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Biomedical subjects

J Panksepp

Publications and source records attributed to J Panksepp.

At least 73 records · Page 4Linked to original sources
PubMed1982

An improved pharmacological procedure for depletion of noradrenaline: pharmacology and assessment of noradrenaline-associated behaviors.

A pharmacological procedure which initially depletes noradrenaline (NA), dopamine (DA) and 5-hydroxytryptamine (5-HT) but permits repletion of DA and 5-HT was used to evaluate the role of NA in feeding behavior and intracranial self-stimulation behavior. The rapid-onset 'reserpine-like' vesicular depletion drug RO 4-1284 reduced NA and 5-HT 99% and DA 90% in rat forebrain within 1 h after administration with complete repletion of all amines occurring within 6 to 12 h. Treatment with the dopamine-beta-hydroxylase inhibitor FLA-63 significantly reduced NA (maximum depletion 42%) but not DA or 5-HT over the 12 h period of evaluation. The two drugs together produced a specific depletion of NA. Forebrain levels of NA in subjects pretreated with FLA-63 then given RO 4-1284 0.5 h later were reduced to 2% of control values for 8 h while vesicular stores of DA and 5-HT were repleted 77% and 93%, respectively, within 8 h after administration. Selective depletion of NA, in this manner, reduced deprivation induced food intake and lateral hypothalamic self-stimulation.

2H-Benzo(a)quinolizin-2-ol, 2-Ethyl-1,3,4,6,7,11b-↗
PubMed1982

Psychomotor stimulants, social deprivation and play in juvenile rats.

Treatment with d-amphetamine (0.125-1 mg/Kg) or methylphenidate (0.5-4 mg/kg caused dose-dependent decreases in play fighting in juvenile rats which were independent of sex and strain. Although brief social isolation profoundly increased play fighting, qualitatively similar drug effects on play were observed in socially housed and isolated animals. By contrast, at the highest doses tested both amphetamine and methylphenidate increased social investigation, but only if the rats were socially isolated. Stimulation of catecholamine systems is evidently incompatible with the expression of playful behavior.

Aggression↗
PubMed1982

The role of norepinephrine in feeding behavior.

When dopamine-beta-hydroxylase is inhibited with FLA-63 (10 mg/kg) free feeding behavior is disrupted in satiated rats. While the average number of meals taken was not different from vehicle injected controls, meal size was decreased 58% in the first 9 hr after treatment with FLA-63. In starved animals, FLA-63, when given alone, produced little effect on feeding behavior, even though norepinephrine depletion was in excess of 40%. When given in combination with RO4-1284 (5 mg/kg), a vesicular reuptake inhibitor, feeding was reduced to 16% of control intake and norepinephrine was specifically depleted 99%. Feeding was reliably reinstated in animals which received FLA-63 plus RO4-1284 with either dl-threo-DOPs, a metabolic precursor to NE, or direct intrahypothalamic injections of NE. These findings suggest that the feeding inhibition observed after treatment with FLA-63 plus RO4-1284 is due to disruption of transmission in brain NE systems. A non-anorectic dosage of L110-140 (3.73 mg/kg), a specific FLA-63. Taken collectively, these findings suggest that the primary role of NE in feeding is maintenance of the consummatory response and that these effects are expressed in relation to activity in other neurochemical systems.

2H-Benzo(a)quinolizin-2-ol, 2-Ethyl-1,3,4,6,7,11b-↗
PubMed1981

Cholinergic modulation of separation distress in the domestic chick.

The effects of nicotine, carbachol, hexamethonium and scopolamine were investigated on distress vocalizations (DBs) of acutely isolated domestic chicks. Nicotine attenuated, while the antimuscarinic scopolamine increased the frequency of separation-induced DVs. Furthermore, the stress attenuating effects of nicotine were blocked by pretreatment with scopolamine. These results implicate muscarinic receptor participation in the control of separation-induced distress, and support the suggestion that nicotine-induced DV suppression may result from activation of behaviorally relevant muscarinic receptors via central release of acetylcholine.

