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J Aceves

Publications and source records attributed to J Aceves.

At least 55 records · Page 3Linked to original sources
PubMed1991

Dendritic activity on neostriatal neurons as inferred from somatic intracellular recordings.

Orthodromic responses after local field stimulation were studied in a neostriatal slice preparation. Single suprathreshold stimuli evoked slow plateau-like orthodromic responses with repetitive firing and duration proportional to the stimulus intensity. Its persistence and apparent threshold upon hyperpolarization, as well as the actions of tetraethylammonium, QX-314 and Sr2+, suggest that this orthodromic response and associated phenomena such as fast prepotentials or Ca-dependent action potentials, may be generated on dendrites.

Action Potentials↗
PubMed1991

L-dopa stimulates the release of [3H]gamma-aminobutyric acid in the basal ganglia of 6-hydroxydopamine lesioned rats.

L-DOPA stimulated the K(+)-induced [3H]GABA (gamma-aminobutyric acid) release from slices of substantia nigra pars reticulata, entopeduncular nucleus, globus pallidus and caudate-putamen isolated from the ipsilateral side of 6-hydroxydopamine-lesioned rats, but the release from ipsilateral subthalamic slices was not affected. In substantia nigra, L-DOPA stimulation (EC50 = 1 microM) of [3H]GABA release was dose-dependently blocked (IC50 = 0.1 microM for the stimulation caused by 10 microM L-DOPA) by the D1 antagonist SCH 23390, but was not affected by (-)-sulpiride, a D2 antagonist. SCH 23390 also blocked the stimulation in the other nuclei. The DOPA decarboxylase inhibitor NSD-1015 (500 microM) did not prevent the stimulation induced by L-DOPA in all of the studied nuclei. The results suggest that L-DOPA is able to activate D1 receptors located on the terminals of striatal projections via the dopamine formed by a decarboxylation mediated by an NSD-1015-resistant enzyme. Activation of the presynaptic D1 receptors results in stimulation of GABA release.

Animals↗
PubMed1991

Gamma-aminobutyric acid (GABAB) receptor-mediated inhibition of tyrosine hydroxylase activity in the striatum of rat.

The effects of GABA and GABA agonists on calcium and depolarization-dependent stimulation of tyrosine hydroxylase activity in striatal slices were studied. gamma-Aminobutyric acid and (-)baclofen inhibited, while muscimol and (+)baclofen did not affect, the stimulation of tyrosine hydroxylase. The inhibitory effect of GABA and (-)baclofen was blocked by the GABAB antagonist, phaclofen but not by the GABAA antagonist, picrotoxin. The data suggest that the activity of tyrosine hydroxylase on dopaminergic nigrostriatal terminals may be modulated by GABA via GABAB receptors.

Animals↗
PubMed1990

Activation of D1 dopamine receptors stimulates the release of GABA in the basal ganglia of the rat.

Here we have explored whether dopamine is able to modulate the release of gamma-aminobutyric acid (GABA) from striatal terminals to substantia nigra pars reticulata, entopeduncular nucleus, globus pallidus and caudate-putamen. The type of dopamine receptors involved was assessed by the blocking effect of either SCH 23390 (D1 antagonist) or (-)-sulpiride (D2 antagonist) of the dopamine effect. Dopamine stimulated (EC50 3.2 microM) the depolarization-induced release of [3H]GABA from slices isolated from all of the above mentioned nuclei. SCH 23390 dose-dependently blocked the dopamine stimulation, but (-)-sulpiride did not show any blocking effect. The results suggest that dopamine via D1 receptors modulates the release of GABA from striatal GABAergic terminals.

Animals↗
PubMed1990

Effect of chronic lead exposure on biopterin metabolism in the rat neostriatum.

Chronic (3 months) lead exposure increased the quinonoid dihydropteridine reductase activity and the tetrahydrobiopterin content but did not affect the GTP-cyclohydrolase activity and the dihydrobiopterin content. These results suggest that lead intoxication may enhance dopamine metabolism in neostriatum by increasing the content of tetrahydrobiopterin, the regulating cofactor of tyrosine hydroxylase activity.

Animals↗
PubMed1990

The influence of culture on pain in Anglo and Hispanic children with cancer.

