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PubMed2003

[Effect of modulator of the signal transmission from opioid receptor to sodium channels on hypothalamus self-stimulation].

We investigated effects of different doses of a new preparation comenic acid as a modulator of the transmission of signals from an opioid receptor to slow sodium channels on the hypothalamic rewarding system in male Wistar rats. Comenic acid has been shown to inhibit the reaction of the hypothalamic self-stimulation (SS) in a dose-dependent fashion with the strongest effect at doses of 28.8-30 mg/kg. We observed a decrease in the rate of lever-pressings, induced by the threshold for SS current intensity, and an increase in the threshold for the response of SS, or its cessation. The similar suppressing effect of the preparation was found at its repeated injections. Thus, those results showed that comenic acid failed in both activation of the rewarding system of the lateral hypothalamus and adaptation to it.

Animals↗
PubMedDate not supplied

Long term potentiation of lateral hypothalamic self-stimulation following parabrachial lesions in the rat.

Two neural systems in the pontine tegmentum have been implicated in reward processes. One is the visceral afferent-column arising from the nucleus of the solitary tract and the pontine tegmental taste area (PTA), the other being the dorsal noradrenergic system that has its origin in the locus coeruleus (LC). Lesions of the LC had no effect on lateral hypothalamic (LH) intracranial self-stimulation (ICSS) whereas lesions of the PTA produce a dramatic and seemingly permanent increase in LH ICSS response rates. These results are discussed in the context of noradrenergic/dopaminergic interactions in the control of goal-directed behaviors.

Afferent Pathways↗
PubMed1976

[Role of the adrenergic system in lateral hypothalamic self stimulation behavior: effects induced by intraventricular injection of epinephrine, norepinephrine, isoproterenol and dopamine].

A bipolar electrode was stereotaxically implanted in or near the medial forebrain bundle at the level of the posterior lateral hypothalamus of male albino Wistar-Imamichi rats. The relationship between the adrenergic system and the lateral hypothalamic self-stimulation (SS) behavior was investigated by intraventricular injection (by the use of the modelled hypodermic needle) of catecholamines. l-Epinephrine(Ep), l-norepinephrine (NE) facilitated the SS behavior dose-dependently. On the other hand, l-isoproterenol and dopamine revealed no detectable effects. Phentolamine inhibited the SS behavior, but propranolol had no marked effects. Facilitation by NE for the SS behavior was not induced when the current was cut off at the time of the injection of NE. These results suggest the following: a) the adrenergic or the noradrenergic system in the brain may play a more important role in the positive reinforcement of the lateral hypothalamic SS behavior than does the dopaminergic system. b) The action of Ep or NE may be facilitated through alpha-receptors rather than through beta-receptors. c) Facilitation by NE for the lateral hypothalamic SS behavior may not be due to the non-specific facilitation of lever pressing, but rather may be related to intracranial stimulation.

Animals↗
PubMed1977

Effect of clonidine on the noradrenergic cyclic AMP generating system in the limbic forebrain and on medial forebrain bundle self-stimulation behavior.

The present results show that clonidine does not mimic the agonist action of norepinephrine (NE) on the noradrenergic cyclic AMP generating system of the limbic forebrain, but antagonizes the stimulatory effect of NE while not influencing the action of isoprenaline. In self-stimulation behavior, clonidine decreases responding and blocks the facilitation caused by d-amphetamine.

Adenosine Monophosphate↗
PubMed1983

Morphine withdrawal produces differential effects on the rate of lever-pressing for brain self-stimulation in the hypothalamus and midbrain in rats.

Rats were implanted with stimulating electrodes either in the medial forebrain bundle-lateral hypothalamus (MFB-LH) or the midbrain-central gray area (MID-CG), and were trained to lever-press for electrical brain self-stimulation (ICSS). The animals were made tolerant to morphine (15 mg/kg) by twice daily injections for a four-day period. Withdrawal was then induced either by substituting saline (spontaneous withdrawal) or by administering naloxone (1.0 mg/kg) (precipitated withdrawal). Changes in body weight, in the incidence of diarrhea, and in rates of lever-pressing for ICSS were recorded during the five-day withdrawal period. In both the MFB-LH implanted and the MID-CG implanted groups, the duration and magnitude of changes in lever-pressing were greater when withdrawal was precipitated than when it was spontaneous. Independently of the type of withdrawal, however, the behavioral disruption was greater for animals implanted in the MFB-LH than for animals implanted in the MID-CG. The changes in body weight were similar for both electrode sites and both types of withdrawal. Diarrhea only occurred in the precipitated withdrawal group and its incidence was similar for animals implanted in the two sites. Three additional groups of animals were implanted in the MFB-LH, made tolerant to morphine, and given naloxone as above. They were administered clonidine (10, 30 or 100 micrograms/kg) 30 min prior to naloxone to attenuate the effects of withdrawal. The 30 micrograms/kg dose of clonidine produced maximal attenuation of the disruption in lever-pressing. None of the doses of clonidine attenuated weight loss, but all three doses reduced the incidence of diarrhea. The ICSS procedure demonstrated that the behavior during withdrawal can be related to the brain area that is stimulated.

