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Formation of functional synapses in the adult cat red nucleus from the cerebrum following cross-innervation of forelimb flexor and extensor nerves. II. Analysis of newly appeared synaptic potentials.

The effects of cross-innervation of peripheral flexor and extensor nerves on the time course and properties of red nucleus (RN) neurons were studied in adult cats. The time course of corticorubral unitary EPSPs was examined. In operated cats, RN neurons innervating upper spinal segments (C-cells) manifested corticorubral unitary EPSPs with shorter time-to-peak and larger amplitude than in normal cats. The mean amplitude of these EPSPs was 0.41 +/- 0.11 mV; the mean time-to-peak was 1.14 +/- 0.51 ms (n = 18). These values differ from normal cats (0.33 +/- 0.09 mV, and 2.68 +/- 0.61 ms, n = 22). RN neuron membrane properties were examined in cross-innervated cats. The main time constant was 5.2 +/- 0.7 ms (n = 10), the shorter equalizing time constant, 0.69 +/- 0.19 ms (n = 10), the input resistance, 2.5 +/- 0.8 M omega. These values were not significantly different from those of normal cats. The electrotonic length was 1.2 (n = 10), somewhat larger than in normal cats. The number of converging interpositorubral synapses, estimated in eight cells from cross-innervated cats, ranged from 37 to 57. This was not significantly different from normal cats, and indicated that there is no large-scale degeneration of interpositorubral synapses after cross-innervation. These results suggest that sprouting and formation of functional synapses occur after cross-innervation of peripheral flexor and extensor nerves.

Animals↗

Origins of post synaptic potentials evoked in spiny neostriatal projection neurons by thalamic stimulation in the rat.

Stimulation of thalamic intralaminar nuclei or structures along the intrathalamic trajectory of thalamostriatal axons evoked complex EPSPs and subsequent hyperpolarizations in rat neostriatal spiny neurons identified by intracellular injection of horseradish peroxidase and/or antidromic activation from substantia nigra. In intact urethane-anesthetized rats, the initial EPSP portion of the response consisted of several components and lasted up to 75 ms. Short (1-10 ms) latency components exhibiting latency variations suggestive of a polysynaptic origin were often observed, and sometimes were the earliest components of the response. However, individual components of the excitatory response could not be clearly distinguished in most neurons and the earliest excitatory component usually appeared to be monosynaptic. After large acute aspiration lesions of ipsilateral cerebral cortex, the early polysynaptic EPSP components of thalamic-evoked EPSPs were absent or greatly attenuated. This suggested that most or all of the short latency polysynaptic EPSP components arose via a thalamo-cortico-striatal route. A short latency (1.6-4.0 ms) monosynaptic EPSP and a second excitatory component with a longer and more variable latency (8-28 ms) remained intact after acute decortication. These were not dependent upon intact corticothalamic or corticostriatal axons, since they were both still present in experiments performed as long as 4 days following ipsilateral hemidecortication. The longer latency excitatory response was shown to be polysynaptic by its latency variation with changes in stimulus intensity and frequency. This component of the response was abolished after acute thalamic hemitransections separating thalamostriatal neurons from their axons. In these experiments, stimulation of thalamostriatal axons rostral to the transection continued to evoke monosynaptic EPSPs in neostriatal spiny neurons. These EPSPs ranged from 1.8 to 3.0 ms in latency, had peak amplitudes up to 11 mV and were 20-37 ms in duration.

Animals↗

Intracellular synaptic potentials of primate motor cortex neurons during voluntary movement.

