[Response of rat lateral hypothalamic neurons to food ingestion and repetitive stimulations at the self-stimulation sites].
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Cholinergic antagonists in ventral tegmentum elevate thresholds for lateral hypothalamic and brainstem self-stimulation.
Frequency thresholds for lateral hypothalamic self-stimulation are elevated following microinjections of atropine into ventral tegmentum (73). Many self-stimulation sites in brainstem are situated near cholinergic cell groups and axons, and ventral tegmentum receives cholinergic afferents terminals. To test the hypothesis that ventral tegmental muscarinic receptors are involved in lateral hypothalamic and brainstem self-stimulation, stimulating electrodes were placed in lateral hypothalamus and dorsal tegmentum near the midbrain-pons border, and cannulae were implanted in ventral tegmentum. Microgram injections of muscarinic antagonists, atropine or scopolamine, or a choline uptake blocker, hemicholinium-3, elevated frequency thresholds for both self-stimulation sites in a dose-dependent and time-dependent fashion. In addition, summation and collision between the two self-stimulation sites was tested using paired-pulse methods (53). Summation ranged from 31 to 87% (i.e., 24 to 47% reductions in frequency threshold were observed at long intrapair intervals), but no collision-like effects were observed at short intrapair intervals. The ventral tegmentum is a likely site for the convergence of dorsal tegmental and lateral hypothalamic self-stimulation pathways.
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Isoosmotic shrinkage by self-stimulated outward Na-K-Cl cotransport in quail erythrocytes.
In mammalian erythrocytes, outward fluxes by the Na-K-Cl cotransporter NKCC have been clearly characterized, but NKCC fluxes are small and their physiological role, if any, is poorly understood. Avian erythrocytes are nucleated cells, in which a physiologically relevant NKCC acts as a cell volume regulator. Therefore, we further investigated outward cotransport and its relation to cell volume by using quail erythrocytes. Unlike human or rat erythrocytes, quail erythrocytes exhibit outward cotransport fluxes: (1) of high magnitude [maximal rate of bumetanide-sensitive Li+ efflux=12.3+/-1.1 mmol (l cells x h)(-1), mean +/-SEM, n=23] and (2) strongly stimulated by hyperosmotic media (by 100-200% in 500 mosmol/l media). Na+- or Li+-loaded quail erythrocytes exhibited rapid cell shrinkage when incubated in K+-free media. Thus, cell volume remained stationary up to 5-10 min and then started to shrink. Shrinkage was first slow, but progressively accelerated, finally reaching a new stationary state where cell volume had decreased by about 20%. Such rapid cell shrinkage was fully inhibited by bumetanide and was associated with outward cotransport stimulation (self-stimulated or an auto-catalytic process, i.e. a reaction stimulated by its product). External K+ reduced all these phenomena, but significant cell shrinkage was still observed at an external K+ concentration of 2.8 mM. K+ removal failed to stimulate outward cotransport in hypotonic media (250 mosmol/l). Finally, reincubation of shrunken erythrocytes in physiological saline revealed that inward cotransport was stimulated more than outward cotransport. In conclusion, isoosmotic hypokalaemia drives a rapid shrinkage of quail erythrocytes, due to auto-catalytic net outward cotransport stimulation. Whether this is an experimental curiosity or indicates that outward cotransport can have some physiological role deserves further investigation.
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Both response effort and current intensity affect self-stimulation train duration thresholds.
Self-stimulation thresholds obtained from rate/intensity functions have often been used to measure brain stimulation reward (BSR) under the assumption that these indices are not contaminated by performance factors. However, very few studies have explicitly examined the effect of performance variables on thresholds. The present experiment examined the joint effects of response effort and current intensity on train duration thresholds. Three levels of stimulation current and lever weightings were factorially combined and train duration thresholds (defined as 50% of maximum response rates) were determined for each condition. It was discovered that changes in both current intensity and response effort produced shifts in thresholds, and that these shifts were of approximately equal magnitude. It was concluded that caution must be exercised when interpreting self-stimulation threshold data since, at least under some conditions, both reward (i.e., train duration) and performance (i.e., effort) manipulations produced similar shifts in self-stimulation response functions.
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Hyperthermia and inhibition of feeding produced by self-stimulation in the septum and preoptic area in dogs.
