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PubMed1983

Cultured cerebellar neurons: endogenous and exogenous components of Purkinje cell activity and membrane response to putative transmitters.

Modified explant cultures of fetal rat cerebellum were developed for electrophysiological and pharmacological studies, at the membrane level, of Purkinje neurons. The goals of the present series of experiments were to identify possible endogenous and exogenous components to the electrical activity of Purkinje neurons, to assess the sensitivity of these neurons to putative excitatory and inhibitory neurotransmitters, and to characterize the membrane response to the transmitters. Intracellular recordings were made from Purkinje neurons, identified on a morphological basis, using conventional electrophysiological techniques. Virtually all Purkinje neurons displayed spontaneous activity. A contribution of both endogenous and exogenous components to the spontaneous activity was indicated by alterations in the pattern and amount of activity when the membrane potential was varied and by the characteristics of the individual potentials themselves. Several types of activity were considered to be endogenous: the most common type consisted of pacemaker-like potentials which generated a pattern of firing similar to that characterized as simple spike activity in previous in vivo studies; another type of endogenous activity consisted of large membrane depolarizations that evoked one or two spikes. These depolarizing responses were similar to the membrane response generated by climbing fiber input to Purkinje cells in vivo. The exogenous components to the spontaneous activity consisted of synaptic potentials including excitatory (EPSPs) and inhibitory (IPSPs) synaptic potentials and biphasic EPSP/IPSPs. Several putative transmitters thought to mediate these synaptic potentials were tested by focal micropressure application to determine if they could mimic the action of the endogenous transmitters. The putative transmitter glutamate depolarized the cultured Purkinje neurons and evoked action potentials, characteristics which were displayed by the excitatory synaptic potentials. The putative inhibitory transmitter GABA hyperpolarized the cultured Purkinje neurons and depressed activity, characteristics which were displayed by the inhibitory synaptic potentials. The putative inhibitory transmitters glycine and taurine were ineffective. Norepinephrine, the transmitter mediating the inhibitory input from the locus coeruleus to Purkinje neurons, was also tested. When applied in the microM range, NE effects were variable. When applied in the mM range, NE depressed the spontaneous activity in a manner suggestive of a presynaptic action.

Animals↗

PubMed2001

[Advancement in mechanisms of long-term potentiation].

Synaptic plasticity in mammalian brain is one of the most widely studied topics in neuroscience over the last decade. Long-term potentiation (LTP), mainly involving post-synaptic mechanisms, is a reflection of neural plasticity. Study on the mechanisms of LTP was formerly focused on the properties of NMDA receptor and the intracellular cascade of reaction after activation of the receptor. However, the definition of "silent synapses" with only NMDA receptors without AMPA receptors was frequently referred in LTP study, showing the importance of AMPA receptor in post-synaptic mechanism of LTP.

Animals↗

PubMed1997

Long-term potentiation induced by single volley activation: a mechanism for bicuculline-induced enhancement of synaptic field potentials in the CA1 hippocampal region.

Long-term potentiation in the CA1 region is often evaluated as the change in the initial slope of the field response following a single test stimulus. This change is thought to represent an alteration of excitatory transmission only. However, it has recently been reported that this initial part of the field response is also controlled by a picrotoxin-resistant GABA(A)ergic response since bicuculline (100 microM), in the presence of picrotoxin, could lead to a substantial increase in the field response initial slope. A disinhibition may then be an important factor underlying expression of what is believed to be long-term potentiation of excitatory synaptic transmission. Alternatively, the bicuculline-induced field response enhancement could be due to an induction of long-term potentiation favoured by the low magnesium (1.25 mM) and high calcium (4 mM) concentrations used in these experiments. Results presented here show that neither picrotoxin (100 microM), nor bicuculline (100 microM), produce any significant change in field response initial slope, when examined using 4 mM magnesium and calcium in the perfusion fluid. In experiments using lower magnesium (1-1.5 mM), the same result was observed in most cases. In some cases, the field response following single test stimuli became temporally paired with spontaneous bursts of spike activity, and its initial slope became considerably enhanced (100%). Similar results could be provoked by a temporary increase in stimulus strength sufficient to evoke spike activity. This potentiation occluded a subsequent long-term potentiation induced by afferent tetanization, and it was not observed when a N-methyl-D-aspartate receptor antagonist was present in the perfusion solution. The present results suggest that the bicuculline-induced enhancement of the field response initial slope represents an induction of long-term potentiation rather than being a direct consequence of pharmacological blockade of a GABA(A)ergic process.

