Biomedical subjects

C Reyes-Vazquez

Publications and source records attributed to C Reyes-Vazquez.

At least 19 recordsLinked to original sources

PubMed2000

The role of intrinsic and agonist-activated conductances in determining the firing patterns of preoptic area neurons in the guinea pig.

Whole-cell and intracellular recordings were made in coronal hypothalamic slices prepared from ovariectomized female guinea pigs. 62% of preoptic area (POA) neurons fired action potentials in a bursting manner, and exhibited a significantly greater afterhyperpolarization (AHP) than did non-bursting POA neurons. The majority (70%) of POA neurons (n=76) displayed a time-dependent inward rectification (I(h)) that was blocked by CsCl (3 mM) or by ZD 7288 (30 microM). In addition, 51% of the cells expressed a low-threshold spike (LTS) associated with a transient inward current (I(T)) that was blocked by NiCl(2) (200 microM). A smaller percentage of POA neurons (29%) expressed a transient outward, A-type K(+) current that was antagonized by a high concentration of 4-aminopyridine (3 mM). Moreover, POA neurons responded to bath application of the mu-opioid receptor agonist DAMGO (93%) or the GABA(B) receptor agonist baclofen (83%) with a membrane hyperpolarization or an outward current. These responses were accompanied by a decrease in input resistance or an increase in conductance, respectively, and were attenuated by BaCl(2) (100 microM). In addition, the reversal potential for these responses closely approximated the Nernst equilibrium potential for K(+). These results suggest that POA neurons endogenously express to varying degrees an AHP, an I(h), an I(T) and an A-type K(+) current. The vast majority of these neurons also are inhibited upon mu-opioid or GABA(B) receptor stimulation via the activation of an inwardly-rectifying K(+) conductance. Such intrinsic and transmitter-activated conductances likely serve as important determinants of the firing patterns of POA neurons.

4-Aminopyridine↗

PubMed1997

Interferon modulates glucose-sensitive neurons in the hypothalamus.

Interferon-alpha (IFN) therapy induces feeding suppression that resembles anorexia. The hypothalamic glucose-sensitive neurons engage in feeding behavior. Coronal sections of rat brains, containing both the lateral hypothalamus (LH) and the ventromedial hypothalamus (VMH), as well as single-cell recordings were used to study the interaction between IFN and glucose-sensitive neurons. IFN suppressed the majority (78%) of LH neurons, while reduction in glucose concentration elicited excitation in the majority (85%) of the same neurons. The opposite effects were observed in the VMH, where IFN excited the majority of neurons (61%), and reduction in glucose concentration exerted the opposite effects in 64% of VMH recordings. Concomitant IFN and glucose reduction exhibited only the effects elicited by IFN, regardless of whether the glucose reduction caused excitation (LH) or suppression (VMH). This observation suggests that IFN causes anorexia by modulating the LH and VMH glucose-sensitive neurons.

Animals↗

PubMed1996

Interferon modulates neuronal activity recorded from the hypothalamus, thalamus, hippocampus, amygdala and the somatosensory cortex.

Neuromodulators interact with classically defined neurotransmitters to regulate a variety of biological processes. The aim of the present study was to study whether interferon-alpha (IFN) can be considered as a neuromodulator. Single cell recordings from five CNS structures were recorded before and following three different routes of IFN administration in Sprague-Dawley rats to substantiate that IFN is a neuromodulator. IFN modulated the majority of the hypothalamic (70%), amygdala (76%), hippocampus (75%) and cortical (82%) cells whether the route of administration was within the brain or given peripherally (i.v. or i.p.). The main difference among the three routes of IFN administration on the neuronal activity of these four CNS sites was the onset of the effect. However, the thalamic neurons responded differently. IFN injection within the brain modulated activity of 43% of thalamic neurons, but only 25% and 17% of the neurons when IFN was given i.v. or i.p., respectively. IFN, in general suppressed hypothalamic neuronal activity while accelerating neuronal activity in all the other studied CNS sites. In conclusion, IFN is an endogenous peptide synthesized and released both peripherally and centrally, with the same effects on neuronal activity whether it is given systemically or locally within the brain. This suggests that IFN can be considered as a neuromodulator.

Animals↗

PubMed1996

Lateral hypothalamus: site involved in pain modulation.

