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PubMed1989

Localization of tetrodotoxin-sensitive field potentials of CA1 pyramidal cells in the rat hippocampus.

1. The role of tetrodotoxin (TTX)-sensitive (Na+) channels in the generation of antidromic and orthodromic field potentials of the CA1 pyramidal cell population was examined by local application of TTX in the in vitro rat hippocampal slice preparation. 2. The sensitivity of alvear (antidromic) and stratum oriens (SO)-evoked potentials to TTX application (10-100 microM) was tested in stratum pyramidale and over the entire extent of pyramidal cell apical dendrites in stratum radiatum. Stratum radiatum (SR)-evoked potentials were examined at the level of pyramidal cell bodies and over the proximal 200 microns of the apical dendritic region. 3. Pressure application of TTX confined to stratum pyramidale or regions of stratum radiatum selectively blocked the negative component of antidromic and SO-evoked population discharge in the cell body layer and over the initial 200 microns of stratum radiatum. 4. SR stimulation evoked a complex field potential in the proximal stratum radiatum (less than 150 microns) composed of at least three components: 1) A short-duration (approximately 3 ms) negativity of shorter peak latency than the population spike recorded simultaneously in stratum pyramidale. This potential was highly sensitive to TTX and appeared to be instrumental in the generation of the cell body population response. 2) A long-duration negativity (approximately 20 ms) evoked at stimulation strengths that were subthreshold for both the short-duration negativity in proximal stratum radiatum and the cell body population spike. Although apparently less sensitive to TTX, this potential was reduced in amplitude with repeated TTX application; and 3) a slow (approximately 12 ms) positive-going potential that was only observed after eliminating all TTX-sensitive conductance mechanisms in the proximal stratum radiatum. 5. The latency difference between the SR-evoked short-duration negativity of proximal stratum radiatum and the population spike in stratum pyramidale decreased or reversed during the course of multiple discharge induced by the addition of bicuculline or picrotoxin (5-10 microM) to the perfusate. 6. These data indicate the presence of TTX-sensitive presumed Na+ channels over the initial 200 microns of pyramidal cell apical dendrites capable of supporting active conduction of population discharge evoked by antidromic or SO stimulation. The sensitivity of SR-evoked potentials to TTX suggests that a synaptic potential generated in the distal apical dendrites is capable of triggering both a slow active depolarization and a fast spike-like discharge in the proximal apical dendritic region.(ABSTRACT TRUNCATED AT 400 WORDS)

Action Potentials↗
PubMed2004

Stabilization of thalamo-cortical long-term potentiation by the amygdala: cholinergic and transcription-dependent mechanisms.

Synaptic potentiation allows neurons to enhance excitability and store information for extended time periods. We examined the role of the amygdaloid complex, known to facilitate long-term memory encoding, to influence synaptic strength at thalamo-cortical synapses. In urethane-anaesthetized rats, theta-burst stimulation of the dorsal lateral geniculate nucleus of the thalamus induced early phase (1-2 h) long-term potentiation (LTP) of the field postsynaptic potential (fPSP) recorded in the ipsilateral primary visual cortex. Electrical stimulation (100 Hz) of the amygdala 5 min after thalamic stimulation converted early phase LTP to stable late-phase (> 4 h) LTP. This effect was not correlated with the degree of electrocorticographic activation of V1 induced by amygdala stimulation. Amygdala stimulation without thalamic theta-burst stimulation did not change thalamo-cortical fPSPs. The centrally acting cholinergic-muscarinic receptor antagonist scopolamine (1 mg/kg, i.p.), but not peripherally acting methyl-scopolamine, completely blocked the amygdala-induced conversion of early to late-phase thalamo-cortical LTP. Further, ventricular application of the transcription inhibitor anisomycin (250 micro g) reduced amygdala-induced late-phase LTP induction. These results demonstrate that the amygdaloid complex transforms time-limited synaptic enhancement of thalamo-cortical transmission into long lasting increases in synaptic strength. These processes are mediated, at least in part, by cholinergic and transcription-dependent mechanisms. These amygdaloid-induced effects provide a potential mechanism underlying long-term enhancement of sensory transmission and information encoding in thalamo-cortical networks.

Amygdala↗
PubMedDate not supplied

Hippocampal long term potentiation: silent synapses and beyond.