2-Amino-5-phosphonovalerate↗

PubMed1987

An interneuronal relay for group I and II muscle afferents in the midlumbar segments of the cat spinal cord.

1. The properties of interneurones located in the 4th lumbar segment of the cat spinal cord (L4 interneurones) have been investigated by intracellular and extracellular recording from individual neurones. The study focused on interneurones projecting to hind-limb motor nuclei and/or interposed in pathways from group II muscle afferents. The projection to motor nuclei was assessed from antidromic activation of the neurones by stimuli applied in the motor nuclei of the 7th lumbar (L7) segment. 2. Interneurones which projected to gastrocnemius-soleus or hamstring motor nuclei were found in laminae VI and VII and at the border between laminae VII and VIII. The dominant peripheral input to most of them was from group II muscle afferents, but they were also influenced by group I muscle afferents and by afferents in cutaneous, joint and interosseous nerves. Both excitatory post-synaptic potentials (e.p.s.p.s) and inhibitory post-synaptic potentials (i.p.s.p.s) were evoked from all of these fibre systems. 3. The same kind of multimodal input was also found in other interneurones in laminae VI and VII. However, their axonal projections were not identified and they might have included neurones projecting to motor nuclei (though outside the areas which were stimulated) as well as neurones with more local actions. 4. Interneurones located in laminae IV and V of the dorsal horn appeared to constitute a separate functional population since both their projections and their input differed from those of the more ventrally located interneurones; none of the dorsal horn interneurones were found to project to motor nuclei and none had input from group I afferents, although they were influenced by group II muscle afferents and by afferents in cutaneous, joint and interosseous nerves. 5. Many of the excitatory actions from group I and II afferents upon L4 interneurones were found to be evoked monosynaptically. A high proportion of L4 neurones synapsing upon motoneurones would thus be interposed in disynaptic reflex pathways from these afferents. In comparison to actions evoked via interneurones of the caudal lumbar segments, any post-synaptic potentials (p.s.p.s) evoked via L4 interneurones would be delayed. These delays would amount to 0.4-0.9 ms for p.s.p.s. from group I afferents and by 0.5-2.5 ms for group II p.s.p.s. 6. In many interneurones, particularly those located ventrally, i.p.s.p.s. were evoked by group I and II muscle afferents at latencies which indicated that they were evoked disynaptically. They may therefore reflect inhibitory interactions between subpopulations of L4 interneurones.(ABSTRACT TRUNCATED AT 400 WORDS)

Action Potentials↗

PubMed2003

Long-term potentiation of polysynaptic responses in layer V of the sensorimotor cortex induced by theta-patterned tetanization in the awake rat.

Although the neocortex in awake, adult animals is resistant to the induction of long-term potentiation (LTP), synaptic potentiation may be enhanced by rhythmic patterns of activation that evoke short- term synaptic facilitation effects. The effectiveness of stimulation patterned after the theta (4-12 Hz) EEG rhythm for the induction of LTP of sensorimotor cortex responses to corpus callosum stimulation was assessed in vivo by inducing LTP using either high- frequency (300 Hz) trains or paired trains delivered at a 100 ms (10 Hz) interval. High-frequency trains caused a reduction of the early field potential component, reflecting a potentiation of direct layer V activation, and a potentiation of the late component, reflecting enhanced polysynaptic activation in layer V. Paired trains resulted in a much larger potentiation of polysynaptic responses than was observed following 300 Hz trains. To determine if short-term facilitation effects contributed to the enhanced LTP induction by theta-patterned trains, facilitation effects induced by the trains were challenged with NMDA receptor antagonists. NMDA-receptor antagonism reduced responses to single pulses, and also reduced facilitated responses evoked by theta-patterned stimulation. The effectiveness of theta-patterned stimulation for the induction of LTP of layer V polysynaptic responses is therefore likely due to frequency-dependent synaptic facilitation effects that enhance NMDA receptor activation.

Animals↗

PubMed2006

Non-NMDA and NMDA receptors are involved in suprathreshold excitation of network of frog tectal neurons by a single retinal ganglion cell.