The present study is an attempt to examine the neuronal circuitry of a supraspinal site engaged in pain modulation. Five physiological measures were postulated as the criteria for defining a central nervous system site engaged in the circuitry of pain modulation. The lateral hypothalamus met these five measures: (i) 81% of the lateral hypothalamus neurons (247/304) responded to noxious stimuli using a single cell recording procedure; (ii) stimulation of the periaqueductal gray-dorsal raphe area or the habenula modulated 98% and 87% of the lateral hypothalamus noxious-evoked activity; (iii) microiontophoretically applied morphine modulated 77% of the lateral hypothalamus noxious evoked activity; (iv) electrical stimulation of the lateral hypothalamus produced behavioral analgesia proportional to the stimulus intensity as assessed by the tail flick assay; and (v) morphine application into the lateral hypothalamus produced behavioral analgesia in a dose-response manner using the tail flick assay. In conclusion, the lateral hypothalamus can be considered one of the pain modulation sites.

Animals↗

PubMed1990

Modification of nociceptively identified neurons in thalamic parafascicularis by chemical stimulation of dorsal raphe with glutamate, morphine, serotonin and focal dorsal raphe electrical stimulation.

The properties of local application of glutamate, morphine and serotonin in the dorsal raphe (DR) area and the effects of DR electrical stimulation on the spontaneous activity and on the nociceptive responses of 135 parafascicularis (PF) neurons were studied. It was observed that local glutamate application within the DR exerts an effect upon the "nociceptive-on" PF neuronal activity similar to that induced by focal electrical stimulation of the DR in intact animals and in animals after dorsal spinal cord section. In addition, local application of morphine and serotonin in the DR area elicits different effects on the spontaneous activity versus the nociceptive responses of PF neurons. These observations suggest that opioids and serotonin at least in part participate in modulation of pathways from DR to PF. This observation is consistent with the hypothesis that the DR ascending path modulates nociceptive input to the PF (at least in part) via activations of both opioid and serotonergic receptors.

Action Potentials↗

PubMed1989

Nociceptive responses in nucleus parafascicularis thalami are modulated by dorsal raphe stimulation and microiontophoretic application of morphine and serotonin.

Single-cell experiments were undertaken to examine the hypothesis that serotonin (5-HT) and morphine participate in ascending pain suppression phenomena. The observations demonstrate that: 1) dorsal raphe stimulation (DRS) modulates the spontaneous activity and the noxious-evoked responses of parafasciculus (PF) neurons, and the modulating effects of DRS are altered by either naloxone or methysergide; 2) morphine ejection into the PF alters the spontaneous activity and the noxious-evoked responses of PF neurons, and naloxone prevents morphine effects; and 3) serotonin ejection into the PF alters the spontaneous activity and the noxious-evoked responses of PF neurons and methysergide prevents the serotonin effects. These findings support the hypothesis that opioid and serotonin participate, at least in part, in the control of ascending pain mechanisms.

Action Potentials↗

PubMed1989

Noxious and non-noxious responses in the medial thalamus of the rat.

Single-cell experiments were undertaken to localize and characterize the medial thalamic (MT) neurons which respond to noxious and non-noxious input in the rat. The observations demonstrated that: (1) 61 and 42% of MT neurons respond to noxious (Nox) and non-noxious (NN) stimulation, respectively; (2) MT neurons exhibit 4 cell types according to their pattern of response; Type A units were excited exclusively by Nox stimulation; Type B units were excited exclusively by NN stimulation; Type C units were excited by both (Nox and NN) stimulation, and Type D units exhibited decreases in firing rate following both stimulation modalities; (3) neurons of the parafascicularis nucleus exhibit more noxious responses (Type A units) than other medial thalamic areas.

Action Potentials↗

PubMed1987

Single injection of three different preparations of alpha-interferon modifies morphine abstinence signs for a prolonged period.

Opiates exert numerous effects on all levels of the central nervous system, with tolerance and physical dependence (addiction) being characteristics of this drug class. The capacity of the immune system to participate in processes primarily considered to be central nervous system phenomena has been suggested recently by several studies demonstrating the ability of various immune-modifiers to attenuate opiate withdrawal severity. Therefore, the immunomodulator agent, interferon was investigated to determine the effect upon the opiate withdrawal signs in an animal model. The degree of morphine dependence is measured by quantifying the various behavioral signs associated with naloxone-induced withdrawal. Three different preparations of human alpha interferon (alpha-IFN) were investigated to determine the duration of their attenuating effect upon the naloxone-induced abstinence syndrome in morphine-addicted rats. All three preparations of alpha-IFN reduced the severity of the opiate withdrawal (i.e., addiction) signs for several weeks. There were differences in the potency and the duration of the effects among the three different preparations of alpha-IFN.

Animals↗

PubMed1986

The parafasciculus thalami as a site for mediating the antinociceptive response to GABAergic drugs.