Long-term, activity-driven synaptic plasticity allows neuronal networks to constantly and durably adjust synaptic gains between synaptic partners. These processes have been proposed to serve as a substrate for learning and memory. Long-term synaptic potentiation (LTP) has been observed at many central excitatory synapses and perhaps most extensively studied at Schaffer collaterals synapses onto hippocampal CA1 neurons. Multiple contradictory models were proposed to account for this form of LTP. However, recent evidence suggests that some synapses are initially devoid of functional AMPA receptors which can be incorporated during LTP. This new model appears to account for most, but not all, properties of this form of plasticity. Indeed, several mechanisms seem to act in parallel to specifically enhance AMPA-receptor mediated synaptic transmission.

Animals↗
PubMed1998

Stimulation-induced responses of the trigeminal caudal neurons in the brainstem preparation isolated from newborn rats.

The brainstem preparation with the trigeminal mandibular nerve attached was isolated from rats postnatal day 0-6 (P0-P6) to test if the potentiation could be induced in neonatal neurons in the trigeminal subnucleus caudalis by stimulation of the primary afferents. The stimulation-induced potentials in 92 neurons recorded extracellularly, and the synaptic potentials in 16 neurons recorded by the whole-cell patch clamp technique were examined. The extracellularly recorded neurons responded to stimulation (0.5 Hz) with either an increase, a decrease, or little change in spike numbers, and were classified as Type 1, Type 2, and Type 3, respectively. Type 1 neurons at P4 and older responded in a low Mg2+ solution with a progressive increase in spike number lasting for several minutes after the cessation of stimulation, i.e., short-term potentiation, STP. This potentiation was antagonized by 20 microM of (+)-MK-801 hydrogen maleate (MK-801) or 25 microM of 2-amino-5-phosphonovaleric acid. In contrast, Type 1 at P3 and younger did not exhibit STP. The age-related distinct response properties were observed between Type 1 neurons at P4-P6 and at P0-P3. The percentage of Type 1 in studied neurons increased from 24% at P0-P3 to 53% at P4-P6. In the intracellular experiment, the mean latency of excitatory postsynaptic potential (EPSP) of recorded neurons indicated that the conduction velocity of the convergent afferents was 0.37 m/s, in the range of C-fiber. Neurons were classified as Type E and Type I. Type E responded with EPSP only, or with both EPSP and inhibitory postsynaptic potentials (IPSP), while Type I responded with IPSP only. In Type E at P4 and older, a single stimulation produced a burst of spike discharges that lasted for several seconds. Stimulation at a hyperpolarized membrane potential showed that aggregated slow EPSPs lay under a burst of spike discharges, and that slow EPSPs, but not a short-latency EPSP, were completely blocked by MK-801. In contrast, Type E at P3 and younger did not evoke a burst of spikes. Morphological examination of recorded neurons showed that the formation of networks was sparse at P1 and rapidly developed up to P4. The results suggest that: (1) short-term potentiation is induced with the development of synaptic network formation in the caudal nucleus at P4 and older; (2) the summation of N-methyl-d-aspartate (NMDA)-mediated slow EPSPs build up a prolonged depolarization; and (3) the brainstem preparation is applicable for neurophysiological studies on the trigeminal pain system.

2-Amino-5-phosphonovalerate↗
PubMed2002

Local circuit plasticity in the rat dentate gyrus: characterization and aging-related impairment.

We have used frequency-dependent inhibition, a form of short-term plasticity mediated by the activation of inhibitory interneurons, to characterize in vivo alterations in local circuit activity and plasticity in the dentate gyrus of the anesthetized rat. The application of the GABA-A receptor blocker, bicuculline, induced a transient reduction in frequency-dependent inhibition, indicating that this form of local circuit activity is GABA-mediated. Delivering theta burst stimulation to the perforant pathway of the hippocampus induced long-term potentiation of the population excitatory post-synaptic potential, reflecting the potentiation of the perforant path-dentate gyrus granule cell synapses. Concomitantly, theta burst stimulation caused a lasting reduction in frequency-dependent inhibition. In aged rats, long-term potentiation could be induced to the same level as in young rats, but while in young rats frequency-dependent inhibition was concomitantly reduced, frequency-dependent inhibition in the old rats did not show this form of plasticity. Our results indicate that theta burst stimulation induces a form of local circuit plasticity independently of its known capacity to induce synaptic plasticity, and that this form of local circuit plasticity is compromised in aging. Based on these results we propose a potential role for plasticity at the level of the local circuit in learning and memory.

