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A Colino

Publications and source records attributed to A Colino.

16 recordsLinked to original sources
PubMed2004

Characterization of release-independent short-term depression in the juvenile rat hippocampus.

Short-term depression strongly influences neuronal activity in cerebral circuits and contributes to low-pass temporal filtering of information. In this work, we show that synaptic depression evoked by stimulation of commissural-Schaffer collateral afferents at 10 Hz is associated with a reduction of the fibre volley. This depression of action potentials is also evident in the absence of extracellular Ca(2+), which underlies its release-independent nature. In addition, this reduction of the excitability is independent of failures in action potential propagation since increasing the distance between the stimulus and recording electrodes does not alter this effect. Whole-cell recordings show that tetanic stimulation at supraminimal intensity induces action potential failures preceded by changes in the repolarization rate of the action potentials leading the membrane potential to hyperpolarized values. This activity-dependent hyperpolarization was blocked by ouabain, an indication of the important role of the Na(+)-K(+)-ATPase in this process. Then again, an alteration of the firing threshold was observed when action potentials were elicited either by somatic current injection or by synaptic stimulation, which indicates that this mechanism could alter the EPSP-spike coupling in these cells. The results suggest that these factors act together to reduce gradually the safety factor for action potential generation and to produce failures in action potential initiation; in fact, experiments made at twice the supraminimal intensity show a dramatic decrease in the rate of these failures. Taken together, the results suggest the existence of a release-independent component of short-term depression that is related to failures in action potential initiation.

Action Potentials↗
PubMed2003

Age-dependent alterations of long-term synaptic plasticity in thyroid-deficient rats.

Thyroid hormone deficiency during a critical period of development profoundly affects cognitive functions such as attention, learning, and memory, but the synaptic alterations underlying these deficits remain unexplored. The present study examines the effect of congenital hypothyroidism on long-term synaptic plasticity. This plasticity is believed to be essential for learning and memory and for activity-dependent regulation of synapse formation in the developing brain. We found that the neonatal expression of long-term potentiation (LTP), long-term depression (LTD), depotentiation, and de-depression in hippocampal slices from hypothyroid animals was similar to that of controls. To examine the postnatal development of these plasticities, we used slices from neonatal (2-3 weeks) and adult (7-8 weeks) rats. This work demonstrates that the ability to express all these forms of synaptic plasticity is reduced in an age-dependent manner in control rats. LTP and depotentiation are also downregulated in adult hypothyroid rats, but we have found that de-depression is not affected during maturation. In addition, these animals express LTD at ages at which controls fail to induce it. In contrast, input/output experiments have shown greater levels of basal synaptic efficacy in hypothyroid adults, and this effect is probably related to the higher probability of release observed by paired-pulse experiments. Nevertheless, these effects appear to be unrelated to the differences observed in long-term synaptic plasticity, as no correlation was found between basal synaptic efficacy and the degree of LTD and de-depression. Furthermore, the NMDA-receptor antagonist amino-phosphonopentanoic acid (APV) completely blocked LTD, which suggests a postsynaptic locus of this alteration. Because LTD has been associated with novelty acquisition, we suggest that the greater LTD observed in adult hypothyroid rats might be related to the hyperactivity of these animals. However, other possibilities such as a retarded maturation of synaptic plasticity must be taken into account.

Aging↗
PubMed2002

Thyroid hormone regulates neurotransmitter release in neonatal rat hippocampus.