This study sought to determine if cultural heritage and acculturation influence the perception and expression of pain and anxiety. The study was based on self-report and observation of Anglo and Hispanic children with cancer undergoing invasive procedures. Seventy-eight children between the ages of 3 and 15 participated. Thirty-five were Anglo and 43 were Hispanic. A significant inverse relationship between age and observed and reported distress was noted in both ethnic groups. The Anglo and Hispanic children had remarkably similar behavioral responses. Hispanic parents, however, reported significantly higher levels of anxiety than Anglo parents.

Acculturation↗
PubMed1990

Degenerative ultrastructural changes observed in the neuropil of caudate nuclei from Parkinson's disease patients.

Degenerative changes of the pars compacta of the substantia nigra are considered the main physiopathological basis of Parkinson's disease, while most authors believe that the neostriatum is well preserved in these cases. This paper deals with the preliminary ultrastructural observations made in the neuropil of the caudate nucleus of Parkinson's disease patients. We have observed (1) astrocytic proliferation, neuronal degeneration, degenerated axons, and hyperdense postsynaptic neurites (dendrites), and (2) that degenerative patterns vary from one case to another. Physiopathological and therapeutical implications are discussed.

Axons↗
PubMed1990

Multidisciplinary analysis of the effectiveness of autologous neural transplant (adrenal medulla) as treatment of Parkinson's disease.

The neurobiological aspects of human neural transplants are far from being understood. We have approached their study by means of a multidisciplinary working team. Nine patients with Parkinson's disease were subjected to open brain surgery for grafting of autologous adrenal medulla. Not all patients improved. Those patients that did so showed different patterns of improvement. Rigidity was the sign most relieved in this group of patients. Electroencephalographic changes were attributable to surgical manipulation. High-performance liquid chromatographic quantification of catecholaminergic metabolites did not correlate with post-grafting outcome. Biopterin levels showed a significant increment after surgery. More interdisciplinary studies ought to be done on neural transplants.

Adrenal Medulla↗
PubMed1989

An early outward conductance modulates the firing latency and frequency of neostriatal neurons of the rat brain.

An in vitro slice preparation was used to obtain intracellular recordings of neostriatal neurons. Indirect evidence for the presence of an early outward conductance in neostriatal neurons is presented. With near threshold stimulation neostriatal neurons fired very late during the pulse. The long firing latency was associated with a slow (ramp-like) depolarization. In the presence of TTX the slow depolarization was lost and outward-going rectification dominated the subthreshold response. This finding demonstrated that both, outward- and inward-going conductances play a role during the ramp-like depolarization. Outward-going rectification during depolarizing responses could be further augmented if the depolarizing stimulus was preceded by a conditioning hyperpolarization. A conditioning hyperpolarization prolonged the firing latency and slowed the firing frequency. A conditioning depolarization had opposite effects. After TTX treatment, the response showed a hyperpolarizing "sag" when depolarizing stimulation was preceded by conditioning hyperpolarization. 4-AP (0.5-2.5 mM) blocked the effects of the conditioning hyperpolarization on the firing latency and on the voltage trajectory. 4-AP also disclosed a slow depolarization which could produce neuronal firing very early during the pulse. This depolarization was TTX-sensitive and Co++-insensitive. In contrast to 4-AP, TEA (20 mM) did not produce a reduction in the firing latency but disclosed a membrane oscillatory behavior most probably produced by the interplay of these opposing conductances: the slow inward (probably Na+) and the transient outward (probably K+). Repetitive firing during 4-AP treatment was of the "phasic-tonic" type with an initial burst riding on the initial Co++-insensitive slow depolarization and a somehow irregular train of spikes during the remainder of the stimulation. Action potentials during 4-AP treatment were followed by an afterdepolarization which dominated the initial part of the interspike interval.

Action Potentials↗
PubMed1989

The role of calcium in the repetitive firing of neostriatal neurons.