NMDA receptors play an important functional role in the neuron excitability and plasticity. The conditions and consequences of their activation are of interest for many neuroscientists. This investigation was designed to explore an activation of the NMDA receptors of frog tectal neurons in vivo by a burst of spikes of individual retinotectal fiber. We show that: (1) the NMDA receptors of tectal neurons can be activated by an intense burst discharge of an individual ganglion cell (likely darkness detector) at physiological conditions. (2) Activation of the NMDA receptors is achieved, primarily, due to temporal summation and frequency facilitation of the fast non-NMDA synaptic potentials. However, it is very likely that spatial summation of the fast retinotectal synaptic potentials with excitatory synaptic potentials of recurrent connections contributes to elicit the NMDA response. (3) The activation of NMDA receptors causes a higher level of activity of tectal neuron network. The suprathreshold excitation of efferent tectal neurons is characteristic for this level. Therefore, the burst discharge of only single retinal ganglion cell can activate the tectobulbospinal tract and lead to the motor reaction.

Action Potentials↗

PubMed1960

Activity patterns of interneurons in the caudal ganglion of the crayfish.

Responses of ascending interneurons from the caudal ganglion of crayfish have been recorded from single units isolated by dissection from the ventral nerve cord; in addition, post-synaptic activity within the ganglionic neuropile has been studied with intracellular micropipettes. The following classes of interneurons have been found: (1) Large fibers which responded to tactile stimuli with single spikes or phasic bursts. These units usually showed broad receptive fields; and spontaneous activity, when present, showed transitory depressions following responses to natural stimuli. (2) A group of fibers, including many small ones, which responded to proprioceptive stimuli with tonic discharges of varying adaptation rate. (3) Interneurons which showed responses both to tactile stimuli and to activation of the sixth ganglion photoreceptor; and (4) units with constant frequency discharges which were unmodifiable by any of the above afferent inputs. Intracellular recording of post-synaptic activity has shown (1) that widely graded excitatory post-synaptic potentials occur; (2) that multiple firing from single synaptic potentials is usual; (3) that the post-synaptic responses to phasic natural stimuli and to electrical stimulation of ganglionic roots are similar. The existence of widely graded post-synaptic potentials and of extensive receptive fields suggests a high degree of convergence from primary afferents to interneurons. The activation of such post-synaptic units involves integrative synaptic transfer, without 1:1 correspondence between pre- and post-fiber activity.

Animals↗

PubMed1995

Lack of evidence for P2X-purinoceptor involvement in fast synaptic responses in intact sympathetic ganglia isolated from guinea-pigs.

Recordings were made from neurons in intact pre- and paravertebral guinea-pig sympathetic ganglia using intracellular microelectrodes. Fast excitatory synaptic responses were evoked by stimulation of preganglionic and peripheral nerve trunks. Suramin (0.1-1 mM) did not affect passive or active membrane properties, nor the amplitude or decay time-course of either synaptic potentials or synaptic currents. Synaptic responses were reversibly reduced in amplitude by hexamethonium (98.7 +/- 0.8%, 50-1000 microM) and d-tubocurarine (95.3 +/- 2.6%, 10-280 microM). ATP (0.5-1 mM) and alpha,beta-methylene ATP (1-40 microM) applied in the bathing solution produced no significant changes in resting membrane potential or input resistance. Prolonged application (up to 25 min) of either compound was also without effect on synaptic responses. These substances also did not affect ganglion cells axotomized one to five days in vivo. These data suggest that activation of P2X-purinoceptors is not involved in the generation of fast excitatory synaptic responses in intact guinea-pig sympathetic ganglia. It appears that dissociation of these neurons must markedly increase their sensitivity to purine nucleotides.

Animals↗

PubMed1992

Pre- and postsynaptic inhibition by opioids in rat striatum.

The physiological role of opioid peptides in the rat striatum was sought by intracellular recording in vitro. Excitatory synaptic potentials (mediated by glutamate or aspartate) and inhibitory synaptic potentials (mediated by GABA) were isolated pharmacologically and/or by positioning the stimulation electrode over the external capsule. Opioid agonists and antagonists selective for mu-, delta-, and kappa-receptors were applied by superfusion. Two main actions of opioids were observed. First, mu- and delta-selective opioids presynaptically inhibited the excitatory postsynaptic potential, whereas only delta-selective opioids decreased the inhibitory synaptic potential. Second, a small subpopulation of cells (not medium spiny neurons) were hyperpolarized by delta-selective agonists. The results indicate that the main action of opioids on striatal neurons is presynaptic inhibition of the corticostriate excitatory synaptic input.

Action Potentials↗

PubMed1982

Effects of rectification on synaptic efficacy.