Thyroid hormone is essential for the normal maturation and function of the mammalian CNS. Thyroid hormone deficiency during a critical period of development profoundly affects cognitive functions such as learning and memory. However, the possible electrophysiological alterations that could underlie these learning deficits in hypothyroid animals remain largely unexplored. In this work, we have studied the possible effect of thyroid hormone on short-term synaptic plasticity, which is hypothesized to be a neural substrate of short-term memory. We compared short-term modification of the excitatory postsynaptic potential in hippocampal slices between control and hypothyroid rats. Electrophysiological studies reveal that paired-pulse facilitation is strongly altered in the hypothyroid rats. In addition, hypothyroid rats exhibit an increase in the Ca(2+)-dependent neurotransmitter release. These alterations are basically reversible when thyroid hormone is administered. In order to examine the possible molecular mechanisms underlying these synaptic changes, we compared the expression of synapsin I, synaptotagmin I, syntaxin, and alpha-Ca(2+)/calmodulin kinase II between control and hypothyroid hippocampus. Our results show that the levels of synapsin I and synaptotagmin I are increased in the hypothyroid rats, which suggests that the genes encoding these proteins are implicated in the action of thyroid hormone on neurotransmitter release. Taken together, the results from this study suggest that thyroid hormone may modulate the probability of neurotransmitter release.

Adenosine↗
PubMed1998

Action potential broadening induced by lithium may cause a presynaptic enhancement of excitatory synaptic transmission in neonatal rat hippocampus.

Lithium enhances excitatory synaptic transmission in CA1 pyramidal cells, but the mechanisms remain unclear. The present study demonstrates that lithium enhances the N-methyl-D-aspartate (NMDA) and alpha-amino-3-hydroxy-5-methyl-isoxazole propionic acid (AMPA) receptor-mediated components of the excitatory postsynaptic current (EPSC). Lithium decreased the magnitude of paired-pulse facilitation and presented an inverse correlation between the lithium-induced enhancement of synaptic transmission and initial paired-pulse facilitation, which is consistent with a presynaptic mode of action. The enhancement of synaptic strength is likely to act, at least in part, by increasing the amplitude of the presynaptic Ca2+ transient. One mechanism which could account for this change of the presynaptic Ca2+ transient is an increase in the duration of the action potential. We investigated action potential in hippocampal pyramidal neurons and found that lithium (0.5-6 mM) increased the half-amplitude duration and reduced the rate of repolarization, whereas the rate of depolarization remained similar. To find out whether the lithium synaptic effects might be explained by spike broadening, we investigated the field recording of the excitatory postsynaptic potential (EPSP) in hippocampal slices and found three lines of evidence. First, the prolongation of the presynaptic action potential with 4-aminopyridine and tetraethylammonium blocked or reduced the synaptic effects of lithium. Second, the lithium-induced synaptic enhancement was modulated when presynaptic Ca2+ influx was varied by changing the external Ca2+ concentration. Finally, both effects, the synaptic transmission increment and the action potential broadening, were independent of inositol depletion. These results suggest that lithium enhances synaptic transmission in the hippocampus via a presynaptic site of action: the mechanism underlying the potentiating effect may be attributable to an increased Ca2+ influx consequent to the broadening effect of lithium on the action potential.

Action Potentials↗
PubMed1997

Lithium enhances synaptic transmission in neonatal rat hippocampus.

The effects of lithium on excitatory synaptic transmission were studied in the CA1 region of hippocampal slices taken from 14- to 30-day-old rats using extracellular recording techniques. Lithium (2-18 mM) reversibly increased the field excitatory postsynaptic potentials in a concentration-dependent manner. Application of lithium for 6-15 min had no effect on the synaptic input-output function, while application of lithium for 20-35 min shifted this curve to the left. Lithium reversibly increased the amplitude of the presynaptic fibre volley in a concentration- and calcium-dependent manner. Lithium decreased paired-pulse facilitation measured at 50-ms interstimulus intervals. The results indicate that lithium enhances excitatory synaptic transmission in CA1 pyramidal cells by at least two different actions.

Animals↗
PubMed1993

Carbachol potentiates Q current and activates a calcium-dependent non-specific conductance in rat hippocampus in vitro.