Aging↗
PubMed1995

Acetylcholinesterase induces long-term potentiation in CA1 pyramidal cells by a mechanism dependent on metabotropic glutamate receptors.

Acetylcholinesterase (AChE) has additional functions within the central nervous system that are unrelated to cholinergic transmission. In the cerebellar cortex AChE has been shown to potentiate synaptic responses evoked by excitatory amino acids. Because AChE is also secreted from the terminal regions of cholinergic nerves within the hippocampus, this study investigates the actions of AChE on synaptic transmission in guinea pig hippocampal slices. Application of AChE produced a long-lasting potentiation of both the field epsp and the resulting population spike evoked by stimulation of the Schaffer/commissural-CA1 pathway. This effect was independent of any cholinergic receptor stimulation since it persisted in the presence of the cholinergic antagonists atropine and mecamylamine. Furthermore, the effect was not mimicked by butyrylcholinesterase despite its cholinolytic activity. However, the effect of AChE was dependent on metabotropic glutamate receptor stimulation since it was prevented by the metabotropic receptor antagonist (+/-)-alpha-methyl-4-carboxyphenylglycine. Perfusion with AChE therefore induces a long-lasting potentiation of hippocampal synaptic transmission which is reminiscent of the classical LTP produced by tetanic stimulation. Consequently the secreted protein could play an important role in the molecular mechanisms of learning and memory in vertebrates.

Acetylcholinesterase↗
PubMed1982

Neural pathway involved in the excitation of motoneurones to jaw-opening muscles by stimulation of the orbital cerebral cortex in the cat.

The pathway and synaptic basis for the efferent discharge in the digastric nerve evoked by stimulation of the orbital cortex were studied in cats anesthetized with alpha-chloralose. Transection of the brain stem at the boundary between the pons and the medulla oblongata abolished discharge. Intracellular recording from anterior digastric motoneurones revealed that the orbital cortical stimulation evoked excitatory post-synaptic potentials with a latency that was longer by one synaptic delay than that of spike potentials evoked in medial bulbar reticular neurones making a direct excitatory projection to anterior digastric motoneurones. It was concluded that the excitatory effects was mediated by the medial bulbar reticular formation.

Animals↗
PubMed2003

Ethanol dual modulatory actions on spontaneous postsynaptic currents in spinal motoneurons.

Recently we have shown that acute ethanol (EtOH) exposure suppresses dorsal root-evoked synaptic potentials in spinal motoneurons. To examine the synaptic mechanisms underlying the reduced excitatory activity, EtOH actions on properties of action potential-independent miniature excitatory and inhibitory postsynaptic currents (mEPSCs and mIPSCs) were studied in spinal motoneurons of newborn rats. Properties of mEPSCs generated by activation of N-methyl-D-aspartate receptors (NMDARs) and non-NMDA receptors and of mIPSCs mediated by glycine and gamma-aminobutyric acid-A receptors (GlyR and GABA(A)R) were examined during acute exposure to 70 and 200 mM EtOH. In the presence of 70 mM EtOH, the frequency of NMDAR- and non-NMDAR-mediated mEPSCs decreased to 53 +/- 5 and 45 +/- 7% (means +/- SE) of control values, respectively. In contrast, the frequency of GlyR- and GABA(A)R-mediated mIPSCs increased to 138 +/- 15 and 167 +/- 23% of control, respectively. Based on the quantal theory of transmitter release, changes in the frequency of miniature currents are correlated with changes in transmitter release, suggesting that EtOH decreased presynaptic glutamate release and increased the release of both glycine and GABA. EtOH did not change the amplitude or rise and decay times of either mEPSCs or mIPSCs, indicating that the presynaptic changes were not associated with changes in the properties of postsynaptic receptors/channels. Acute exposure to 200 mM EtOH increased mIPSC frequency two- to threefold, significantly higher than the increase induced by 70 mM EtOH. However, the decrease in mEPSC frequency was similar to that observed in 70 mM EtOH. Those findings implied that the regulatory effect of EtOH on glycine and GABA release was dose-dependent. Exposure to the higher EtOH concentration had opposite actions on mEPSC and mIPSC amplitudes: it attenuated the amplitude of NMDAR- and non-NMDAR-mediated mEPSCs to ~80% of control and increased GlyR- and GABA(A)R-mediated mIPSC amplitude by ~20%. EtOH-induced changes in the amplitude of postsynaptic currents were not associated with changes in their basic kinetic properties. Our data suggested that in spinal networks of newborn rats, EtOH was more effective in modulating the release of excitatory and inhibitory neurotransmitters than changing the properties of their receptors/channels.

