Lateral Hypothalamus GABAergic Neurons Modulate Consummatory Behaviors Regardless of the Caloric Content or Biological Relevance of the Consumed Stimuli.

It was recently reported that activation of a subset of lateral hypothalamus (LH) GABAergic neurons induced both appetitive (food-seeking) and consummatory (eating) behaviors in vGat-ires-cre mice, while inhibition or deletion of GABAergic neurons blunted these behaviors. As food and caloric-dense liquid solutions were used, the data reported suggest that these LH GABAergic neurons may modulate behaviors that function to maintain homeostatic caloric balance. Here we report that chemogenetic activation of this GABAergic population in vGat-ires-cre mice increased consummatory behavior directed at any available stimulus, including those entailing calories (food, sucrose, and ethanol), those that do not (saccharin and water), and those lacking biological relevance (wood). Chemogenetic inhibition of these neurons attenuated consummatory behaviors. These data indicate that LH GABAergic neurons modulate consummatory behaviors regardless of the caloric content or biological relevance of the consumed stimuli.

Neurobiology of consummatory behavior: mechanisms underlying overeating and drug use.

Consummatory behavior is driven by both caloric and emotional need, and a wide variety of animal models have been useful in research on the systems that drive consumption of food and drugs. Models have included selective breeding for a specific trait, manipulation of gene expression, forced or voluntary exposure to a substance, and identification of biomarkers that predict which animals are prone to overconsuming specific substances. This research has elucidated numerous brain areas and neurochemicals that drive consummatory behavior. Although energy homeostasis is primarily mediated by the hypothalamus, reinforcement is more strongly mediated by nuclei outside the hypothalamus, in mesocorticolimbic regions. Orexigenic neurochemicals that control food intake can provide a general signal for promoting caloric intake or a more specific signal for stimulating consumption of a particular macronutrient, fat, carbohydrate, or protein. The neurochemicals involved in controlling fat ingestion--galanin, enkephalin, orexin, melanin-concentrating hormone, and the endocannabinoids--show positive feedback with this macronutrient, as these peptides both increase fat intake and are further stimulated by its intake. This positive association offers some explanation for why foods high in fat are so often overconsumed. Consumption of ethanol, a drug of abuse that also contains calories, is similarly driven by the neurochemical systems involved in fat intake, according to evidence that closely relates fat and ethanol consumption. Further understanding of the systems involved in consummatory behavior will enable the development of effective therapies for the treatment of both overeating and drug abuse.

Neural substrates for sexual and thermoregulatory behavior in the male leopard gecko, Eublepharis macularius.

The preoptic area-anterior hypothalamus (POAH) continuum is critical for the integration of environmental, physiological, and behavioral cues associated with reproduction in vertebrates. In the present study, radiofrequency lesions in the POAH abolished sexual behavior in the leopard gecko (Eublepharis macularius). Furthermore, results suggest a differential effect of POAH lesions on those behaviors regarded as appetitive (tail vibration and grip) and those regarded as consummatory (mounting and copulation), with consummatory behaviors being affected to a greater extent. E. macularius is an ectothermic vertebrate that modulates body temperature behaviorally relative to ambient temperature. In vertebrates, the POAH is also an important integrator of thermoregulation. Thus, the present study investigated whether lesions that disrupt reproductive behavior also disrupt body temperature regulation. While virtually all males displayed diurnal rhythms in thermoregulatory behavior prior to surgery, this pattern was abolished in a small proportion of animals bearing POAH lesions. Lesions that abolished thermoregulatory rhythms involved the suprachiasmatic nucleus (SCN), whereas lesions confined to the POAH, while dramatically influencing sexual behavior, did not affect thermoregulatory rhythms or temperature set point. Together, these findings identify the POAH as an important neural locus regulating sexual behavior but not thermoregulation and suggest that the SCN acts as a pacemaker controlling daily behavioral temperature regulation in this species.

Hindbrain catecholamine neurons mediate consummatory responses to glucoprivation.