Intracellular recordings were made from CA1 neurons in rat hippocampal slices maintained in vitro. When Na+ currents were blocked with tetrodotoxin and K+ conductances known to be sensitive to suppression by muscarinic agonists were blocked by 2 mM Ba2+, CA1 cells were depolarized by carbachol (3-10 microM) with an attendant conductance increase, whereas prior to Ba2+ the agonist produced a decrease or no change in conductance. Under voltage clamp at approximately -60 mV and in the presence of tetrodotoxin and Ba2+, carbachol (3-10 microM) induced a variable-latency biphasic inward current of up to 380 pA associated with a conductance increase of approximately 50%. The first phase was associated with an increase (more than 2-fold) of the Cs(+)-sensitive, hyperpolarization-activated cationic current, IQ. Carbachol also accelerated the kinetics of IQ at -100 mV with an average 24% reduction in its activation time constant. The second phase reflected an additional inward current that was Cs(+)-resistant, displayed little apparent voltage sensitivity and had a mean extrapolated reversal potential, determined in the presence of external Cs+ (< or = 5 mM), of approximately -20 mV. In a small proportion of cells the second phase of inward current was followed (or overlapped) by an outward current, also associated with a conductance increase, which reversed at approximately -70 mV. These carbachol actions were prevented by extracellular 300 microM Cd2+ and 2 mM Mn2+, by high levels (> 5 mM) of extracellular Mg2+ or Ca2+, and by omission of Ca2+ or reduction of extracellular Na+ to 25 mM by substitution of NaCl with Tris or N-methyl-D-glucamine. Carbachol action was not mimicked by oxotremorine (< or = 60 microM), but was irreversibly blocked by this drug. Likewise, atropine (100 nM) irreversibly and gallamine (10 microM) reversibly antagonized carbachol's action. The action of carbachol was blocked shortly after prior exposure of slices to 2-5 mM caffeine. Chronic or acute incubation of slices with 2 mM Li+ potentiated (between 1- and 2-fold) carbachol responses. The data indicate that muscarinic activation increases cationic flux by a calcium-dependent potentiation of IQ and activation of a non-selective conductance. The probability that inositol phospholipid metabolism is involved in triggering these events is discussed.

Animals↗
PubMed1993

Mechanisms underlying induction of long-term potentiation in rat medial and lateral perforant paths in vitro.

1. The mechanisms underlying the induction of long-term potentiation (LTP) in the medial and lateral perforant paths were studied by recording excitatory postsynaptic potentials (EPSPs) from rat dentate granule cells in vitro using extracellular and whole-cell recording techniques. 2. Paired stimuli (interstimulus interval, 50-1,000 ms) resulted in facilitation of the lateral and depression of the medial perforant path-evoked EPSPs, respectively. This physiological difference was used to isolate responses evoked by stimulation of a single path. 3. Tetanic stimulation induced LTP in both pathways, although the magnitude of LTP in the lateral perforant path was significantly less than that in the medial perforant path. Both forms of LTP were blocked by the N-methyl-D-aspartate (NMDA) receptor antagonist D-2-amino-5-phosphonovaleric acid (D-APV). 4. Buffering intracellular calcium by loading granule cells with the calcium chelator bis (O-aminophenoxy) ethane-N,N,N',N'-tetraacetic acid prevented LTP in both pathways. 5. Pairing of low-frequency (0.25 Hz) afferent stimulation with postsynaptic depolarization induced LTP in the medial but not the lateral perforant path. However, pairing of higher-frequency stimulation (1-4 Hz) with postsynaptic depolarization did potentiate the lateral perforant path-evoked EPSP in some cells. 6. Both the medial and lateral perforant path-evoked EPSPs had two components; a fast component blocked by the non-NMDA receptor antagonist 6-cyano-7-nitroquinoxaline-2,3-dione and a slower, voltage-dependent component blocked by D-APV. 7. The results indicate that the induction of LTP in both the medial and lateral perforant paths requires activation of postsynaptic NMDA receptors and a rise in intracellular calcium.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1992

The influence of prior synaptic activity on the induction of long-term potentiation.