Electrophysiological (single cell) experiments were undertaken to examine whether neurons in the rat parafasciculus thalami (PF) are involved in mediating the antinociceptive response to GABAergic drugs. The results indicated that: noxious stimuli excite most PF neurons; microiontophoretic application of morphine, GABA or the GABA agonist, THIP, attenuated the spontaneous firing rate of PF neurons; morphine, THIP and GABA reduced the neuronal excitation induced by noxious stimuli; application of the GABA receptor antagonist, bicuculline, prevented the effects of THIP and GABA on PF activity; while naloxone blocked the response to morphine on PF neurons, it failed to influence the actions of GABA and THIP; and the injection of THIP or GABA into the PF produced an antinociceptive response as assessed by the rat tail-immersion assay, whereas pentobarbital was inactive. The findings suggest that GABA receptors located in the PF may mediate the antinociceptive response to GABAergic drugs, and that the action of these agents is unrelated to opiate receptors.

Animals↗

PubMed1986

Rat pineal exhibits two electrophysiological patterns of response to microiontophoretic norepinephrine application.

The spontaneous activity of 117 pineal units was recorded in urethane-anesthetized rats. The pineal units exhibited a wide range of firing rates of which 50% were on average slower than 14 spikes per second. Superior cervical ganglion (SCG) stimulation was studied in 76 pineal units; this stimulation caused excitation in 55% of the units. Microiontophoretic application of norepinephrine (NE) induced changes of firing rates in 61% of the pineal units tested. Two patterns of activity following NE microiontophoresis was observed: increase in firing rate (64%) and decrease in firing rate (36%). NE-induced excitation was observed only in those units excited by SCG stimulation. When NE and SCG stimulation were applied together, partial summation of the excitation induced by each one alone was observed. None of the units in which NE depressed the firing rate responded to SCG stimulation. Local application of propranolol blocked the excitation initiated by SCG stimulation as well as the excitation and the depression induced by NE microiontophoresis.

Action Potentials↗

PubMed1985

Interaction of norepinephrine and superior cervical ganglion input in the rat pineal body.

The effects of superior cervical ganglion stimulation and the local application of norepinephrine or its antagonist propranolol were studied in 18 pineal cells. In 61% of the pineal cells, stimulation elicited excitation; the same cells also responded by excitation to norepinephrine ejection. When stimulation and norepinephrine ejection were applied together, summation (of the excitation) was observed in these cells. Several cells that failed to respond to stimulation did respond to norepinephrine ejection, but with the opposite pattern, i.e., decrease of firing rates. Propranolol prevented the norepinephrine-induced excitation and inhibition, as well as the excitation produced by stimulation. We suggest that norepinephrine regulates pineal activity by two routes: activation of the sympathetic neuronal input and inhibition by way of the circulation.

Animals↗

PubMed1985

Three different types of alpha-interferons alter naloxone-induced abstinence in morphine-addicted rats.

The opiate abstinence syndrome represents a fundamental feature of the addictive process, with the degree of addiction being directly correlated to the intensity of withdrawal. Therefore, the discovery of substances capable of attenuating withdrawal signs may provide insights into the dynamics of opiate addiction. The present study demonstrates that three different types of alpha-interferons modify the behavioral signs associated with naloxone-induced abstinence in rats addicted to morphine. These observations suggest that opiate addiction may, in part, be due to an immune response in that immunomodulators (interferon) are capable of altering the naloxone-induced abstinence syndrome in morphine-dependent rats.

Animals↗

PubMed1985

Does the immune system communicate with the central nervous system? Interferon modifies central nervous activity.

The present investigation determined whether an immunomodulator agent modified the central nervous system activity as measured behaviorally and neurophysiologically. Two types of interferons (IFNs), alpha (alpha) and gamma (gamma), were applied locally (microiontophoretically) into various regions of the rat brain simultaneously with single neuron recording from the cerebral cortex, hippocampus, thalamus and hypothalamus. Of the various IFNs, only alpha-IFN altered single cell activity in all brain structures in a dose-dependent manner. Moreover, systemic administration of alpha-IFN altered the naloxone-induced abstinence syndrome in morphine-dependent rats. These observations suggest that immunomodulators such as alpha-IFN are capable of influencing directly central nervous system function as well as the immune system.

Animals↗

PubMed1984

Does interferon exert its actions through opiate receptors.