The Ca++ -dependence of the repetitive firing of neostriatal neurons was studied in an in vitro slice preparation of the rat neostriatum. Neuronal firing was evoked by injecting depolarizing currents of 100-200 ms duration. In normal conditions, the mode of firing was tonic and showed very little adaptation. The frequency-current relation was linear over a wide range of frequencies. The repetitive firing was first enhanced and later suppressed by Co++, Mn++ and Cd++. These effects on the repetitive firing by the Ca++ -channel blockers paralleled the suppression of the slow afterhyperpolarizing potential. The lowering (0.2 mM) of Ca++ had similar effects. In the presence of TEA (up to 10 mM), the cell fired both Na+ and Ca+ action potentials. The results suggest that, as in other CNS neurons of the vertebrate, in neostriatal neurons the slow afterhyperpolarizing potential (AHP) is due to a Ca++ -activated K+ -conductance, and that the AHP plays a crucial role in the repetitive firing of these neurons.

Action Potentials↗
PubMed1988

Physostigmine stimulates phosphoinositide breakdown in the rat neostriatum.

The reversible acetylcholinesterase inhibitor, physostigmine, stimulated in a dose-dependent manner the accumulation of [3H]inositol monophosphate ([3H]IP1) in lithium-treated neostriatal slices. The muscarinic agonists, carbachol and oxotremorine, also stimulated [3H]IP1 accumulation. Atropine completely blocked the physostigmine-induced accumulation but had no effect on the basal accumulation. Tetrodotoxin partially inhibited the physostigmine-induced [3H]IP1 accumulation but had no effect on the carbachol-induced accumulation. 4-Aminopyridine stimulated the basal [3H]IP1 accumulation and potentiated the physostigmine-induced accumulation. This potentiation was blocked by tetrodotoxin. The physostigmine dose-response curve for the stimulation of [3H]IP1 accumulation was similar to its dose-response curve to inhibit acetylcholinesterase activity in the neostriatum. The results suggest that, under our experimental conditions, the acetylcholine released spontaneously from intrinsic cholinergic neurons does not activate the striatal muscarinic receptors coupled to phosphoinositide breakdown unless the intrinsic acetylcholinesterases are inhibited.

4-Aminopyridine↗
PubMed1988

Presynaptic modulation of the release of GABA by GABAA receptors in pars compacta and by GABAB receptors in pars reticulata of the rat substantia nigra.

The effect of GABA agonists and antagonists on K+-stimulated [3H]GABA release was studied to assess how presynaptic GABA receptors modulate GABA release. The release was affected in a quite different manner in the pars compacta and in the pars reticulata. Muscimol markedly inhibited the release from the pars compacta but had no effect on the release from the pars reticulata. Baclofen inhibited the release from the pars reticulata without affecting the release from the pars compacta. Bicuculline itself facilitated the release from the pars compacta but inhibited the release from the pars reticulata. Picrotoxin facilitated the release from the pars compacta and had no effect in the pars reticulata. The results suggest that the release of GABA from GABAergic terminals in the substantia nigra of the rat brain is modulated by GABAA autoreceptors in the pars compacta and by GABAB receptors in the pars reticulata.

Animals↗
PubMed1988

Congenital optic atrophy and brachytelephalangy: the Berk-Tabatznik syndrome.

Here we report on a prepubertal boy with the Berk-Tabatznik syndrome. Manifestations included short stature, congenital optic atrophy, and hypoplasia of the cervical vertebral bodies and distal phalanges. Prognosis was adversely affected by visual and auditory difficulties. The cause of this condition remains unknown.

Deafness↗
PubMed1988

Electrotonic properties of neostriatal neurons are modulated by extracellular potassium.

In order to assess the effects of [K+]o on the passive membrane properties of neostriatal neurons, the cable properties of these cells were determined at two extracellular potassium concentrations (6.25 and 3.0 mM). The effect of tetraethylammonium (TEA) on cable properties was also studied at 6.25 [K+]o. At 6.25 mM [K+]o, the mean input resistance at the resting membrane potential (RMP), and the mean membrane time constant (tau o) were 27 +/- 1.5 M omega and 6.9 +/- 0.5 ms respectively (n = 17), while at 3 mM [K+]o they were 62.9 +/- 4.8 M omega and 14.3 +/- 0.6 ms (n = 15) (mean +/- SEM). With one of the methods used to calculate the electronic parameters, the total electrotonic length of the dendrites (L) and the dendritic to somatic conductance ratio (rho) were 1.3 +/- 0.05 and 5 +/- 0.8 at the higher [K+]o respectively, while they were 0.95 +/- 0.04 and 3 +/- 0.7 at the lower [K+]o. Cells were depolarized in 6.25 as compared to 3 mM [K+]o (RMP = -66 +/- 1.3 mV vs RMP = -80.5 +/- 1.4 mV). After one hour exposure to TEA (10 mM), the input resistance and time constant tripled at 6.25 mM [K+]o. TEA slightly depolarized the cells bathed in 6.25 mM [K+]o. The results suggest that changes in [K+]o, within the physiological range, markedly affect the cable properties of neostriatal neurons, possibly modifying subthreshold, voltage-dependent K+-conductances. TEA seems to block some of these channels.