Animals↗
PubMed1981

Effects of chlorpheniramine, pyrilamine and astemizole on intracranial self-stimulation in rats.

Rats implanted in the lateral hypothalamus were used to assess lever pressing for brain stimulation. Lever pressing was increased dose-dependently by chlorpheniramine and decreased dose-dependently by pyrilamine. Astemizole, a new orally long-acting antihistamine did not affect self-stimulation. Evidence from pharmacological tests based on altered neurotransmitter functions suggests that the central anticholinergic activity of chlorpheniramine is probably responsible for the increased response rate, whereas the central dopamine receptor blocking activity of pyrilamine may be responsible for the decreased response rate. Astemizole is a specific antihistamine devoid of any central activity.

Animals↗
PubMed1985

Lateral hypothalamic self-stimulation persists in rats after destruction of lateral hypothalamic neurons by kainic acid or ibotenic acid.

Bilateral injections of 1 microgram/microliter of kainic or ibotenic acid into the lateral hypothalamus (LH) of rats destroyed most of the cells in the LH. This treatment did not prevent electrical self-stimulation from electrodes placed in the LH, indicating that intrinsic neurons of the LH alone are not crucial elements of the neural system that mediates reinforcing hypothalamic stimulation.

Animals↗
PubMed2002

Effects of isolation-rearing on intracranial self-stimulation reward of the lateral hypothalamus: baseline assessment and drug challenges.

There is evidence that isolation rearing produces down-regulation of the dopamine D2 receptor. Therefore, isolation rearing should also modify the effects of D2 antagonists on intracranial self-stimulation (ICSS) reward. This study investigated the effect of isolation rearing on ICSS reward, and modulation of that reward by SCH23390, Raclopride and MK-801. Sprague-Dawley rats were reared alone (isolates) or in pairs from day 21 postnatal to day 75 postnatal. At this time, all rats were implanted with monopolar stimulating electrodes in the lateral hypothalamus. The ICSS rate-frequency curve-shift method was used to assess reward and operant motor function at baseline and after administration of SCH-23390 (D1 antagonist: 0.02, 0.06, 0.2 mg/kg), Raclopride (D2 antagonist: 0.01, 0.025, 0.06 mg/kg), and MK-801 (non-competitive NMDA receptor antagonist: 0.1, 0.2 mk/kg). Isolation-reared rats displayed similar measures of both basal reward and motor function when compared to socially reared controls. Isolation-reared rats were subsensitive to the reward decreasing effects of Raclopride. Socially reared rats were observed to have more variant baseline reward measures, and could be divided into distinctly different groups with different basal reward function. Isolation-rearing down-regulates D2 function but does not affect basal reward function, but some unknown factor in the social rearing environment did have a substantial effect on basal reward function.

Animals↗
PubMedDate not supplied

A comparison of the effects of mesencephalic injections of neurotensin(1-13) and neuromedin N on brain electrical self-stimulation.

Neuromedin N (NM-N), a hexapeptide that shares a four amino acid C-terminal homology with the tridecapeptide, neurotensin (NT), has been suggested as a potential neurotransmitter or neuromodulator that could interact with the NT-sensitive receptors. In this experiment, we compared the effects of an equimolar concentration of NM-N and NT(1-13) injected in the ventral tegmental area (VTA) on brain electrical self-stimulation (SS), a behavior previously shown to be potentiated by VTA injections of NT(1-13). Rats implanted with a stimulating electrode in the mesencephalic central gray and a guide cannula in the VTA were trained to lever press to obtain rewarding electrical stimulations. Functions relating the rate of lever pressing to the stimulation frequency were determined, on separate daily tests, before and after the injection of 3 nmol of NM-N, NT(1-13), or an equal volume of saline vehicle. At this concentration, both NM-N and NT(1-13) produced a significant facilitation of SS when compared to saline vehicle, an effect that was not seen when the peptides were injected outside the VTA. The facilitation of SS by NM-N, however, was much weaker and of a shorter duration than the one produced by NT(1-13). The shorter time course and the weaker behavioral effect of NM-N compared to NT(1-13) are consistent with its lower potency at the NT receptor and its faster rate of enzymatic degradation in the VTA, and suggest that NM-N potentiated the reward-relevant neural signal by acting on mesencephalic NT receptors.

Animals↗
PubMed1996

Bicuculline microinjections into the ventral tegmental area of the rat: alteration of self-stimulation thresholds and of cytochrome oxidase activity in the brain.