2-Amino-5-phosphonovalerate↗
PubMed1985

Synaptic block of a transmitter-induced potassium conductance in Aplysia neurones.

A voltage-clamp study was made of a slow excitatory post-synaptic potential (slow e.p.s.p.) that can be elicited in the medial cells of the left pleural ganglion of Aplysia californica by the firing of at least three different presynaptic neurones (labelled I, II and III). Each of these three neurones elicits other permeability changes in addition to the slow e.p.s.p., and all elements of these synaptic responses were shown to be mediated monosynaptically. The slow e.p.s.p., associated with an increase in membrane resistance, was shown to be due to a decrease in K permeability. When the slow e.p.s.p. was present spontaneously, it could be blocked by three compounds (tetraethylammonium (TEA), phenyltrimethylammonium (PTMA), or methylxylocholine (beta-TM 10], all previously shown to block the cholinergic receptor that mediates an increase in K conductance in the medial cells (see Kehoe, 1972b). Furthermore, in ganglia in which no slow e.p.s.p. was seen in response to firing of the neurones I, II, and III, such a response became manifest when agonists capable of activating the cholinergic receptor were applied (e.g. acetylcholine (ACh), carbachol, arecoline, or F2268). The slow e.p.s.p. thus appears to result from the reduction, induced by any one of three 'blocking neurones', of a cholinergically controlled K conductance. Finally, when presynaptic neurone I (the only neurone tested) was fired shortly before or during the activation of presynaptic neurone IV, previously shown to be cholinergic (Kehoe, 1972b), the K component of the cholinergic post-synaptic inhibitory potential was markedly reduced. The concentration at which a given agonist caused the manifestation of the synaptic diminution in K conductance (i.e. the slow e.p.s.p.) was found to be the same as that at which it caused a reduction in the synaptically activated, cholinergic, K-dependent conductance elicited by presynaptic neurone IV. Intracellularly injected adenosine 3',5'-cyclic monophosphate (cyclic AMP) imitated the effect of the 'blocking neurones' on the K conductance activated by bath-applied cholinomimetics. This effect was superimposed on a cyclic-AMP-induced, voltage-dependent inward current that disappeared when the cell was bathed in Na-free sea water, or when the extracellular Ca concentration was increased to 60 mM. The effect of cyclic AMP on the cholinergic K conductance remained even after this cyclic-AMP-activated inward current was eliminated.(ABSTRACT TRUNCATED AT 400 WORDS)

1-Methyl-3-isobutylxanthine↗
PubMed2002

Differential thresholds of local field potentials and unit discharges in rat auditory cortex.

Thresholds for responses to tone bursts in the primary auditory field of pentobarbital-anesthetized rat are significantly lower for local field potentials (5.60 dB+/-1.76 S.E.M.) than for multiple unit discharges (17.80 dB+/-3.17), recorded simultaneously from the same microelectrode. The characteristic frequencies (CFs) of local field potentials provide a good 'predictive' estimate of unit CFs at their higher thresholds. The findings are consistent with the view that local field potentials in the auditory cortex reflect summed synaptic potentials rather than cellular discharges.

Acoustic Stimulation↗
PubMed1989

Long-term potentiation in hippocampal CA3 neurons: tetanized input regulates heterosynaptic efficacy.

Three excitatory synaptic inputs to hippocampal CA3 neurons--the mossy fibers, Schaffer collateral/commissural fibers, and fimbrial fibers--were determined to be separate and independent in the pharmacologically disinhibited in vitro slice. Long-term synaptic potentiation (LTP) was induced in one of these three synaptic inputs, and subsequent synaptic efficacy changes in the other two nontetanized inputs were characterized using current and voltage clamp techniques. LTP in the mossy fiber input was accompanied by potentiation of Schaffer and fimbrial responses, whereas the induction of LTP in the Schaffer pathway was associated with the potentiation of fimbria responses and a depression of mossy fiber responses. LTP induced in the fimbrial response was confined to that input alone.