Previous work using the retrogradely transported immunotoxin, saporin (SAP) conjugated to a monoclonal antibody against dopamine-beta-hydroxylase (DBH; DSAP), to selectively lesion norepinephrine (NE) and epinephrine (E) neurons projecting to the medial hypothalamus, demonstrated the essential role of these neurons for appetitive ingestive responses to glucoprivation. Here, we again utilized this lesion to assess the importance of these same neurons for the consummatory phase of glucoprivic feeding. To test consummatory responses, milk was infused intraorally through a chronic cheek fistula until rejected. Appetitive responses were tested in the same rats using pelleted food. Feeding responses to insulin-induced hypoglycemia, 2-deoxy-D-glucose (2DG)-induced blockade of glucose utilization, mercaptoacetate (MA)-induced blockade of fatty acid oxidation, 0.9% saline, and 18-h food deprivation were assessed. Unlike unconjugated SAP controls, the DSAP rats did not increase their food intake in response to glucoprivic challenges in either the pelleted food or the intraoral feeding tests. However, the DSAP rats did not differ from SAPs in their ingestive responses to food deprivation and blockade of fatty acid oxidation. The selective impairment of glucoprivic feeding responses indicates that DSAP did not impair the underlying circuitry required for either appetitive or consummatory ingestive responding but eliminated the mechanism for control of this circuitry specifically by glucoprivation. Results suggest that both appetitive and consummatory responses to glucoprivation are controlled and coordinated by multilevel terminations of the same catecholamine neurons.

Excitotoxic lesions of the gustatory thalamus spare simultaneous contrast effects but eliminate anticipatory negative contrast: evidence against a memory deficit.

Using consummately contrast procedures and the same taste stimuli (0.15% saccharin and 1.0 M sucrose), the authors tested the hypothesis that lesions of the gustatory thalamus disrupt gustatory memory in 2 experiments. In Experiment 1, irrespective of the duration of the intersolution interval (0 s, 30 s, 1 min, 2 min, 4 min, 8 min), thalamic lesions had no influence on the expression of simultaneous contrast effects. In Experiment 2, thalamic lesions abolished anticipatory negative contrast at the 0-s intersolution interval. These results provide no support for the experimental hypothesis. Rather, the data seem best interpreted as a lesion-induced disruption of the comparison mechanism responsible for anticipatory negative contrast. By this analysis, different comparison mechanisms underlie simultaneous and anticipatory contrast effects.

Gustatory thalamus lesions in the rat: III. Simultaneous contrast and autoshaping.

The performance of rats with electrophysiologically guided electrolytic lesions of the gustatory thalamus (GT) was compared to that of control subjects in two experiments. In Experiment 1, the lesioned rats showed normal simultaneous contrast effects (both positive and negative) during brief, alternating access to 0.15% saccharin and 1.0 M sucrose. There was, however, a substantial lesion-induced impairment in the level of conditioned stimulus-directed maintenance responding on the autoshaping procedure of Experiment 2. These findings are discussed with respect to the anticipatory contrast deficit recently reported in GT-lesioned rats.

Stress-related behavior and central norepinephrine concentrations in the REM sleep-deprived rat.

Rapid eye movement sleep deprivation (REMd) is a potent stressor in the rat. Behavioral abnormalities are among the earliest overt symptoms of REMd, the mechanisms for which remain largely unknown. The phenomena of hyperphagia and weight loss that are associated with REMd may contribute to its later morbidity; however, little is known about the onset of these phenomena or the neurotransmitter mechanisms that are involved. The aim of this study was to determine whether the earliest effects of REMd on consumatory behavior in the rat and its performance in the swimming cylinder of Porsolt are related to changes in norepinephrine (NE) concentrations in the cerebral cortex and selected areas of the hypothalamus. Sprague-Dawley rats were divided into three groups (n = 6): the REMd group resided in a water tank on 6.5-cm diameter pedestals for 96 h; the tank control (TC) group resided in the water tank on 15-cm pedestals for 96 h; the cage controls (CC) remained in their home cages for the duration of the study. In the first series of experiments, body weights and caloric intake were recorded daily, along with the performance of all animals in the swimming cylinder of Porsolt. In the second series of experiments, body weights and caloric intake were recorded, but the Porsolt test was not employed and the brains were dissected after 96 h for NE analysis by HPLC. It was observed that the REMd group had lower immobility times (p < 0.05) in the Porsolt test after only 24 h, compared to groups TC and CC.(ABSTRACT TRUNCATED AT 250 WORDS)

Ca2+/calmodulin system: participation on rat sexual hypothalamic differentiation.

Modifications of male rat hypothalamic sexual differentiation after neonatal administration of drugs that participate on the Ca2+/calmodulin system (haloperidol, trifluoperazine, penfluridol, pimozide, and verapamil) were studied. Pups treated 72 h after birth were behaviorally tested on day 120 of extrauterine life. Five tests for homotypical behavior were conducted. Afterwards animals were castrated and tested twice for heterotypical (female) behavior under replacement hormonal therapy. Fifty percent (80% in the case of pimozide) of all treated males showed lordotic behavior compared with none of the controls. Haloperidol (39%, lordosis quotient) and pimozide (40%, lordosis quotient) were more active than the others. Results obtained with verapamil were not statistically different from the controls. Pimozide was the most active agent influencing the appetitive masculine behavior (mount latency, intromission latency, and postejaculatory interval). Verapamil was more efficient than the rest of the drugs on the consummatory behavior (mount latency, intromission frequency, interintromission interval, and ejaculatory latency). Our results support the participation of the Ca2+/calmodulin system in hypothalamic sexual differentiation and in the differential modulation of the masculine and feminine behavioral patterns.