We have investigated the effects of postsynaptic membrane properties on the shape of synaptic potentials generated by time-varying synaptic conductances. We used numerical simulation techniques to model cells of several different geometrical forms, from an isopotential sphere to a neuron with a soma and a dendritic tree. A variety of postsynaptic membrane properties were tested: (a) a passive resistance-capacitance membrane, (b) a membrane represented by the Hodgkin and Huxley (HH) equations, and (c) a membrane that was passive except for a delayed rectification represented by a voltage- and time-dependent increase in GK. In all cases we investigated the effects of these postsynaptic membrane properties on synaptic potentials produced by synaptic conductances that were fast or slow compared with the membrane time constant. In all cases the effects of postsynaptic rectification occurred on postsynaptic potentials of amplitudes as low as 1 mV. The HH model (compared with the passive model) produced an increased peak amplitude (from the increase in GNa) but a decreased half-width and a decreased time integral (from the increase in GK). These effects of the HH GK change were duplicated by a simple analytical rectifier model.

Animals↗

PubMed1996

Neural parameters contributing to temperature compensation in the flight CPG of the locust, Locusta migratoria.

Elevated thoracic temperature increases the wingbeat frequency of flying locusts. We investigated the extent to which temperature-induced changes in resting membrane potential and postsynaptic potential amplitude contribute to the effects of increased temperature on the frequency of the central flight rhythm. Flight neurons were hyperpolarized by changing the K+ concentration of the superfusing saline from 10 mM to 2 mM. 5 min of low-K+ superfusion hyperpolarized flight motoneurons from -42.8 mV to -50.1 mV with a concomitant decrease of the frequency of the central flight rhythm from 11.6 Hz to 10.5 Hz. The amplitude of postsynaptic potentials was halved after 10 min of zero Ca2+/high Mg2+ superfusion, but the frequency of the central rhythm did not change significantly. GABAergic inhibitory connections were reduced in amplitude using picrotoxin. This treatment increased the frequency of the central rhythm from 11.6 Hz to 12.9 Hz, and increased the thermosensitivity of the rhythm frequency. We conclude that the excitatory effect of increased temperature on rhythm frequency is not mediated by temperature effects on membrane potential and/or synaptic potential amplitude. We propose that the inhibitory effect of temperature-induced hyperpolarization of the membrane potential compensates for the excitatory effect of temperature on rhythm frequency (e.g. via increased conduction velocity). We further suggest that some measure of temperature compensation is afforded by equal effects on the amplitudes of excitatory and inhibitory postsynaptic potentials, such that the net effect on the level of excitation is zero.

Animals↗

PubMed1987

Observations on the actions of substance P and [D-Arg1,D-Pro2,D-Trp7,9,Leu11)substance P on single neurons of the guinea pig submucous plexus.

Intracellular recordings were made from neurons of the guinea pig submucosal plexus and the effects of substance P and the substance P analogue [D-Arg1,D-Pro2,D-Trp7,9,Leu11]substance P were examined. Substance P (20-200 nM) depolarized all submucosal neurons; these depolarizations were shown to be due to a decrease in the resting (or "leak") potassium conductance of the membrane. In approximately 50% of the 46 neurons tested, superfusion with [D-Arg1,D-Pro2,D-Trp7,9,Leu11]substance P (0.2-20 microM) produced a dose-dependent membrane hyperpolarization. This hyperpolarization was prevented by the alpha 2-adrenoceptor antagonist idazoxan (300 nM) or by concentrations of cobalt which abolished all spontaneous and evoked synaptic potentials, indicating that it resulted from release of noradrenaline from sympathetic nerve terminals. [D-Arg1,D-Pro2,D-Trp7,9,Leu11]substance P depressed the amplitude of the three synaptic potentials recorded from submucosal neurons; the concentrations that caused 50% of the maximal inhibition of the fast excitatory postsynaptic potential, the inhibitory postsynaptic potential, and slow excitatory postsynaptic potential were 40 microM, 600 nM and 20 microM, respectively. When idazoxan was present, the substance P analogue was less effective in depressing the amplitudes of the fast and slow excitatory synaptic potentials suggesting that much of its presynaptic inhibition also resulted from release of noradrenaline. These results provide evidence that [D-Arg1,D-Pro2,D-Trp7,9,Leu11]substance P releases noradrenaline from sympathetic nerves in the submucosal plexus. One effect of this is a membrane hyperpolarization; another is a presynaptic inhibition of transmitter release. These actions much limit the usefulness of this "substance P antagonist" in efforts to show that synaptic potentials, such as the slow excitatory synaptic potential, are mediated by substance P.

