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Neuronal responses in monkey lateral hypothalamus during operant feeding behavior.

Single neuron activity was recorded from monkey lateral hypothalamus to investigate neuronal events correlated with operant bar press feeding behavior. The behavioral paradigm was divided into three phase: visual (discrimination), bar press (procurement), and ingestion (consummatory). Of 669 neurons tested, 158 (24%) responded in one or more phases. During the visual phase, 106 neurons (16%) responded. Of 80 neurons that responded in the visual phase and were tested systematically, 33 (41%, 33/80) responded selectively to the sight of food or nonfood objects associated with a juice reward, but not to the sight of nonfood or objects associated with aversive saline. Neuronal activity related to discrimination was modulated by satiation and learning (i.e., acquisition and extinction). During the bar press phase, 51 neurons (7.6%) responded. These responded tonically during the early or late stage of the bar press period, but did not depend on individual bar pressing motions. During ingestion, 90 neurons (13%) responded. The ingestion response was modulated by palatability of food and satiation. Data suggest that the LHA is deeply involved in operant feeding behavior; discrimination of food, drive to get food, and perception of reward, all of which are affected by learning and internal states such as hunger and satiety.

Animals↗

Chemical and visual control of feeding and escape behaviors in the channel catfish Ictalurus punctatus.

Channel catfish, maintained individually in aquaria with dark substrate, responded to visual stimuli from above with escape behavior and to amino acid stimuli with feeding behavior. Feeding behavior was composed of a) appetitive patterns, such as barbel movements, orienting posture, and search swimming and b) consummatory patterns that included a halt in swimming, turning, snapping-biting, ingestion, mastication, and swallowing. The conditioning procedure, which consisted of 90 s presentations of a single amino acid followed by a food reward, influenced the duration and speed of the search swim. Swimming behavior was quantified by counting the number of turns greater than 90 degrees. Catfish turned 40-75 times to the conditioned stimuli, L-proline and L-arginine, but only 20-40 times to the nonconditioned stimuli. Olfaction rather than taste was involved in the conditioned response to L-proline because the highest possible contact concentration (3 x 10(-6) M) of L-proline within the stimulus eddies was at least 30 times lower than the estimated L-proline electrophysiological taste threshold (> 10(-4) M).

Animals↗

Electrical activation of visual pathways substitutes for tonic light input in triggering EEG correlates of food reward during conditioned behavior in cats.

Cats trained to press a lever for 1 cc of milk reward normally show during the consummatory response high voltage 6--8 c/sec EEG synchronization associated with epicortical positive steady potential shift over the primary and secondary visual projections. The emergence of this postreinforcement synchronization (PRS) and Reward Contingent Positive Variation (RCPV) is known to depend upon appropriate gustatory input and presence of ambient light, although visual perception of reward and/or environment is not essential as shown in cats wearing translucent "milky" contact lenses. Training the animals in a paradigm in which a "light-off" cue signaled the availability of reward, and thus assigned positively reinforcing quality to the dark condition, also failed to restore the PRS-RCPV phenomenon in the absence of light. However, brief electrical stimuli applied to either the optic tract or the lateral geniculate nucleus substituted for unpatterned light input and fully restored the PRS-RCPV in the dark. The suprathreshold stimuli were effective only during the consummatory response. Maximum effect could be produced during a brief time period between 0.8 and 1.5 sec after the onset of consummatory response as judged by lapping activity, thus showing the specificity of the effect of visual input. Even during a relaxed wakefulness after satiation or during slow wave sleep or REM sleep the same electric stimuli were ineffective although they produced well-developed evoked potentials with all characteristic wave components. The results indicate that brain pathways utilize unpatterned i.e. noisy visual input in complex integrative processes involving gustatory input.

Animals↗

The nitric oxide synthase inhibitor L-NAME suppresses androgen-induced male-like pseudocopulatory behavior in whiptail lizards.

The synthesis of nitric oxide by the enzyme nitric oxide synthase (NOS) is involved in the androgen-dependent gating of male-typical copulatory behavior, both centrally, particularly in the preoptic area, and peripherally, notably through its role in penile erection. In the all-female whiptail lizard species Cnemidophorus uniparens, individuals display copulatory behaviors indistinguishable from males of similar species if gonadectomized and treated with testosterone. In this experiment, androgenized individuals were treated with a NOS inhibitor, which eliminated male-like behavior in half the individuals, suggesting that the central role of nitric oxide synthesis is conserved in this species. The deficit was principally in mounting, suggesting that sexual motivational systems were affected, rather than consummatory mechanisms.