It had been reported that alpha interferon (alpha-IFN) induces endorphin-like effects such as analgesia and catatonia. These effects, reversed and prevented by naloxone, suggest that the alpha-IFN effect is mediated via opiate receptors. In order to examine this hypothesis, the present study was initiated. Extracellular cortical cell recording and microiontophoretic application of alpha-IFN, morphine, and naloxone, as well as the application of these three drugs on the coaxially stimulated guinea-pig ileum preparation were used. alpha-IFN application induced excitation in cortical cells and on the guinea-pig ileum. In contrast, the main effect elicited by morphine was a decrease in both preparations. Naloxone was able to reverse and/or prevent the morphine effects in both preparations, but failed to alter the effects induced by alpha-IFN. The present observations using the guinea-pig ileum preparation and cortical neurons recording failed to support the hypothesis that alpha-IFN effects are mediated via opiate receptors.

Animals↗

PubMed1984

Microiontophoretic application of morphine and naloxone to neurons in hypothalamus of rat.

The present experiments used urethane-anesthetized rats and single cell recording to study the electrophysiological properties of ventromedial hypothalamic (VMH) cells following different doses of morphine and naloxone, applied microiontophoretically. More than 45% of ventromedial hypothalamic units reacted in a dose-response fashion to local application of morphine. In the majority of the ventromedial hypothalamic neurons, naloxone failed to reverse the effects of morphine. Naloxone alone had effects on 37% of the ventromedial hypothalamic units. The ventromedial hypothalamic units exhibited different response patterns from those observed from other CNS sites in response to the microiontophoretic application of morphine and naloxone; this difference is discussed. The present neurophysiological findings support the existence of opiate target sites with multiple opiate receptors within the ventromedial hypothalamus.

Animals↗

PubMed1984

Alpha and gamma interferons' effects on cortical and hippocampal neurons: microiontophoretic application and single cell recording.

Responses of 96 extracellular spontaneous active cortical and hippocampal neurons to microiontophoretically applied four types of alpha interferons (alpha-IFNs), one type of gamma interferon (gamma-IFN) as well as three fractions of gamma-IFNs were examined. All four types of alpha-IFN ejections increased the discharge of the majority of neuron tested. Significant differences of the number of cells excited and the intensity of the excitation among the 4 types of alpha-IFN were observed. The most significant effects were induced by Cantell's human leukocyte alpha-IFN followed by the Hoffman-LaRoche recombinant alpha-IFN which exhibited a dose dependent effect (i.e., each higher dose of IFN affected more neurons and intensified the excitation) on the hippocampal and cortical cells respectively. Neither the IFN carrier (albumin), nor the gamma-IFNs and its fractions, as well as current ejection, altered the extracellular spontaneous active of these 96 cortical and hippocampal neurons respectively. These observations show that the immunomodulator alpha-IFNs, but not gamma-IFNs, exerts excitatory effects on neuronal activity recorded from these two brain structures and support the view that the brain is capable of communicating with the immune system.

Action Potentials↗

PubMed1984

Microiontophoretically applied morphine and naloxone on single cell activity in the parafasciculus nucleus of naive and morphine-dependent rats.

Responses of parafasciculus (PF) thalamic neurons to microiontophoretically applied morphine and naloxone were examined in morphine-naive and morphine-dependent rats. The PF neurons exhibited high responsiveness (65%) to microiontophoretically applied morphine. Five different patterns of response to morphine in naive animals were obtained from the PF neurons. In morphine-dependent rats, the total responsiveness to microiontophoretic application of morphine was reduced dramatically (to 30%) and the response patterns to morphine were significantly (P less than .01) altered; this indicates that the PF neurons exhibit tolerance to morphine. Naloxone applied together with morphine only blocked the morphine-induced decreases in firing rates, but not the increases to which naloxone exhibited opiate agonist effects. Microiontophoretic application of naloxone alone, before morphine ejections in morphine-naive rats, induced changes in 51% of the PF neuronal population studied. Most of them (73%) responded with decreased firing rates. In morphine-dependent rats, more units responded to naloxone ejection (64%) as compared with the morphine-naive group. Excitation was the dominant response (73%) to naloxone treatment. The application of naloxone alone in naive and morphine-dependent rats demonstrated that the PF units responded in a characteristic dose-response manner to incremental naloxone administration. The present observations support our previous experiments using systemic applications of morphine and naloxone in freely behaving animals.

Animals↗

PubMed1983

Differential effects of interferon on ventromedial hypothalamus and dorsal hippocampus.

Three incremental doses of recombinant alpha-interferon (IF) were applied iontophoretically to hippocampal and hypothalamic cells. IF produced a dose-dependent long-lasting excitation in hippocampal neurons, whereas, in the hypothalamus alpha-IF elicited biphasic responses. The highest IF currents induced changes in the amplitude of the action potentials on both structures. Our observations suggest that IF could have a selective effect on the specific areas studied.

Animals↗