Methylphenidate dose-response behavioral and neurophysiological study of the ventral tegmental area and nucleus accumbens in adolescent rats.

The psychostimulant methylphenidate (MPD) is the most common medication used in treating ADHD in children. Studies have shown an increasing prevalence among adolescents without ADHD to take MPD as a cognitive booster and recreational drug, even though it is a Schedule II drug and has a high potential for abuse. The objective of this study is to explore if there is an association between the animals' behavioral and neurophysiological responses to acute and/or chronic methylphenidate exposure within the ventral tegmental area and the nucleus accumbens, and to compare how these two brain structures fire in response to methylphenidate.

Locus coeruleus neuronal activity correlates with behavioral response to acute and chronic doses of methylphenidate (Ritalin) in adolescent rats.

The objective of this study is to gain insight into the behavioral and neuronal changes induced by acute and chronic methylphenidate (MPD) administration. Specifically, there is limited knowledge of the effects of MPD on the locus coeruleus (LC), the main site of norepinephrine synthesis in the brain. In this study, LC neuronal firing rate was recorded simultaneously with locomotor activity in freely moving adolescent rats.

Comparison of the VTA and LC response to methylphenidate: a concomitant behavioral and neuronal study of adolescent male rats.

Methylphenidate (MPD), also known as Ritalin, is a psychostimulant used to treat attention deficit hyperactivity disorder. However, it is increasingly being misused by normal adolescents for recreation and academic advantage. Therefore, it is important to elucidate the behavioral and neurophysiological effects of MPD in normal subjects.

Morphine administration and abrupt cessation alter the behavioral diurnal activity pattern.

In mammals, there is an underlying mechanism that dictates the organism's biological functions and daily activity schedule, known as circadian rhythms, which play a major role in maintaining steady metabolism, homeostasis, and immunity. Limited research has been done investigating the effects of continuous opiate administration on the circadian rhythm activity pattern. A change in circadian activity pattern is suggested as an experimental model to demonstrate long-term effect of the drug.

Interferon modulates central nervous system function.

The interferons (IFNs) are an endogenous pleiotropic family of cytokines that perform fundamental physiological functions as well as protecting host organisms from disease and in maintaining homeostasis. This review covers the effects of endogenous IFN on the nervous system. It starts with the description of its receptors, followed how it modulate neuronal activity, mood, sleep, temperature, the endocrine system, the opioid system and how it regulate food consumption and the immune system.

Melatonin attenuates the decrement of dendritic protein MAP-2 immuno-staining in the hippocampal CA1 and CA3 fields of the aging male rat.

Neuronal death during brain aging results, at least in part, from the disruption of synaptic connectivity caused by oxidative stress. Synaptic elimination might be caused by increased instability of the neuronal processes. In vitro evidence shows that melatonin increases MAP-2 expression, a protein that improves the stability of the dendritic cytoskeleton, opening the possibility that melatonin could prevent synaptic elimination by increasing dendritic stability.

Sex differences in tail-flick latency of non-stressed and stressed rats.

The present study was conducted to assess whether there are sex differences between male and female subjects in their response to noxious stimuli under non-stressed and stressed conditions. Tail-flick latency assay was used as an experimental tool on 12 adult male and 12 adult female Sprague-Dawley rats before immobilization (i.e.

Methylphenidate and amphetamine modulate differently the NMDA and AMPA glutamatergic transmission of dopaminergic neurons in the ventral tegmental area.

Behavioral and neurochemical studies suggest that the induction of behavioral sensitization to psychostimulants involves transient changes at the synapses of the ventral tegmental area's dopaminergic neurons (VTA-DA). Differences in the behavioral response to amphetamine (Amph) and methylphenidate (MPD) were observed. In an attempt to understand these behavioral differences at the neuronal level, the dose-response characteristics of these two psychostimulants on electrophysiologically identified VTA-DA neurons at the glutamatergic synapse were investigated.

ATP-sensitive potassium channels and endogenous adenosine are involved in spinal antinociception produced by locus coeruleus stimulation.

The effects of locus coeruleus stimulation on nociceptive evoked discharges of thalamic parafascicular (PF) neurons were investigated in lightly urethane-anesthetized rats, aiming to study the mechanisms underlying these effects. Intrathecal (i.t.