Analysis of Variance↗

The effects of microinjection of d-amphetamine into the n. accumbens during the late maintenance phase of an ethanol consumption bout.

The microinjection of d-amphetamine into the n. accumbens of rats, prior to the start of an operant ethanol self-administration session, increases operant behavior and the amounts of ethanol presented as the reinforcer. Although this effect could result by blocking termination processes regulating a consummatory bout, it could also be a result of enhancing the stimulus control regulating the maintenance of a drinking bout. To explore this issue, rats were trained to self-administer 10% ethanol in an operant situation. Following establishment of stable behavior, they were surgically instrumented so that the n. accumbens could be microinjected with d-amphetamine during a drinking bout, without having to handle the animal. The microinjection of d-amphetamine in the rats self-administering ethanol at the late phase of the drinking bout resulted in a prolonged bout and increased self-administration. During extinction testing, a reinstatement of responding was found following the amphetamine microinjection. The data suggest the most likely action of the amphetamine microinjection was to alter stimulus control factors, which normally regulate the maintenance of drinking, thereby prolonging the bout and increasing intake.

Alcohol Drinking↗

The kappa-opioid U-50,488H suppresses the initiation of nocturnal spontaneous drinking in normally hydrated rats.

The effect of a systemic (IP) treatment with 1.0, 3.0 and 9.0 mg/kg U-50,488H (U50), a highly selective kappa-agonist, on spontaneous, nocturnal ingestive behavior of the rat was studied using a microcomputer controlled data acquisition system. The latency to initiate drinking was increased and drinking behavior was suppressed in the first hour after injection in a dose-dependent manner. The consummatory indices of drinking were not affected. After this period of adipsia, a phase of polydipsia, that was probably due to the diuretic effect of U50, was evident. This prophagic effect of U50 was evident only at the dose of 3 mg/kg and was accompanied by an increased duration of feeding episodes but not by a reduced latency to feed. These results suggest that kappa-receptors play a pivotal role in modulating spontaneous drinking in the normally hydrated rat and that this control is mainly exerted on the motivational aspect of drinking.

3,4-Dichloro-N-methyl-N-(2-(1-pyrrolidinyl)-cycloh↗

Autoshaping the pigeon's gape response: acquisition and topography as a function of reinforcer type and magnitude.

The pigeon's key-pecking response is experimentally dissociable into transport (head movement) and gape (jaw movement) components. During conditioning of the key-pecking response, both components come under the control of the conditioned stimulus. To study the acquisition of gape conditioned responses and to clarify the contribution of unconditioned stimulus (reinforcer) variables to the form of the response, gape and key-contact responses were recorded during an autoshaping procedure and reinforcer properties were systematically varied. One group of 8 pigeons was food deprived and subgroups of 2 birds each were exposed to four different pellet sizes as reinforcers, each reinforcer signaled by a keylight conditioned stimulus. A second group was water deprived and received water reinforcers paired with the conditioned stimulus. Water- or food-deprived control groups received appropriate water or food reinforcers that were randomly delivered with respect to the keylight stimulus. Acquisition of the conditioned gape response frequently preceded key-contact responses, and gape conditioned responses were generally elicited at higher rates than were key contacts. The form of the conditioned gape was similar to, but not identical with, the form of the unconditioned gape. The gape component is a critical topographical feature of the conditioned key peck, a sensitive measure of conditioning during autoshaping, and an important source of the observed similarities in the form of conditioned and consummatory responses.

Animals↗

Dopamine and preparatory behavior: III. Effects of metoclopramide and thioridazine.

The effects of metoclopramide and thioridazine on feeding behaviors of male hooded rats were investigated in 2 experiments. Metoclopramide (2.5-7.5 mg/kg) attenuated conditioned preparatory responses to a conditional stimulus signaling delivery of a meal. However, consummatory responses were affected only by the highest dose. Similar effects had previously been observed following administration of pimozide (Blackburn, Phillips, & Fibiger, 1987). Thioridazine (10-30 mg/kg) had no significant effect on any measure of feeding behavior. The different effects of the 2 drugs may be related to their preferential actions at dopamine terminals in anatomically distinct regions of the forebrain.