Dogs bearing electrodes implanted in the anterior part of the basal forebrain were tested for their response to food upon electric stimulation of rewarding sites, and for self-stimulation-produced hyperthermia. Self-stimulation and forced (experimenter-induced) stimulation of 12 out of 16 loci evoked a negative reaction to food the strength of which was determined according to occurrence and persistence of three effects: ignoring food (the dog performing self-stimulation in the presence of readily available meat), food rejection (the dog's failure to take meat offered together with passive stimulation of the rewarding site), and food ejection (throwing meat out of the mouth upon passive stimulation). The rise in body temperature during self-stimulation was positively correlated with the rate of responding. Hyperthermia was significantly higher during self-stimulation in sites where stimulation produced a strong negative reaction to food, as compared with those where stimulation failed to stop the animal from eating. The stimulus-contingent negative reaction to food may reflect a short-term satiety which is supposed to play an essential role in the mechanism of reinforcement. Hyperthermia, and particularly stabilization of hypothalamic temperature on an elevated but fairly constant level, argues for a shift of the set-point for temperature regulation. Occurrence of the two effects supports the claim that self-stimulation produces some complex activation of neural processes controlling energy homeostasis.
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Effects of electrical stimulation of the nucleus tractus solitarius on self-stimulation behavior.
The electrical stimulation of the nucleus tractus solitarius (NTS) produced profound suppression of self-stimulation (ICSS) in cats. This effect depended on the sequence and side of NTS stimulation, as well as on the stimulus parameters and locus of self-stimulation. The suppressive effect of NTS stimulation on ICSS was not abolished by ipsilateral vagotomy, thus the vagal bradycardia probably is not involved in the suppression of ICSS.
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Post-stimulation excitability of mediodorsal thalamic self-stimulation.
The post-stimulation excitability of the substrate for brain stimulation reward in the mediodorsal thalamus was assessed using equal- and unequal-pulse procedures. In 3 rats, refractory periods were found to begin no earlier than 1 ms and to end as late as 10 ms. Using test (T) pulses 1.5 times the amplitude of condition (C) pulses, the contribution of absolute and relative refractory periods was determined in one subject. No change in the slope of the recovery function was obtained in this condition, suggesting that several populations of neurons with different absolute refractory periods compose the behaviorally relevant substrate. A large supernormal contribution, evaluated by increasing the C amplitude to 1.5T, occurred between 3 and 10 ms with a peak at 7.5 ms. These results suggest that mediodorsal thalamic self-stimulation is mediated by a wide range of small, probably unmyelinated fibers.
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Effects of naloxone and chlordiazepoxide on lateral hypothalamic self-stimulation in rats.
Lateral hypothalamic self-stimulation behavior of rats in an operant chamber was investigated under the treatments of the first injection of naloxone (5 mg/kg) or saline followed by the second injection of chlordiazepoxide (4 mg/kg) or saline. Both inhibitory effect of naloxone and facilitatory effect of chlordiazepoxide on self-stimulation response were statistically significant, but the interaction between the two effects was not obtained. The results indicate that the facilitatory effect of chlordiazepoxide upon self-stimulation is independent of endogenous opioid system. Further, the obtained effect of naloxone was discussed in terms of interaction of the drug with aversive, rather than rewarding, component of self-stimulation.
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Simultaneous dopamine and single-unit recordings reveal accumbens GABAergic responses: implications for intracranial self-stimulation.
Intracranial self-stimulation (ICS) is a motivated behavior that results from contingent activation of the brain reward system. ICS with stimulating electrodes placed in the medial forebrain bundle (MFB) is particularly robust. However, the neurons that course through this pathway use a variety of neurotransmitters including dopamine and GABA. For this reason, the neurotransmitters that are central to this behavior, and the specific roles that they subserve, remain unclear. Here, we used extracellular electrophysiology and cyclic voltammetry at the same electrode in awake rats to simultaneously examine cell firing and dopamine release in the nucleus accumbens (NAc) during ICS and noncontingent stimulation of the MFB. ICS elicited dopamine release in the NAc and produced coincident time-locked changes (predominantly inhibitions) in the activity of a subset of NAc neurons. Similar responses were elicited with noncontingent stimulations. The changes in firing rate induced by noncontingent stimulations were reversed by the GABA(A) receptor antagonist bicuculline. Most time-locked unit activity was unaffected by D1 or D2-like dopamine-receptor antagonists, or by inhibition of evoked dopamine release, although, for a minority of units, the D1 dopamine-receptor antagonist SCH23390 attenuated neural activity. Thus, neurons in the NAc are preferentially inhibited by GABA(A) receptors after MFB stimulation, a mechanism that may also be important in ICS.