Serotonin modulates hypothalamic neuronal activity.

Effects of serotonin (5-HT) on electrophysiological activities of single hypothalamic arcuate neurons in rat brain slices were observed by extracellular recording. The results showed that (1) of 385 arcuate neurons observed, the patterns of spontaneous firing were divided into 3 categories: "slow irregular" (46.0%), "fast continuous" (22.

Dopaminergic ventral tegmental neurons modulated by methylphenidate.

Treatment of psychostimulants leads to the development of behavioral sensitization, an augmented behavioral response to drug re-administration. The induction of behavioral sensitization to psychostimulants such as amphetamine and cocaine occurs at the ventral tegmental area's dopaminergic neurons (VTA-DA). Currently, there is limited experimental data about the physiological properties of methylphenidate (MPD) on VTA-DA neurons.

Galphimine B modulates synaptic transmission on dopaminergic ventral tegmental area neurons.

Galphimine B (GB) is a bioactive compound isolated from the plant Galphimia glauca Cav. (Malpighiaceae) and has been shown to have central nervous system depressant properties. In an earlier study, it was reported that both systemic and local administration of GB modified the extracellular spontaneous spiking activity in the ventral tegmental area (VTA) neurons.

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).

Galphimine-B modifies electrical activity of ventral tegmental area neurons in rats.

Galphimine-B (G-B) is a bioactive compound isolated from the plant Galphimia glauca Cav. (Malpighiaceae) with central nervous system depressant properties previously described. In the present study, extracellular spiking activity records in either somatosensorial cortex or ventral tegmental area (VTA) neurons, were performed in rats after i.

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.

Apamin blocks the direct relaxant effect of melatonin on rat ileal smooth muscle.

The present study investigated the mechanisms of melatonin-induced inhibition of the ileal smooth muscle contraction. Rat isolated ileal smooth muscle strips were stimulated in an organ bath using carbachol (CAR) or potassium chloride (KCl) depolarization. Under these conditions, melatonin produced a concentration-dependent inhibition of muscle contraction (mean inhibitory concentration, IC50: 17.

Melatonin modulates cholinergic transmission by blocking nicotinic channels in the guinea-pig submucous plexus.

Melatonin, a hormone produced and released by the pineal gland is also synthesized by cells of the gastrointestinal wall, where it might be a local regulator of gut functions. In this study, we investigated the possible role of melatonin as a modulator of the enteric nervous system. Intracellular recordings were made in neurons of the submucosal plexus from the guinea-pig ileum to measure the melatonin effects on their electrophysiological properties.

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.

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.

Alpha-interferon suppresses food intake and neuronal activity of the lateral hypothalamus.

Alpha-interferon (alpha-IFN) treatment in humans induces anorexic effects. However, the mechanisms and sites of action are unknown. Rats implanted with an intracerebroventricular (i.

[Uterine contraction induced by carbachol is inhibited by melatonin].

It has been suggested that the pineal gland has a specific role in the regulation of reproductive functions. Melatonin, secreted by pineal gland, is involved in the control of mammalian reproduction. Previous investigations have show that melatonin reduced the smooth muscle contraction.

Effects of acute and chronic toluene inhalation on behavior, monoamine metabolism and specific binding (3H-serotonin and 3H-norepinephrine) of rat brain.

The present study deals with the effect of chronic toluene inhalation (30,000-40,000 ppm in air, 15 min/day for 30 days) that induced abnormal behavior states resembling the serotonin syndrome in rats: resting tremor, hindlimb abduction, Straub tail, head weaving and rigidity. The head weaving latencies were significantly decreased when assessed at 15 and 30 days of exposure to toluene vapors. The sequence pattern signs of serotonin syndrome were changed after 15 and 30 days of exposure, indicating possible cumulative effects and/or tolerance development.

Melatonin modifies the spontaneous multiunit activity recorded in several brain nuclei of freely behaving rats.

Melatonin, a pineal hormone, released photoperiodically, was administered systemically in rats, previously implanted with semimicroelectrodes into six different brain structures. The multiunit electrical activity of these structures was recorded for 10 min before and 60 min after melatonin administration in unanesthetized, freely moving rats. Different melatonin doses (100, 200, 500, and 1000 micrograms/kg) produced changes in the electrical activity of all tested structures.

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.

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.