Animals↗
PubMed1987

Spontaneous synaptic potentials in dopamine-denervated neostriatal neurons.

Intracellular spontaneous activity was recorded in neostriatal slices from rats with 6-hydroxydopamine-induced lesion of the left nigrostriatal dopaminergic system. Recordings were made at different times after denervation. Dopaminergic denervation caused the appearance of spontaneous synaptic potentials, which were present even after 8 months. The results suggest a tonic inhibitory influence of the dopaminergic innervation on the synaptic input of neostriatal neurons.

Action Potentials↗
PubMed1987

Platelet dysfunction associated with Wilms tumor and hyaluronic acid.

Acquired von Willebrand disease (AVWD) has been described in two cases of nephroblastoma. We studied a patient with nephroblastoma who presented with a coagulopathy suggestive of AVWD. The subject had undetectable levels of F.VIIIR:Ag, diminished F.VIIIR:WF (16.3%), F.VIII:C activity (37%), and lack of platelet aggregation to ADP, epinephrine, collagen, and arachidonic acid. These results were associated with abnormally high serum levels (850 mg/dl) of hyaluronic acid (HA), which made the patient's serum hyperviscous. Examination of the neoplasm revealed HA in the tumor matrix. All abnormalities of coagulation resolved after chemotherapy and extirpation of the neoplasm, which produced normal serum HA levels. To study the effects of HA on platelet function, we added HA to normal platelet-poor plasma (NPP), which rendered F.VIIIR:Ag undetectable; treatment of HA with hyaluronidase eliminated F.VIIIR:Ag assay interference caused by HA. F.VIII:C activity decreased in vitro when HA was mixed with normal platelet-poor plasma (NPP). HA reduced the initial slope of normal platelet aggregation. Partial correction of platelet aggregation occurred after hyaluronidase treatment of HA-spiked PRP. Experiments in rabbits exposed to HA (serum level 400 mg/dl) demonstrated abnormalities similar to those noted in the patient. Shear rate studies of whole blood containing HA (500 mg/dl) yielded high shear stress, 27-136 dynes/cm2 over shear rates of 10-216 sec-1. We conclude that the coagulopathy demonstrated in this case is secondary to hyperviscosity produced by elevated levels of HA, which interferes with the assay for F.VIIIR:Ag. Thus the acquired coagulopathy associated with other cases of nephroblastoma may present as spurious von Willebrand disease.

Animals↗
PubMed1985

The binding of doxepin to histamine H1-receptors in guinea-pig and rat brain.

The affinity constant for doxepin obtained from inhibition of histamine-induced contraction of guinea-pig intestinal smooth muscle at 30 degrees C was 2.6 +/- 0.18 X 10(10)M-1. The slope of a Schild plot was not significantly different from unity. The affinity constant of doxepin did not vary markedly with temperature. At 37 degrees C it was 3.75 +/- 0.02 X 10(10)M-1 and at 25 degrees C 2.1 X 10(10)M-1. Doxepin was a competitive inhibitor of [3H]-mepyramine binding to guinea-pig cerebellar homogenates. The affinity constant derived for doxepin at 30 degrees C was 1.12 +/- 0.45 X 10(10)M-1. Hill coefficients for curves of doxepin or mepyramine inhibition of [3H]-mepyramine binding in guinea-pig cerebellum, cerebral cortex and hippocampus did not differ significantly from unity. The mean affinity of mepyramine for histamine H1-receptors in rat brain homogenates at 30 degrees C was 3.5 X 10(8)M-1. Hill coefficients for curves of doxepin or mepyramine inhibition of [3H]-mepyramine binding to homogenates of rat cerebral cortex or rat whole brain were near unity. These studies provide no evidence that doxepin binds preferentially to a sub-class of histamine H1-receptors in rat brain.

Animals↗