Abuse of drugs that potentiate GABAergic neurotransmission, namely benzodiazepines, is difficult to understand because this potentiation should elicit, among other effects, a decrease in activity within the mesolimbic system. Abuse of benzodiazepines is difficult to understand since the opposite, namely an increase in mesolimbic activity, has been implicated in drug abuse as well as in the rewarding effect of direct mesolimbic stimulation. In order to evaluate how the activity of the mesolimbic system depends on mesolimbic GABAergic influence, a GABAA receptor antagonist, bicuculline methiodide, was unilaterally injected into the ventral tegmental area and its effect on self-stimulation thresholds derived from stimulations applied to the same area was evaluated. Microinjection of 15, 20 and 30 ng increased the stimulation threshold. This decrease in stimulation efficiency lasted no more than 15 min after which baseline levels were obtained. Such a decrease is paradoxical considering that the manipulation should have released the ventral tegmentum from a tonic inhibitory influence. The metabolic consequences of repeated injections of 30 ng bicuculline were furthermore evaluated by cytochrome oxidase histochemistry. The staining was found to be weak around the injection site and dense in the ipsilateral nucleus accumbens. Release of a tonic GABAergic inhibition added to some cytotoxic damage probably resulted in an increased metabolic activity of this system. The presently reported paradoxical response of the ventral tegmentum and mesolimbic system to a GABAergic challenge may account for the paradoxical relationship between some behavioral properties of the mesolimbic system and GABAergic drugs.

Animals↗
PubMed1997

Intracranial self-stimulation in female and male rats: no sex differences using a rate-independent procedure.

Given gender differences in human drug use and dependence, this study examined sex differences in reinforcement processes that may underlie such behavior. A psychophysical determination of reinforcement threshold was made using an intracranial self-stimulation (ICSS) paradigm, electrically activating the medial forebrain bundle (MFB) as it passes through the lateral hypothalamus (LH). Using this response rate-independent procedure, basal reinforcement thresholds were not significantly different in male vs. female rats (119.4 +/- 3.3 microA vs. 110.8 +/- 4.0 microA, respectively; N = 8/sex). Further, baseline reinforcement threshold did not fluctuate systematically across stages of the estrous cycle in female rats. The psychostimulants D-amphetamine (0.056-0.56 mg/kg s.c.) and cocaine (1.8-18.0 mg/kg i.p.) dose-dependently lowered reinforcement threshold, with no significant sex difference. The opioid morphine (0.56-5.6 mg/kg s.c.) did not significantly lower reinforcement threshold in either sex. These results contrast those of some previous studies that have used response rate-dependent measures of reinforcement threshold; procedures which are less rate-dependent may be more appropriate when examining subject variables such as sex and stage of estrous.

Animals↗
PubMed1977

Relationships of hippocampal theta cycles with bar pressing during self-stimulation.

Previous reports have demonstrated a relationship between hippocampal rhythmical slow activity (theta) and movement, and have suggested that rhythmical movements tend to occur during certain phase of theta. Therefore, the relationships between theta cycles and voluntary motor activity were investigated. Bar pressing for electrical brain stimulation provided the reference to relate hippocampal activity. Ongoing theta increased in amplitude and frequency before and after pressing. Periodic waves preceding and following pressing. These waves only appear if the presses occur at particular phases of the theta cycles. They gradually disappeared during sessions lasting 4 to 8 hr. Light weights ( less than 90 g) added to the lever did not alter theta, but heavier weights (greater than 90 g) produced averages without periodic waves and with movement-related potentials. Introduction of a delay between pressing and electrical stimulation delayed evoked potentials, while averaging indicated that periodical waves persisted before and after bar pressing. Total lesions of the septum or superior fornix abolished theta and increased the frequency of self stimulation. In animals with partial lesions, theta reappeared during pressing. The above results indicating that the rats tended to lever press during particular phases of theta, suggest that phase-locked theta may be a corollary of motor mechanisms, and perhaps of the timing of motor responses.

Animals↗
PubMed1982

Dissociation of hunger and self-stimulation by trigeminal deafferentation in the rat.

Section of trigeminal orosensory or oromotor nerves reduces food intake and disrupts performance of a food-reinforced lever pressing response but increases the rate of an identical level pressing response reinforced by electrical stimulation of the lateral hypothalamus. Our findings suggest that trigeminal orosensation plays a critical role in the neural control of hunger in the rat. The results also fail to support a response-oriented theory of intracranial self-stimulation where the latter is thought to involve selective facilitation of sensorimotor circuits underlying species-typical consummatory behavior.

Afferent Pathways↗
PubMed1989

Interactions between RO 15-4513 and ethanol on brain self-stimulation and locomotor activity in rats.