Adaptation, Physiological↗
PubMed1996

B64, a newly identified central pattern generator element producing a phase switch from protraction to retraction in buccal motor programs of Aplysia californica.

1. Buccal motor programs in Aplysia are characterized by two phases of activity, which represent protraction and retraction of the radula in intact animals. The shift from protraction to retraction is caused by synaptic activity inhibiting neurons that are active during protraction and exciting neurons that are active during retraction. 2. B64, a newly identified neuron present bilaterally in the buccal ganglia, is partially responsible for the phase shift. Stimulating a single B64 causes bilateral inhibition of neurons B31/B32 and other neurons active during protraction and cause bilateral excitation of neurons B4/B5 and other neurons active during retraction. B64 is active throughout retraction. The amplitude and waveforms of the synaptic potentials caused by firing B64 are similar, but not identical, to those seen during retraction. 3. Some of the effects of B64 on B31/B32 and on B4/B5 are monosynaptic, as shown by their maintained presence in high divalent cation seawater, which blocks polysynaptic activity. 4. A brief depolarization of B64 leads to a long-lasting depolarization and firing. The ability of B64 to respond in this way is at least partially caused by an endogenous plateau potential, as this property is still seen after synaptic transmission is blocked. 5. Hyperpolarization of B64 bilaterally and preventing the somata from firing unmasks a large excitatory postsynaptic potential in B64. This procedure does not block the shift from protraction to retraction, indicating that spiking in the B64 somata is not necessary for the phase shift. 6. The firing pattern and synaptic connections of B64 are consistent with the hypothesis that the neuron is part of a central pattern generator underlying buccal motor programs. B64 is monosynaptically inhibited by neurons that are active along with B31/B32, which are responsible for producing the protraction phase of a buccal motor program. During the later portion of the protraction phase B64 is excited. In addition, firing B64 can phase advance and phase delay buccal motor programs. 7. Regulating the firing of B64 can regulate the expression of buccal motor programs. Stimulation of B64 at frequencies of 0.5-1.0 Hz leads to complete inhibition of buccal motor programs, whereas steady-state depolarization of B64 can lead to repetitive bursts of activity.

Animals↗
PubMed1988

Long-term changes in neuromuscular synapses with altered sensory input to a crayfish motoneuron.

Prolonged changes in crayfish motoneuron electrical activity result in adaptations in neuromuscular synapses which are consistent with findings at other synapses. In this study we establish that this long-term adaptation (LTA) of crayfish neuromuscular synapses to increased activation of the motoneuron does not require the activation of any other neurons. Selectively increasing the impulse activity of the relatively inactive fast closer excitor motoneuron (FCE) over a period of 7 days results in a 41% reduction in initial amplitude of the excitatory postsynaptic potential (EPSP), and a 42% decrease in synaptic fatigue. These changes in EPSP properties have been previously shown to be due to decreased initial transmitter release and greater sustained release of transmitter during prolonged stimulation. Chronic stimulation of sensory receptors known to produce subthreshold synaptic potentials in the central processes of the FCE elicits LTA of its neuromuscular synapses. The initial EPSP is decreased by 21%, and the synaptic fatigue is reduced by 17%. These results lead to the hypothesis that the primary event leading to LTA of neuromuscular synapses is depolarization of the motoneuron.

Adaptation, Physiological↗
PubMed2002

Differential discrimination of fast and slow synaptic waveforms by two low-voltage-activated calcium channels.

Electrophysiological analysis of human embryonic kidney 293 cells stably expressing recombinant channels was used to compare how the biophysical properties of the low-voltage-activated Ca(2+) channels encoded by the alpha(1G) (Ca(V)3.1) or alpha(1I) (Ca(V)3.3) subunits shape their responses to excitatory synaptic potentials. In medium containing 2 mM extracellular Ca(2+) standard current-voltage relationships demonstrated both channel types to be clearly low-voltage activated with significant slowly activating current responses being observed at -66 mV. At all test potentials examined, activation of Ca(V)3.3 was substantially slower than that of Ca(V)3.1. To probe how these different T-type channels might respond to excitatory postsynaptic potentials (EPSPs), mock EPSPs with different kinetic profiles were created from the sum of exponentials. These waveforms were then used as command templates in voltage-clamp experiments. Ca(V)3.1-mediated channels responded effectively to both rapidly decaying mock EPSPs and slowly decaying EPSPs. In contrast, Ca(V)3.3-mediated channels were poorly gated by rapidly decaying EPSPs but were effectively activated by the more prolonged synaptic response. When activated with mock EPSPs Ca(V)3.3-mediated currents were more resistant to steady-state depolarisation of the pre-stimulus holding potential. Ca(V)3.3 currents were also more resistant to repetitive application of prolonged EPSPs, which caused substantial inactivation of Ca(V)3.1-mediated currents. The addition of a single mock action potential to the peak of a rapidly decaying EPSP voltage-clamp template greatly enhanced the currents produced by either Ca(V)3.1 or Ca(V)3.3-expressing cells. This facilitatory effect was considerably greater for Ca(V)3.3-mediated channels. From these data we suggest that the slow activation kinetics of Ca(V)3.3-mediated T-type channels enable them to respond selectively to either slow or suprathreshold synaptic potentials.