Animals↗

Suppressing effect of the cannabinoid CB1 receptor antagonist, SR 141716, on alcohol's motivational properties in alcohol-preferring rats.

Administration of the cannabinoid CB(1) receptor antagonist, SR 141716 [N-piperidino-5-(4-chlorophenyl)-1-(2,4-dichlorophenyl)-4-methyl-3-pyrazole-carboxamide], has been reported to reduce alcohol intake and alcohol self-administration in different models of excessive alcohol consumption, including the selectively bred Sardinian alcohol-preferring (sP) rats. The present study investigated whether SR 141716 was also capable of decreasing, in this rat line, alcohol's motivational properties. Extinction responding for alcohol, defined as the maximal number of lever responses reached in the absence of alcohol in rats trained to lever-press for alcohol, was used as index of alcohol's motivational properties. Rats were initially trained to lever-press for oral alcohol (15%, v/v) under a fixed ratio (FR) schedule of FR4. Once self-administration behavior was established, extinction sessions were conducted. SR 141716 (0, 0.3, 1 and 3 mg/kg; i.p.) was acutely administered before extinction sessions. In order to assess the specificity of SR 141716 action on extinction responding for alcohol, a separate group of sP rats was trained to lever-press for a 3% (w/v) sucrose solution under an FR4 schedule. SR 141716 administration produced a dose-dependent, virtually complete suppression of extinction responding for alcohol. In contrast, extinction responding for sucrose was not significantly altered by treatment with SR 141716. Further to the consummatory aspects, these results also extend the suppressing effect of SR 141716 to the appetitive aspects of alcohol drinking behavior in sP rats. The results also implicate the cannabinoid CB1 receptor in the neural substrate mediating alcohol's motivational properties in this rat line.

Alcohol Drinking↗

Chronic fluoxetine inhibits sexual behavior in the male rat: reversal with oxytocin.

RATIONALE: Selective serotonin reuptake inhibitors, used widely in the treatment of depression, progressively inhibit sexual orgasm in many patients and induce a transient inhibition of sexual desire. OBJECTIVES: We attempted to model the effects of these drugs in sexually experienced male rats during tests of copulation in bilevel chambers. These chambers allow the study of both appetitive and consummatory sexual responses of male rats. METHODS: Males were treated daily with fluoxetine hydrochloride (0, 1, 5, or 10 mg/kg) and tested for sexual behavior with receptive females at 4-day intervals. Rats were treated with oxytocin (200 ng/kg) or saline after ejaculations had decreased. RESULTS: Fluoxetine decreased ejaculatory responses of male rats in a dose- and time-dependent fashion, but left the copulatory efficiency of the males intact. In contrast, conditioned level changing, a measure of appetitive sexual excitement, was inhibited following acute and chronic treatment with 10 mg/kg, although tolerance may have developed to the effect of 5 mg/kg. Subsequent administration of oxytocin restored the ejaculatory response but not the measure of sexual excitement to baseline levels. CONCLUSIONS: The reversal by oxytocin of the fluoxetine-induced deficit in ejaculations is consistent with the hypothesis that serotonin suppresses ejaculatory mechanisms by interrupting the action of oxytocin, which normally accompanies sexual behavior. Co-administration of oxytocin may help to alleviate the predominant sexual side effect of serotonin reuptake blockers.

Animals↗

Scopolamine reverses haloperidol-attenuated lever-pressing for water but not haloperidol-attenuated water intake in the rat.

The operant lever-pressing response has previously (Ljungberg, Pharmacol Biochem Behav 27: 341-350, 1987) been found to be inhibited by lower doses of haloperidol than the corresponding consummatory act, i.e., water intake. In the present study it was found that the attenuation of the lever-pressing response caused by the neuroleptic, but not the attenuation of the water intake, could be counteracted by scopolamine. The results support the notion that blockade of operant responding by low doses of neuroleptics are probably related to the extra-pyramidal side-effects of neuroleptics seen in the clinic, as both phenomena can be counteracted by anticholinergics. These results therefore conflict with the anhedonia hypothesis put forward as an explanation of the attenuating effects of neuroleptics in operant settings. The findings also have a clear bearing on the role of dopamine in feeding and drinking behavior, as the results implies that different aspects of the control of water intake (i.e., the operant vs. the consummatory phase) are governed by different mechanisms in the CNS.