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Analysis of the relationships between self-stimulation sniffing and brain-stimulation sniffing.
Determination of current thresholds for self-stimulation and electrically elicited sniffing from electrodes placed into lateral hypothalamic and ventral tegmental areas of rats revealed a tight correlative relationship between the two phenomena (r values of approx 0.9 at both sites). Thresholds for sniffing were never higher than those for self-stimulation, while approximately half the animals had higher self-stimulation than sniffing thresholds, suggesting that electrically elicited sniffing may better index the underlying psychobiological process that mediates self-stimulation. That both phenomena reflect the same basic process was suggested by the fact that 48 h of food deprivation consistently reduced the thresholds for both self-stimulation and sniffing, while 24 h of food deprivation had only marginal effects on both. The implications for understanding the nature of self-stimulation processes is discussed.
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[Astressin blockade of amygdaloid corticoliberin receptors eliminates the stimulating effects of amphetamine, morphine and leu-enkephalin on brain self-stimulation].
Amphetamine (1 mg/kg), morphine (1 mg/kg), and ethaminal sodium (5 mg/kg) activated self-stimulation reaction of lateral hypothalamus in rats. In contrast, intraamygdalary injections of astressin (1 microg/microl), which is a nonselective antagonist of corticoliberin receptors, inhibited this reaction. The astressin blockade of extrahypothalamic corticoliberin receptors in the central nucleus of amygdala modified the effects of various narcogens on self-stimulation reaction. On this background, amphetamine did not activate self-stimulation, ethaminal sodium retained significant psychoactivating effect, whereas the effect of morphine switched from stimulant to depressant. Leu-enkephalin exhibited a stable depressant effect, thus potentiating the action of astressin. The astressin-induced enhancement of the inhibiting action of leu-enkephalin on cerebral self-stimulation is probably related to a temporary switch-off of the activating influence of the central nucleus of amygdala on hypothalamus.
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[Effects of various psychotropic drugs on self-stimulation behavior in the rat].
Effects of various psychotropic drugs on tegmental and hypothalamic self-stimulation behavior in rats with chronically implanted electrodes in the brain were studied. Effects of elecrtical stimulation in several brain structures on self-stimulation behavior and influences of drugs on the stimulation effect were also investigated. The hypothalamic self-stimulation behavior was more markedly inhibited by chlorpromazine than the tegmental self-stimulation, whereas the latter was more strongly inhibited by diazepam. The effects of pentobarbital on the self-stimulation behavior were similar to those of diazepam. Methamphetamine facilitated both the tegmental and hypothalamic self-stimulation behavior. Suppressive effect of hypothalamic stimulation on the tegmental self-stimulation behavior was inhibed by chlorpromazine, while those of amygdaloid and septal stimulation were augmented. All the effects of hypothalamic, amygdaloid and septal stimulating on the tegmental self-stimulation behavior were inhibed by diazepam and pentobarbital, while these were facilitated by methamphetamine. Suppressive effects of tegmental, amygdaloid and septal stimulation on the hypothalamic self-stimulation behavior were all facilitated by both chlorpromazine and methamphetamine. The effects of amygdaloid and septal stimulation on this behavior were inhibed by diazepam and pentobarbital, while those of tegmental stimulation were enhanced. The effects of imipramine, in all experiments, were variable in each rat and not significant.
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Cocaine facilitation of prefrontal cortex self-stimulation: a microstructural and pharmacological analysis.
A novel self-stimulation methodology involving a fixed-interval (FI-5 s) schedule of reinforcement, microanalysis and threshold evaluation was used to investigate the effects of cocaine on rats lever pressing for electrical stimulation of the prefrontal cortex. Cocaine (15 mg/kg) increased medial prefrontal cortex (MPC) self-stimulation rates under FI-5 by a mean of 269% and reduced current thresholds for self-stimulation. A similar facilitation was evident with self-stimulation of the sulcal prefrontal cortex. Microanalysis showed that cocaine decreased inter-response times and post-reinforcement pauses, increased responding in the second and third quartiles of the inter-reinforcement interval (IRI) and decreased responding in the fourth IRI quartile. Schedule control of responding was still evident following cocaine despite the profound facilitation of response rates. Increased response rates were seen up to 48 h following a single dose of cocaine, suggesting sensitization of the PFC reinforcement substrate. The acute effects of cocaine on MPC self-stimulation were completely reversed by the dopamine (DA) D1 antagonist SCH 23390 0.02 mg/kg) and the D2 antagonist raclopride (0.3 mg/kg) but not by naloxone (0.5 mg/kg). These results are consistent with previous studies demonstrating the PFC as part of the neural substrate mediating cocaine reward. Further, these results implicate DA receptors in the reinforcing properties of both cocaine and MPC self-stimulation.