Animals↗
PubMed1988

The development of sensorimotor synaptic connections in the lumbosacral cord of the chick embryo.

We have examined the development of synaptic connections between afferents and motoneurons in the lumbosacral spinal cord of the chick embryo between stages 28 and 39. The central projection of afferents was visualized following injection of dorsal root ganglia with HRP. Afferent fibers first entered the dorsal gray matter between stages 29 and 31. They grew in a ventrolateral direction, reaching motoneuron dendrites by stage 32. Quantitative analysis of axon numbers suggested that individual axons did not begin to branch extensively until they approached the lateral motor column at stage 36. Connectivity between afferents and motoneurons was assessed by stimulating dorsal roots or nerves supplying the femorotibialis muscle and recording the resulting motoneuron synaptic potentials intracellularly or from the cut ventral roots. At stages 37-39, low-intensity stimulation produced a short-latency positive potential that was followed at higher stimulus currents by slower positive potentials. All of these potentials were abolished in solutions that block chemical synaptic transmission (zero Ca2+/2 mM Mn2+). The early potential, which includes the monosynaptic EPSP produced by muscle afferents, persisted in the presence of the N-methyl-D-aspartate antagonist, 2-amino-5-phosphonovaleric acid (APV), but was largely eliminated by the more general excitatory amino acid antagonist, kynurenic acid. Therefore, in the chick, as in other species, a glutamate-like transmitter appears to be released at the synapses between muscle afferents and motoneurons. The APV-resistant potential was reduced in amplitude during bath application of the glycine and GABA antagonists, strychnine and picrotoxin, suggesting that it was composed of depolarizing inhibitory as well as excitatory components at these stages. The monosynaptic EPSP could be recorded in ventral roots as early as stages 32-33, when muscle afferents first grew into the vicinity of motoneuron dendrites. The EPSP in these young embryos was unaffected by picrotoxin and strychnine, but responded to APV and kynurenate in a manner similar to that at later stages. Between stages 28 and 32, only long-latency, slowly rising potentials could be evoked in the ventral roots by afferent activation. These potentials were abolished by superfusion with zero Ca2+/2 mM Mn2+, APV, or kynurenic acid, and could be revealed before stage 31 only by removing Mg2+ from the bath.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed2002

Ifenprodil and ethanol enhance NMDA receptor-dependent long-term depression.

Long-term alterations in synaptic transmission are thought to underlie various types of alcohol-related brain disorders. While ethanol effects on synaptic potentiation are well documented, ethanol effects on synaptic depression have not been addressed. Herein, we performed experiments to assess the role of ethanol on long-term depression (LTD) formation. In rat hippocampal slices, prolonged low-frequency stimulation (LFS) of CA1 Schaffer collaterals (1 Hz for 7 min) induced saturable, long-lasting, reversible N-methyl-D-aspartate (NMDA) receptor-dependent LTD of stimulus-evoked dendritic population excitatory postsynaptic potentials. This depression (-26% LTD amplitude) was observed in young rats (12-20 days old), but not adult rats (28-35 days old). Induction of LTD was blocked (-3% LTD amplitude) when the LFS was delivered in the presence of the NMDA receptor antagonist D-2-amino-5-phosphonovaleric acid. When the conditioning LFS was delivered in the presence of ethanol, there was a significant enhancement in the induction of NMDA receptor-dependent LTD versus control LTD (-36% LTD amplitude). Ifenprodil, an N-methyl-D-aspartate receptor subunit 2B (NR2B)-selective antagonist, also significantly facilitated the induction of LTD (-40% LTD amplitude). Consistent with this result, ifenprodil did not affect the NMDA receptor-dependent component of the baseline synaptic response, whereas D-2-amino-5-phosphonovaleric acid caused significant depression of the NMDA component. These data indicate that whereas ethanol is known to inhibit NMDA receptor function in a variety of systems, it significantly enhances the induction of NMDA receptor-dependent LTD. Furthermore, since ifenprodil is known to select for ethanol-sensitive subtypes of NR2B-NMDA receptors, these data also suggest that NR2B-containing NMDA receptor subpopulations do not contribute to LTD, but instead may actually play inhibitory roles in LTD induction.