Animals↗

PubMed2003

Spike timing-dependent serotonergic neuromodulation of synaptic strength intrinsic to a central pattern generator circuit.

Neuromodulation is often thought to have a static, gain-setting function in neural circuits. Here we report a counter example: the neuromodulatory effect of a serotonergic neuron is dependent on the interval between its spikes and those of the neuron being modulated. The serotonergic dorsal swim interneurons (DSIs) are members of the escape swim central pattern generator (CPG) in the mollusk Tritonia diomedea. DSI spike trains heterosynaptically enhanced synaptic potentials evoked by another CPG neuron, ventral swim interneuron B (VSI-B), when VSI-B action potentials occurred within 10 sec of a DSI spike train; however, if VSI-B was stimulated 20-120 sec after DSI, then the amplitude of VSI-B synaptic potentials decreased. Consistent with this, VSI-B-evoked synaptic currents exhibited a temporally biphasic and bidirectional change in amplitude after DSI stimulation. Both the DSI-evoked enhancement and decrement were occluded by serotonin and blocked by the serotonin receptor antagonist methysergide, suggesting that both phases are mediated by serotonin. In most preparations, however, bath-applied serotonin caused only a sustained enhancement of VSI-B synaptic strength. The heterosynaptic modulation interacted with short-term homosynaptic plasticity: DSI-evoked depression was offset by VSI-B homosynaptic facilitation. This caused a complicated temporal pattern of neuromodulation when DSI and VSI-B were stimulated to fire in alternating bursts to mimic the natural motor pattern: DSI strongly enhanced summated VSI-B synaptic potentials and suppressed single synaptic potentials after the cessation of the artificial motor pattern. Thus, spike timing-dependent serotonergic neuromodulatory actions can impart temporal information that may be relevant to the operation of the CPG.

Action Potentials↗

PubMed1999

Effect of long-term elevated corticosteroid levels on field responses to synaptic stimulation, in the rat CA1 hippocampal area.

Daily injections with high doses of corticosterone for 3 weeks were previously found to result in atrophy of the dendritic tree of hippocampal CA3 neurons, which form a major input source to CA1 pyramidal cells. In this study we examined if exposure of rats to a similar chronic corticosterone treatment is associated with changes in field responses of CA1 neurons to stimulation of Schaffer collateral/commissural fibers. In line with earlier studies, we observed that corticosterone injections for 1 day or 1 week reduce the maximal amplitude of the population spike and synaptic potentiation observed after theta burst stimulation, respectively. Yet, animals which were exposed to high corticosterone levels during 3 weeks did not exhibit significant suppression of either the field potential amplitude or the synaptic potentiation compared with the control group. The data suggest that exposure of rats for 3 weeks to very high corticosterone levels induces adaptational changes in the CA1 hippocampal network function which partly normalize the effects seen with less prolonged corticosterone treatment.

Adrenal Cortex Hormones↗

PubMed2004

Stress enables synaptic depression in CA1 synapses by acute and chronic morphine: possible mechanisms for corticosterone on opiate addiction.

The hippocampus, being sensitive to stress and glucocorticoids, plays significant roles in certain types of learning and memory. Therefore, the hippocampus is probably involved in the increasing drug use, drug seeking, and relapse caused by stress. We have studied the effect of stress with morphine on synaptic plasticity in the CA1 region of the hippocampus in vivo and on a delayed-escape paradigm of the Morris water maze. Our results reveal that acute stress enables long-term depression (LTD) induction by low-frequency stimulation (LFS) but acute morphine causes synaptic potentiation. Remarkably, exposure to an acute stressor reverses the effect of morphine from synaptic potentiation (approximately 20%) to synaptic depression (approximately 40%), precluding further LTD induction by LFS. The synaptic depression caused by stress with morphine is blocked either by the glucocorticoid receptor antagonist RU38486 or by the NMDA-receptor antagonist D-APV. Chronic morphine attenuates the ability of acute morphine to cause synaptic potentiation, and stress to enable LTD induction, but not the ability of stress in tandem with morphine to cause synaptic depression. Furthermore, corticosterone with morphine during the initial phase of drug use promotes later delayed-escape behavior, as indicated by the morphine-reinforced longer latencies to escape, leading to persistent morphine-seeking after withdrawal. These results suggest that hippocampal synaptic plasticity may play a significant role in the effects of stress or glucocorticoids on opiate addiction.