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Energy balance and hypothalamic self-stimulation.
The effects of negative energy balance on self-stimulation are a matter of considerable disagreement. This disagreement undoubtedly reflects the inadequacies of the continuous reinforcement self-stimulation procedures used in this type of experimentation. The present experiment uses a new fixed-interval reinforcement shuttle-box procedure which provides indices of reward and stimulation escape that are free from the numerous performance altering effects that confound continuous reinforcement performance. Whereas 24 h of food deprivation had no effect on stimulation initiation or escape rates, 48 h of food deprivation selectively increased initiation rates. The enhancement of reward was seen over virtually the entire anterior-posterior extent of the lateral hypothalamus and occurred irrespective of the occurrence of any stimulus-bound behaviors. Thus negative energy balance appears to selectively increase the excitability of reward-related neurons in the lateral hypothalamus. The self-stimulating rats became clearly hyperphagic, yet their weight gains were not significantly different from those of controls. The self-stimulation must, therefore, have greatly increased energy expenditure. Thus, not only does energy balance affect self-stimulation, but self-stimulation appears to affect energy balance.
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Concurrent intracranial self-stimulation and amphetamine self-administration in rats.
In a two-lever testing chamber, rats had concurrent access to intravenous amphetamine and brain stimulation reinforcers. Responding for each reinforcer was generally increased above baseline rates taken when only one reinforcer was available. Amphetamine stereotypy was observed, but did not interfere with rapid lever-pressing for brain stimulation.
Amphetamine↗
Effects and interactions of naloxone and amphetamine on self-stimulation of the prefrontal cortex and dorsal tegmentum.
Naloxone (0.1 to 10 mg/kg) caused a dose-dependent depression of self-stimulation of the medial prefrontal cortex (PFC) lateral hypothalamus (LH) and a region in the dorsal tegmentum lateral to the central gray (DT). The DT contains many enkephalin fibers and is a site for stimulation-produced analgesia, while the PFC contains little enkephalin and does not support stimulation-produced analgesia. However, self-stimulation rates of the PFC, DT and LH were all equally depressed by naloxone. In order to study possible opiate-dopamine interactions, we examined the effects of naloxone on the facilitatory effects of D- and L-amphetamine (1.0 mg/kg) on self-stimulation of the DT and PFC. If amphetamine mildly facilitated self-stimulation (L-amphetamine on DT self-stimulation and D-amphetamine on PFC self-stimulation) then the addition of naloxone was without effect. If amphetamine greatly increased self-stimulation (D-amphetamine on DT self-stimulation), naloxone caused a depression of the amphetamine effect. It is argued that naloxone's effects in this and other reports reviewed is related to the level of self-stimulation performance, and not to the level of enkephalin at the self-stimulation site, nor to amphetamine's effects on dopamine activity.
Amphetamine↗
Electrical hypothalamic stimulation in rats induces hyperthermia if and only if they learn to self-stimulate.
Handling and exposure to a novel environment has been shown to produce an emotional fever in rats. Electrical stimulation of lateral hypothalamus sites produced a rise of intracranial temperature not different from this emotional fever. Once the rats learned to self-stimulate, the same electrical stimulation produced a rise of the intracranial temperature significantly higher than the emotional fever. During the autoshaping for self-stimulation a significant relationship was found between the rise of the intracranial temperature and time expressed as successive days of self-stimulation training, or between the rise of intracranial temperature and the increasing frequency of operant responses. This seems to indicate that when the rats learned to self-stimulate, an initially nonsense signal, without specific thermal effect, was transformed into a neural or neurochemical code producing a new or modified effect which was a significantly higher fever.
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[The effect of different gas mixtures under increased pressure on the self-stimulation reaction of rabbits].
Self-stimulation of rabbits in heliox at high pressure was decreased. That effect was potentiated by rapid compression. Addition of 2% or 6% nitrogen to heliox exerted no influence on the self-stimulation behavior.
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