Animals↗

Limits of habituation and extinction: implications for relapse prevention programs in addictions.

Problems in the application of exposure techniques to the management of long term dishabituation in addicts are discussed in the light of human and animal evidence. Extinction and habituation of responses to drug cues or drug aftereffects are unstable and strongly dependent on context, thus limiting the effectiveness of cue exposure treatments in the prevention of relapse. Several strategies are suggested to improve the stability of extinction and habituation in order to enduringly prevent relapse in addictions. (i) Warning patients about the episodic resurgence of unexpected urges or cravings precipitated by conditioned contexts and exposing them to such contexts. (ii) To obtain a maximum protection against relapse, extinction should 'recreate' all the original learning contexts (i.e. all possible drug cues). (iii) The behavioral chains involved in self administering drugs ought to be incorporated into cue exposure treatments (without permitting consummatory responses) in order to decrease their signal value as cues for drugs.

Animals↗

Obsessive-compulsive disorder as a disturbance of security motivation: constraints on comorbidity.

Patients with OCD often meet criteria for additional psychiatric disorders, with the incidence of comorbidity being as high as 75% in some studies. Here we examine the theoretical plausibility that in OCD much of the domain of co-morbid presentations encompasses related perturbations of the security motivation system. According to a recent proposal, the security motivation system represents a biologically primitive special motivation that is activated by potential (as opposed to imminent) danger to self or intimate others and engages a set of specialized species-typical behaviors (such as checking and washing) to handle potential danger. Because the task of security motivation is open ended, in the sense that no consummatory stimuli can exist in the real world to indicate the absence of potential danger, the shutdown of security motivation is produced by a self-generated feeling of knowing, a satiety signal termed yedasentience. In this schema, OCD results from a failure to generate or respond to the yedasentience signal: without this negative feedback the patient persists abnormally long in a strong motivational state having to do with primal, basic threats to existence, a condition that leads to prolonged engagement in security-related behaviors, such as the checking and washing, characteristic of OCD compulsions and obsessions. Considering the proposed neuronatomy of security motivation system and OCD, we discuss the likelihood that the phenomenon of "spread of allied reflexes" can produce other security-related psychiatric conditions, as well as the possibility that disturbances along different pathways of the security motivation system can lead to apparently different disorders.

Anxiety↗

Effects of punishing elements of a simple instrumental-consummatory response chain.

Rats were trained to press a lever, with every response reinforced with water. After responding was established, nine rats were administered a brief shock after each lever press, and nine others were shocked after drinking. The two procedures resulted in similar suppression of responding, and examination of the latency data when responding was partially suppressed indicated that under both conditions response suppression was due primarily to an increase in the latency of the instrumental response, rather than to pausing between the instrumental and consummatory responses. Thus, punishment following either the instrumental or consummatory component of the simple response sequence reduced the number of sequences initiated, rather than selectively suppressing the punished behavior.

Animals↗

Antagonism by abecarnil of enhanced acetylcholine release in the rat brain during anticipation but not consumption of food.

Changes in the extracellular concentration of acetylcholine (ACh) were evaluated in the prefrontal cortex and hippocampus of freely moving rats habituated for 35 days to consume their daily meal during a fixed 2-h period. During the 40 min immediately before presentation, ACh output increased by 49 and 55% in the prefrontal cortex and hippocampus, respectively. ACh release increased further during the first 40 min of consumption phase in the prefrontal cortex (+220%) and hippocampus (175%). Administration of abecarnil (0.1 mg/kg, IP) 40 min before food presentation prevented the increase in ACh output in both brain regions during the anticipatory phase. In contrast, although abecarnil reduced the ACh content achieved during the consummatory phase, it did not prevent the increase in ACh release in the prefrontal cortex or hippocampus induced by food intake. Finally, the binding of [35S]TPBS to cerebral cortex, hippocampus, or septum of rats killed 20 min before food presentation was significantly higher than the values for animals killed 2 h after food presentation. These results suggest that during ingestive behavior ACh release is regulated by at least two independent mechanisms: one, associated with the anticipatory phase, that is sensitive to the activation of GABA(A) receptors. and a second, associated with the consummatory phase, that is insensitive to abecarnil.

Acetylcholine↗