An intracellular recording technique was applied to the precentral motor cortex of the unanesthetized, chronically behaving monkey. Postsynaptic potentials, responsible for an initiation of the voluntary movement, were recorded. In total, 22 pyramidal tract neurons (PTNs) and 40 non-pyramidal tract neurons (non-PTNs) were successfully penetrated in 5 monkeys while the monkey was performing a flexion-extension wrist movement after a visual cue (reaction time, 200--350 msec). The neurons showed a negative membrane potential shift of at least 30 mV for more than 30 sec. A slowly rising PSP appeared 80--180 msec after the visual cue, and was 70--180 msec prior to an onset of the movement. Spike activities were superimposed upon this slow PSP with 20--80 msec rise time and 2--6 mV depolarization (8 PTNs and 6 non-PTNs). Since these depolarizations were variable in magnitude and latency, these were considered to be summated potentials of small EPSPs and hidden IPSPs. Membrane resistance was measured from an IR drop by a hyperpolarizing current (1.2 X 10(-9) A) passed through a recording electrode, and was 3.5 +/- 1.7 Momega in 18 PTNs and 4.5 +/- 2.5 Momega in 28 non-PTNs. There was a linear relationship in PTNs between membrane resistance and antidromic latency from the pontine pyramid. Because of the time course of PSPs, their possible dendritic origins were discussed.

Animals↗

Excitatory synaptic potentials and morphological classification of tectal neurons of the frog.

Under electrical stimulation of the optic nerve, intracellular recording and staining techniques were applied to tectal neurons of the frog. In the first part of this study, two response types in 25 cells were examined. One type (type I; 21 cells) was composed of an EPSP followed by an IPSP. The other type (type II; 4 cells) was composed of two successive EPSPs followed by an IPSP. The initial EPSP of type II response was concluded to be monosynaptic, while the other ones were assumed to be disynaptic. These responses were produced by myelinated fibers. Under stronger stimulus intensities, a pair of depolarization and hyperpolarization appeared at longer latencies. In the later part of this study, 22 cells were stained with Procion Yellow. Neurons were classified into three morphological types, i.e. vertical type (V-type; 10 cells), multipolar type (MP-type; 11 cells) and small neuron (S-neuron; one cell). All V-type neurons gave rise to type I response, while either type I or type II responses were recorded from MP-type neurons.

Animals↗

Identification of a GABA-activated chloride-mediated synaptic potential in rat pars intermedia.

Intracellular recordings from melanotrophs in acutely isolated, intact pituitaries revealed inhibitory postsynaptic potentials (IPSPs) resulting from both pituitary stalk stimulation and exogenous gamma-aminobutyric acid (GABA) application. The stalk-stimulated and GABA-evoked IPSPs displayed identical conductance increases to chloride ions. Both responses reversed in polarity at the same membrane potential and were blocked with bicuculline, a GABAA antagonist. We conclude that activation of this synapse releases GABA which acts on a classical GABAA receptor to increase conductance to chloride in the melanotroph.

Action Potentials↗

Synaptic potentials in the rat neostriatum in dissociated embryonic cell culture.

Neostriatal cells of embryonic days 19-21 were grown in dissociated cell culture. To test whether the cultures contained predominantly neostriatal cells, a glyoxylic acid staining procedure was used which, after dopamine loading, stained neostriatal cells but not neurons of embryonic neocortical tissue. Whole cell current clamp recording was performed in the neurons after 1-2 weeks in cell culture. Although cells could be driven to discharge by direct depolarization, spontaneous activity was low. All cells responded to gamma-aminobutyric acid (GABA) (0.1-0.5 mM), and the majority of them responded to glutamate (Glu) (0.1 mM). Only about 50% were depolarized by acetylcholine (ACh) (0.1-0.5 mM). Atropine (1-10 microM) did not block this depolarization. Barrages of postsynaptic potentials (PSPs) were induced by applications of Glu or ACh, even if the neuron under observation was not depolarized. All PSPs were depressed by bicuculline (50 microM), indicating their mediation by GABAergic receptors. Exclusively GABAergic PSPs were also observed in cultures raised in the presence of nerve growth factor. The study indicates that neostriatal cells form GABAergic, but not excitatory cholinergic synapses when cultured at this embryonic age under our conditions, resembling the pattern of development observed in slices obtained from neonatal rats.

Acetylcholine↗

Competitive inhibition by NBQX of kainate/AMPA receptor currents and excitatory synaptic potentials: importance of 6-nitro substitution.