Long-term potentiation (LTP) is an extensively studied model of synaptic plasticity, in part because it is a plausible biological correlate for the Hebbian synaptic modification that forms the basis for theoretical models of neural development, learning, and memory. Although these models must incorporate algorithms that constrain synaptic weight changes, physiological evidence for such mechanisms is limited. Examination of LTP in area CA1 of the hippocampus revealed that the threshold for LTP induction was not fixed but could be strongly influenced by the recent history of synaptic activity. This effect was transient, synapse-specific, and dependent on postsynaptic N-methyl-D-aspartate (NMDA) receptor activation. These results suggest that the threshold for LTP induction may be continually adjusted according to the recent history of NMDA receptor activation and provide a physiological mechanism by which LTP can be transiently inhibited.

2-Amino-5-phosphonovalerate↗
PubMed1992

Characterization of the integration time for the stabilization of long-term potentiation in area CA1 of the hippocampus.

In area CA1 of the hippocampus, synaptic activation of NMDA receptors during postsynaptic depolarization can generate either a decremental synaptic potentiation termed short-term potentiation (STP) or stable, long-term potentiation (LTP). Examining the relationship between these two forms of synaptic enhancement should provide information about the intracellular processes responsible for the stabilization of LTP. Using the hippocampal slice preparation, initial experiments confirmed that STP can be generated either by a weak tetanus or by pairing a single EPSP with postsynaptic depolarization. Following the generation of submaximal LTP, application of a weak, STP-inducing tetanus resulted in STP (not LTP), suggesting that the processes responsible for stabilizing LTP must be activated during induction and cannot be accessed at later times. To determine the interval over which processes activated during STP can be integrated and result in stable LTP (the "integration time" for the stabilization of LTP), a fixed number of afferent stimuli were given at varying intervals (5-60 sec) during postsynaptic depolarization. Using either extracellular or whole-cell recording, LTP was rarely (11% of experiments) elicited at 1 min intervals and frequently (76% of experiments) elicited at 10 sec intervals. These results indicate that following a single EPSP during postsynaptic depolarization, the processes responsible for the stabilization of LTP decay significantly within approximately 1 min, although this value may depend on the level of activation of the requisite intracellular processes.

Animals↗
PubMed1987

Commissural component of the stria terminalis: electrophysiological properties.

The commissural component of the stria terminalis (S. T.) was studied in Equi-Thesin (92.7 mg/kg) anesthetized rats after their exposure in the caudothalamic surface of both hemispheres. Two types of connection between right and left S. T. across the anterior commissure are described: A "direct" connection set up by fibres that run through the S. T. and join the contralateral S. T., and another "indirect" component, formed by cell axons that receive excitatory synaptic contacts from fibres running in the S. T.

Action Potentials↗
PubMed1986

Inhibitory response in entorhinal and subicular cortices after electrical stimulation of the lateral and basolateral amygdala of the rat.

The present study concerns an electrophysiological investigation of the responses of entorhinal and subicular neurons to electrical stimulation of the lateral and basolateral amygdaloid nuclei. All the neurons exhibited suppression of cell firing after the stimulation of these amygdaloid nuclei. Initial excitation following by the suppression characterized 91% of the units and 9% showed initial inhibition. The suppression effect was observed in association with an extracellularly recorded positive deflection. These data suggest that this inhibitory response is mediated by an interneuron.

Amygdala↗
PubMed1986

Electrical activity generated in subicular and entorhinal cortices after electrical stimulation of the lateral and basolateral amygdala of the rat.

Evoked field potentials and extracellular unitary activity were recorded from entorhinal lateral and subicular ventral cortices under conditions of amygdala stimulation in equithesin-anesthetized rats. The stimulation of the lateral and basolateral nuclei of the amygdaloid complex evoked field potentials consisting of negative-positive waves in layers III-VI and positive-negative deflections in the superficial layers of the ventral subdivision of the entorhinal cortex. The stimulation of the lateral nucleus evoked similar potentials in the dorsal subdivision of this cortex. And the stimulation of the lateral and basolateral nuclei of the amygdala evoked negative-positive field potentials in layer III of the subicular cortex. Cellular activity of the entorhinal and subicular cells evoked by stimulation of the lateral and basolateral nuclei consisted of an excitatory response followed by a prolonged suppression period. This activation coincided with the negative potential recorded in the deeper layers of these cortices. Such observations provide support for amygdaloid projection to the entorhinal and subicular cortices as recent anatomical findings suggested. The functional significance of these observations indicate an amygdaloid influence on entorhinal-hippocampal neurotransmission as well as on the ventral subiculum which provides the major output from the hippocampus.