Experiments were conducted to elucidate the behavioral effects of RO 15-4513, a putative alcohol antagonist, when administered alone or in combination with alcohol. Two groups of animals were trained to lever-press for brain self-stimulation (ICSS) on either a fixed ratio:15 or a fixed interval:15 second schedule of reinforcement. RO 15-4513 (0.1-3.0 mg/kg) reduced the rate of lever-pressing for ICSS in both groups. RO 15-4513 (1.0 mg/kg) further reduced rates when combined with alcohol (0.1-1.7 g/kg), and this effect was especially marked in the fixed ratio paradigm. Other groups of animals were tested in a locomotor activity apparatus. In contrast to the depression of lever-pressing in the ICSS experiments, RO 15-4513 produced a graded increase in locomotor activity. When combined with alcohol (0.1-1.7 g/kg), 1.0 mg/kg RO 15-4513 also increased locomotor activity. Thus, the depression in schedule-controlled behavior was not associated with a generalized behavioral depression. These results demonstrated that RO 15-4513 has potent behavioral effects of its own that are consistent with its classification as an anxiogenic compound.

Animals↗
PubMed1996

Mediation by neurotensin-receptors of effects of neurotensin on self-stimulation of the medial prefrontal cortex.

1 Intracortical microinjections of neurotensin (NT) selectively decreased intracranial self-stimulation (ICSS) of the medial prefrontal cortex in the rat. 2 To elucidate whether this effect is mediated by NT receptors or by the formation of NT-dopamine complexes, we investigated the effects on ICSS of intracortical microinjections of neurotensin (1-11), an NT fragment that forms extracellular complexes with dopamine but does not bind to NT receptors. 3 We also studied the effects of the peripheral administration of SR 48692, a selective antagonist of NT receptors, on the inhibition of ICSS produced by the intracortical administration of NT. 4 Unilateral microinjections of neurotensin (1-11) at doses of 10, 20 and 40 nmol into the medial prefrontal cortex did not change the basal ICSS rate of this area. 5 The intraperitoneal administration of SR 48692 at doses of 0.08 and 0.16 mg kg-1 30 min before microinjection of 10 nmol of NT into the medial prefrontal cortex, antagonized the inhibition of ICSS produced by the neuropeptide. 6 These results demonstrate that the inhibitory effect of NT on ICSS is mediated by NT receptors.

Animals↗
PubMed1982

Self-stimulation response decrement patterns differentiate clonidine, baclofen and dopamine antagonists from drugs causing performance deficit.

Fouriezos and co-workers have reported that rats treated with the neuroleptics, pimozide or d-butaclamol, barpress at baseline rates at the start of an intracranial self-stimulation (ICSS) session, but cease responding within a few minutes. They suggested that this response decrement pattern (RDP) resembles natural extinction, indicating attenuation of reward by neuroleptic treatment. In the present experiments, the RDPs produced by several different drug classes were systematically compared. Two dopamine receptor antagonists, haloperidol and metoclopramide, produced an extinctionlike RDP. In contrast, the alpha-1 adrenoceptor blocker, prazosin, and the muscle relaxant, methocarbamol, caused uniformly low response rates that did not decrease further as the session progressed. Clonidine, an alpha-2 adrenoceptor agonist, and baclofen, a novel GABAB receptor agonist, were associated with RDPs that resembled those of the dopamine antagonists tested. Analysis of drug-induced RDPs is characterized as a valuable tool for exploring the nature of drug effects on ICSS responding.

Animals↗
PubMed1990

Decreased intracranial self-stimulation in a new animal model of endogenous depression.

Neonatal treatment of rats with clomipramine may produce adult animals which model endogenous depression. We report here that a major factor of depression in humans, the diminished capacity for pleasure, appears present in these rats. At age 7 months, bar-press responding for rewarding hypothalamic stimulation is reduced across a range of intensities. At age 4 or 5 months this effect is not seen, although other behavioral abnormalities are present at the younger age. The delayed onset of diminished intracranial self-stimulation may relate to the gradual insidious onset of endogenous depression in humans.

Animals↗
PubMed1977

Reward versus performance in self-stimulation: electrode-specific effects of alpha-methyl-p-tyrosine on reward in the rat.

The hypothesis that alpha-methyl-p-tyrosine (AMPT), an inhibitor of catecholamine synthesis, reduces brain stimulation reward was tested, using a measure of reward previously shown to be relatively unaffected by variables that alter performance but not reward. The rewarding effectiveness of stimulation was determined by the location of the sharp rise in the function relating running speed in an alley to the number of pulses received as a reward. For some electrodes, AMPT depressed self-stimulation performance (speed of running) without producing any sizable effect on the measure of reward (location of rise). For other electrodes, the rewarding effectiveness of the stimulation was greatly reduced by AMPT and restored by L-dopa. These opposing results could be repeatedly demonstrated on different electrodes in the same rat. The electrode-specific differential sensitivity to AMPT suggests neurochemically disparate substrates for reward.

Animals↗