial septal nucleus on the excitability of the commissural path-CA1 pyramidal cell synapse in the hippocampus of freely moving mice.

Changes in the excitability of the commissural path-CA1 pyramidal cell synapse were studied by varying the interval between the application of a conditioning pulse in the medial septal nucleus and a test pulse in the contralateral hippocampus in freely moving mice. The results showed that septal prestimulation results in marked changes in the excitability of pyramidal cells (population spikes) without any associated changes in the averaged evoked excitatory post synaptic potentials. Thus, as a result of septal stimulation, population spikes were first potentiated for interpulse intervals ranging from 10 to 30 ms; this was followed by inhibition at intervals between 40 and 60 ms and then by another phase of hyperexcitability between 100 and 160 ms. Possible mechanisms underlying this phenomenon are discussed and these successive changes in excitability are compared to the phase-locked ones which occur spontaneously during theta waves.

Afferent Pathways↗