Amygdala↗
PubMedDate not supplied

Differential modulation of three separate K-conductances in hippocampal CA1 neurons by serotonin.

The hippocampus receives a dense serotonin-containing innervation from the divisions of the raphe nucleus. Serotonin applied to hippocampal neurons to mimic the action of endogenous transmitter often produces complex and variable responses (see for example ref. 3). Using voltage-clamp methods and new ligands that are selective for subtypes of serotonin receptors, we have been able to clarify the mechanism of serotonin action on CA1 cells in rat hippocampal slices. We describe three distinct actions of serotonin (or 5-HT) on identified K-conductances in these cells. First, it activates a Ca-independent K-current which is responsible for neuronal hyperpolarization and is inhibitory. Second, it simultaneously suppresses the slow Ca-dependent K-conductance that is largely responsible for the accommodation of cell firing in CA1 neurons: this produces a paradoxical increase in neuronal discharge in response to a depolarizing input. Third, serotonin produces a more slowly developing and long-lasting suppression of an intrinsic voltage-dependent K-conductance, Im (ref. 9), leading to neuronal depolarization and excitation. The hyperpolarizing response is mediated by class 1A serotonin receptors, whereas the other responses are not. Modulation of these different conductances by endogenously released serotonin could therefore change the probability or the duration (or both) of neuronal firing in the mammalian brain in different ways to give inhibitory, excitatory or mixed effects.

Action Potentials↗
PubMedDate not supplied

[The usefulness of a diagnostic study of mental retardation].

INTRODUCTION: The etiological diagnosis of mental retardation is of interest for several reasons, such as being able to inform parents of the risk of recurrence, and offer the possibility of prenatal diagnosis when possible. It is therefore not surprising that doctors use all means available for this, although the real usefulness of this has not been fully studied. OBJECTIVE: To find the frequency with which an etiological diagnosis is made after relevant investigations. PATIENTS AND METHODS: We describe a retrospective study of persons aged between 0 and 14 years, who were seen by specialists in the hospitals of Gandia and Denia over a period of 7 years. Cases in which the diagnosis was already known or there was isolated motor or language retardation were excluded from the study. RESULTS: An etiological diagnosis was established in 15.4% of the 65 children who fulfilled the criteria of inclusion or exclusion. CONCLUSIONS: The little help obtained from the tests done, and the fact that the number of such tests did not affect the possibility of reaching a diagnosis, made us reconsider the habitual complementary investigations. It would be useful if other centres carried out similar studies so that the results may be compared.

Adolescent↗
PubMedDate not supplied

[Short term synaptic plasticity].

INTRODUCTION: At many chemical synapses, the amount of transmitter released by each action potential can increase or decrease markedly after the onset of specific temporal patterns of activity. OBJECTIVES: This review focuses on mechanisms and functions of short term presynaptic plasticity that last from milliseconds to minutes. The short term enhancement of neurotransmitter release is due to three calcium dependent presynaptic processes differing in their durations: about one second or less (facilitation), about 30 seconds (augmentation) and several minutes (post tetanic potentiation). These forms of short term potentiation are usually attributed to a transient elevation in presynaptic calcium ions (Ca2+) concentration following the arrival of the action potential. Otherwise, presynaptic depression processes, as well as the facilitation ones, depend on neurotransmitter release probability. Thus, synapses with high release probability show few facilitation and are easily depressed because of their ability to deplete faster all synaptic vesicles of the ready releasable pool. CONCLUSIONS: Short term synaptic plasticity appears to serve as a flexible mechanism for temporal information processing in higher cortical integration.

Action Potentials↗