Animals↗
PubMedDate not supplied

Septal fetal tissue transplants restore long-term potentiation in the dentate gyrus of fimbria-formix-lesioned rats.

Two groups of Sprague-Dawley male rats received bilateral aspirative lesions of the fimbria fornix under chloral hydrate anesthesia. One group (n = 9) received no further treatment (lesioned). In the second group (n = 8), a piece of septal fetal tissue, obtained at day E15-16, was implanted into each lesion cavity (transplanted). A third group consisted of shamlesioned rats (controls, n = 14). Two months after the operations, a recording electrode was implanted in the hilar region of the dentate gyrus of each animal, and a bipolar stimulating electrode was implanted in the perforant path. Long-term potentiation at 400 Hz was induced and followed for two hours. FF-lesioned rats showed an impaired potentiation of the field excitatory post-synaptic potential, which rapidly declined to basal levels within 15 minutes. The transplanted rats showed a normal potentiation of this parameter, similar to that seen in the control animals. A decrease in choline acetyltransferase activity in the hippocampi of the lesioned animals showed a tendency toward recovery after septal fetal tissue transplantation. In all the dorsal hippocampal areas of the lesioned animals, acetylcholinesterase histochemistry showed an almost complete loss of enzymatic activity, which was partially restored by the transplants. The improved synaptic plasticity in the transplanted animals might be related to septal transplant-induced recovery of mnemonic functions.

Acetylcholinesterase↗
PubMed2000

The influence of single VB thalamocortical impulses on barrel columns of rabbit somatosensory cortex.

Extracellular recordings were obtained from single neurons in ventrobasal (VB) thalamus of awake rabbits while field potentials were recorded at various depths within topographically aligned and nonaligned barrel columns of somatosensory cortex (S1). Spike-triggered averages of cortical field potentials were obtained following action potentials in thalamic neurons. Action potentials in a VB neuron elicited a cortical response within layer 4 with three distinct components. 1) A biphasic, initially positive response (latency <1 ms) was interpreted to reflect activation of the VB axon terminals (the AxTP). This response was not affected by infusion of an alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA)/kainate receptor antagonist within the barrel. In contrast, later components of the response were completely eliminated and were interpreted to reflect focal synaptic potentials. 2) A negative potential [focal synaptic negativity (FSN)] occurred at a mean latency of 1.65 ms and lasted approximately 4 ms. This response had a rapid rise time ( approximately 0.7 ms) and was interpreted to reflect monosynaptic excitation. 3) The third component was a positive potential (the FSP), with a slow rise time and a half-amplitude duration of approximately 30 ms. The FSP showed a weak reversal in superficial cortical layers and was interpreted to reflect di/polysynaptic inhibition. The amplitudes of the AxTP, the FSN, and the FSP reached a peak near layer 4 and were highly attenuated in both superficial and deep cortical layers. All components were attenuated or absent when the cortical electrode was missaligned from the thalamic electrode by a single cortical barrel. Deconvolution procedures revealed that the autocorrelogram of the presynaptic VB neuron had very little influence on either the amplitude or duration of the AxTP or the FSN, and only a minor influence (mean, 11%) on the amplitude of the FSP. We conclude that individual VB thalamic impulses entering a cortical barrel engage both monosynaptic excitatory and di/polysynaptic inhibitory mechanisms. Putative inhibitory interneurons of an S1 barrel receive a highly divergent/convergent monosynaptic input from the topographically aligned VB barreloid, and this results in sharp synchrony among these interneurons. We suggest that single-fiber access to disynaptic inhibition is facilitated by this sharp synchrony, and that the FSP reflects a consequent synchronous wave of feed-forward inhibition within the S1 barrel.

Action Potentials↗