[Evoked potentials of the brain limbic structures during a change in the motivational state of dogs and during the realization of unconditioned reflex reactions]. / Vyzvannye potentsialy limbicheskikh struktur mozga pri izmenenii motivatsionnogo sostoianiia sobak i osushchestvlenii bezuslovnoreflektornykh reaktsii.

In experiments on 6 dogs it has been shown that in the EPs led from the hippocampus in response to electrostimulation of limbic structures and from the latters at the hippocampus stimulation, initial negativity, after positivity and late negative wave are the most stable components. At transition from one functional state to another two latter waves are subjected to the greatest changes. Amplitude-temporal characteristics of intralimbic EPs depend on the level and type of motivation, degree of emotional stress and properties of conditioned reaction.

Amine accumulation in behavioural pathology.

When nigro-striatal and meso-cortical neurons degenerate there is a loss of dopamine in the terminal fields and an accumulation of amines in the axons of these systems as they traverse the hypothalamus through the medial forebrain bundle. Traditional lines of thought have attributed the occurrence of motor and consummatory deficits which occur after dopamine neuron degeneration to the loss of functional dopamine neurotransmitter in the terminal fields. However, we have hypothesized that hypothalamic amine accumulation represents an area of brain tissue where processes such as neurotransmitter release, ephaptic transmission or local axon swelling may be affecting adjacent neurons and may thereby participate in the production of behavioural deficits. There is a considerable amount of evidence from studies on both peripheral and central catecholamine-containing neurons indicating that when their axons degenerate a release of functional neurotransmitter can occur. Information from neuropharmacological studies indicates that several drugs which facilitate behavioural recovery from dopamine-depleting lesions may do so by affecting amine release or receptor sensitivity near areas of accumulation rather than depleted terminal fields. We conclude that amine accumulation is a component of dopamine neuron degeneration which should be considered when assessing the role of the central catecholamine systems in the control of various behavioural and physiological processes.

Conative regulation of cortical activity by the reticular formation, hypothalamus, and thalamus.

Evolution of neural regions suggests the requirement for a common format for information units exchanged among regions. Short-term memory experiments suggest a format of six or seven items. A similar number of configurations of primary cerebral interactions is proposed, associated with arousal, sleep, approach, withdrawal, perseveration, alert scanning, and commanded by the reticular formation. A comparable number of basic states (feeding, mating, grooming, shelter-seeking, fighting, etc.) is proposed as operating within these configurations, under regulation by the hypothalamus. Conative variables from this region are transformed into patterns of regulation for local cortical populations by the thalamus. Elaboration of these configurations and states by higher structures leads to new forms of cortical activity only loosely coupled to brain stem systems.

[Avoidance mechanisms during self stimulation]. / Issledovanie mekhanizmov izbeganiia pri samostimuliatsii

Increased negative discordance of the dominating mode of the pressing duration histogram (PDH), which correlates with the growth of fixed bursts of stimulation is accompanied by a progressive decrease in the reinforcing properties of self-stimulation (SS), avoidance of the pedal and at the same time by a change of behavioral grooming reactions in the intervals between SS for search and consummatory reactions. Hunger considerably shortens the preferable duration of pressing or leads to the appearance of an additional mode on the PDH. With the change of the dominating PDH mode from positive discordance to a negative one, brain stimulation acquires aversive properties which are apparently due to the activation of the mechanisms of specific motivations.

Tail pinch-induced eating, gnawing and licking behavior in rats: dependence on the nigrostriatal dopamine system.

Mild-tail-pinch induces a syndrome of eating, gnawing and licking behavior in rats in the presence of food. Detailed behavioral, pharmacological and biochemical analyses of this phenomenon resulted in the following conclusions. (1) This is an unusually reliable phenomenon, demonstrable in each of more than 200 animals tested. (2) Eating is by far the predominant response to tail-pinch. (3) Tail-pinch behavior is critically dependent on the nigrostriatal dopamine system. (4) There are striking pharmacological parallels between tail-pinch behavior and schizophrenia.