Animals↗

PubMed1972

A comparison of chemical and electrical synaptic transmission between single sensory cells and a motoneurone in the central nervous system of the leech.

In leech ganglia, three sensory cells of different modality converge on a motoneurone, where they form chemical and electrical synapses. Each of these synapses behaves in a characteristic manner and the nature of the transmission mechanism has significant functional consequences for the operation of the reflexes. An analysis has been made of the effects of trains of impulses on synaptic transmission through these pathways, using frequencies that correspond to natural firing.1. At the chemical synapse between the nociceptive sensory cell and the motoneurone, two opposing events occur: facilitation and depression. Thus, with trains of impulses, the synaptic potentials first increase in amplitude and then decrease. The two processes could be separated by altering the Mg and Ca content of the bathing fluid. In concentrations of Mg that reduced the amplitude of a single control chemical synaptic potential, pure facilitation occurred during a train. Depression predominated during brief trains in raised concentrations of Ca, although synaptic potentials were initially larger. These results suggest that changes in the amount of transmitter released by each presynaptic action potential can account for the changes observed in chemical synaptic transmission.2. In contrast, electrical transmission between the sensory cell responding to touch and the same motoneurone did not show facilitation or depression. The electrical coupling potential in the motoneurone was relatively constant when the touch cell fired at high or low frequencies in normal Ringer fluid, high Mg, or high Ca fluid.3. Further differences between chemical and electrical synapses were apparent when the preparation was cooled to 4 degrees C. In the cold the latency of chemically evoked synaptic potentials in the motoneurone increased and their amplitude declined drastically with repetitive stimulation, while electrical coupling potentials were unaffected.4. A brief hyperpolarization of the presynaptic cell by injected current produced a marked and prolonged increase in chemically evoked synaptic potentials, but did not influence electrical synaptic transmission.5. The synapses of the sensory cell responding to pressure, which are both chemical and electrical, behaved as expected: the chemical synaptic potentials showed facilitation and depression while electrical transmission remained relatively constant.6. These experiments emphasize the different functional consequences of electrical or chemical synapses in reflex pathways for the transmission of signals that arise as a result of natural sensory stimuli.

Action Potentials↗

PubMed2001

Modulation of hippocampal long-term potentiation by the amygdala: a synaptic mechanism linking emotion and memory.

Why are emotionally arousing experiences well-remembered? Since the amygdala and hippocampus play pivotal roles in emotion and memory, respectively, the interaction between these brain regions may underlie the formation of enhanced memory for emotionally arousing events. Behavioral experiments using animals have demonstrated that lesions of the amygdaloid nuclei or infusions of drugs into the amygdaloid nuclei impair or enhance hippocampal-dependent learning. In addition, we have obtained direct evidence that neural inputs from the amygdala modulate synaptic plasticity in the hippocampus, through electrophysiological experiments using anesthetized rats. Electrical stimulation of the basolateral amygdala evoked synaptic potentials in the dentate gyrus of the hippocampus, indicating that there is a neural connection from the amygdala to the hippocampus. Lesion of the basolateral or basomedial, but not central, amygdala resulted in attenuation of long-term potentiation (LTP) at the perforant path-dentate gyrus granule cell synapses. High-frequency stimulation of the basolateral or basomedial amygdala alone did not induce LTP in the dentate gyrus, but facilitated the induction of LTP when applied at the same time as tetanic stimulation of the perforant path. The activity-dependent facilitation of hippocampal LTP by the basomedial and basolateral amygdala may be a synaptic mechanism underlying memory enhancement associated with emotions.

Amygdala↗

PubMedDate not supplied

Use of artificial ion channels for quasi-intracellular recording of cerebral cortex neuron activity.

Action potentials and synaptic potentials were recorded in vivo from cortical neurons in baby rats aged 20-25 days using a new method based on the ionophore nystatin. Nystatin solution was used to fill a standard glass extracellular microelectrode, and became inserted into membranes. Spikes which were initially recorded as extracellular spikes showed increases in amplitude and were transformed into unipolar quasi-intracellular spikes at 0.5-5.0 min after formation of the high-conductance contact. This method allows stable recording of neuronal activity from cells for at least 1 h, and provides a good signal-to-noise ratio. The electrode does not puncture the neuron membrane, with the result that experiments do not require any isolation from vibration. Thus, the results obtained demonstrate that the method is highly efficient for recording the in vivo activity of small nerve cells.

Action Potentials↗