We evaluated the inhibitory potencies at excitatory amino acid receptors of 2,3-dihydroxy-7-sulfamoyl-benzo[f]quinoxaline (BQX) and its 6-nitro derivative, NBQX. Currents activated by kainate or (RS)-alpha-amino-3-hydroxy-5-methyl-4-isoxazole-propionic acid (AMPA) in two-electrode voltage-clamp recordings of Xenopus oocytes injected with rat cortex mRNA were inhibited by BQX and NBQX: the apparent Ki values versus kainate were 14 microM and 78 nM, respectively, and versus AMPA were 23 microM and 63 nM, respectively. Thus, to a degree even more marked than with other quinoxalinedione derivatives, 6-nitro substitution of BQX to yield NBQX increases potency (200-fold) at the non-NMDA ionotropic receptor, but does not confer selectivity for kainate or AMPA. Schild analysis of the NBQX inhibition of the kainate and AMPA currents yielded pA2 values of 7.17 +/- 0.05 and 7.05 +/- 0.10, respectively, and slopes near unity confirming the competitive nature of the inhibition. Neither BQX nor NBQX significantly inhibited the current activated by glycine plus NMDA. The selectivity ratio of NBQX (greater than 5000-fold) is by far the greatest of any quinoxalinedione derivative antagonist of the kainate/AMPA receptor. BQX and NBQX also inhibited the excitatory postsynaptic field potentials mediated by kainate/AMPA receptors in the CA1 region of hippocampal slices after stimulation of the Schaffer collateral-commissural pathways with IC50 values of 130 and 0.90 microM, respectively. The 10-fold differences between the IC50 values in hippocampal slices and the Ki values in Xenopus oocytes correlate closely with data for other quinoxalinedione derivative antagonists.

Animals↗

Effects of 5-HT1A and 5-HT4 receptor agonists on slow synaptic potentials in enteric neurons.

Intracellular electrophysiological methods were used to examine the effects of 5-hydroxytryptamine (5-HT), 5-carboxamidotryptamine (5-CT), 5-methoxytryptamine (5-MeOT), 4-amino-5-chloro-2-methoxy-N-(4-[1-azabicyclo[3,3,1]nonyl]) benzamide hydrochloride (renzapride), cis-4-amino-5-chloro-N[1-[3- (4-fluorophenoxy)propyl]-3-methoxy-4-piperidinyl[-2-methoxybenzamide monohydrate (cisapride) and endo-N-(8-methyl-8-azabicyclo[3.2.1]oct-3-yl)-2,3-dihydro-3- (1-methyl)ethyl-2-oxo-1 H-benzimidazole-1-carboxamidehydrochloride (BIMU 8) on noncholineric slow excitatory postsynaptic potentials (slow EPSPs) in myenteric afterhyperpolarization (AH) neurons of guinea pig ileum. 5-HT (0.01-1 microM) and 5-CT (0.001-0.1 microM) produced a concentration-dependent inhibition of slow EPSPs. The 5-HT1A receptor antagonist 1-(2-methoxyphenyl)-4-[4-(2-phthalimidobutyl]piperazine (NAN-190) produced rightward shifts in 5-HT and 5-CT concentration-response curves; facilitation of slow EPSPs was never observed. 5-MeOT caused a depolarization and inhibited spike afterhyperpolarizations in a concentration-dependent manner but this effect was not blocked by the 5-HT3/5-HT4 receptor antagonist, tropisetron (1 microM). Renzapride (0.01-0.3 microM), cisapride (0.01-1.0 microM) and BIMU 8 (0.01-1.0 microM) did not change the membrane potential of any neuron tested. Renzapride and BIMU 8 did not change the amplitude of slow EPSPs. In 13 of 19 neurons cisapride did not change the amplitude of slow EPSPs; in 6 neurons cisapride (1 microM) reversibly inhibited the slow EPSP. Responses to substance P which mimicked the slow EPSP were not affected by cisapride.(ABSTRACT TRUNCATED AT 250 WORDS)

5-Methoxytryptamine↗