Animals↗
PubMed1981

Ascending endorphin inhibition of distress vocalization.

Distress vocalizations were produced in adult guinea pigs by electrical stimulation of the dorsomedial thalamus or the septum-preoptic area. Both of these forebrain-derived vocalizations were increased by systemic administration of naloxone and were inhibited by analgesic periventricular gray stimulation. Naloxone blocked the inhibitory effects of the analgesic stimulation on thalamic vocalizations. Stimulation of nonanalgesic mesencephalic sites in close proximity to the periventricular gray increased the anterior-elicited vocalizations. These data provide evidence for ascending endorphin-mediated inhibition of excitatory forebrain sites for distress vocalizations.

Animals↗
PubMed1981

The ontogeny of play in rats.

Play behavior, as indicated by frequency and duration of pinning behavior, was studied in young rats between 18 and 64 days of age. The incidence of play was markedly increased by social isolation. Play increased from 18-28 days of age, peaked between 32 and 40 days of age, and gradually declined thereafter. Animals developed stable "dominance hierarchies" during the course of testing so that one animal pinned the other on the average 70% of the time. Also "dominant" animals exhibited the longer pin durations. The data indicate that social play can be efficiently studied in the laboratory rat and, further, that one function of play may be to establish stable social relationships.

Aging↗
PubMed1981

Opioid modulation of ingestive behavior.

Supportive evidence for an important role of endogenous opioid systems in modulation of ingestive behaviors is presented. Low doses of morphine (1.0-5.0 mg/kg) increase and low doses of naloxone (0.5-2.5 mg/kg) decrease food and water intake during both acute and chronic testing in mildly-deprived rats. Chronic infusions of naloxone with implanted osmotic mini-pumps elicited sustained dose-related suppression of food, water, and saccharin solution intakes but did not reduce ingestion of 10.0% glucose solution or food following 12 hr deprivation. Finally, naloxone treatment did not antagonize nocturnal ingestion of food any more than it reduced day time feeding when the latter was enhanced by prior food deprivation. These results indicate that an opiate agonist and an opiate antagonist modify ingestive behaviors oppositely, affirming that endogenous opioid systems may be involved in control of feeding and drinking. However, their role may be restricted to only indirect participation in homeostatic regulation via neural systems modulating emotional tone or goal-directed behaviors in general.

Animals↗
PubMed1981

D-glucose infusions into the basal ventromedial hypothalamus and feeding.

Following symmetrical bilateral infusion of D-glucose into the basal ventromedial hypothalamus (BVMH), using Alzet minipumps (1 microliter/h of 10% D-glucose for 6 days), average daily food intake was reduced by 27% for the period of treatment. Symmetrical bilateral infusions into the posterior medial hypothalamus had a transitory effect on feeding, as did asymmetrical and unilateral infusions. Infusion of L-glucose into the BVMH did not yield a chronic reduction in food intake. Included in the infused solutions were tracer amounts of [14C]glucose, [14C]proline or [14C]leucine to permit radioautographic estimations of infusate dispersal in the brain and axonal transport patterns from the infusion sites. Infusions were generally well-restricted to 1-1.5 mm of the cannulae tips, and descending transport of amino acids was highest in substantia nigra and midline structures of the mesencephalon and pons including central gray, ventral tegmental area, raphe and ventral tegmental nuclei. These results provide evidence for an energy intake regulatory mechanism situated in the BVMH whose outputs may modulate activity in the substantia nigra and midline brain stem areas.

Animals↗
PubMed1981

An autoradiographic map of (3H)diprenorphine binding in rat brain: effects of social interaction.

(3H)Diprenorphine binding was analyzed autoradiographically in the brains of 33 day old rat pups. A photographic atlas of diprenorphine binding in the coronal plane is provided to highlight the dispersion of opioid receptor systems through the brain. To determine whether brain opioid release may be induced by social interactions, half the animals were sacrificed following a 30 min period of social interaction while the other half were sacrificed following 30 min of social isolation. Opioid binding was higher in isolate-tested animals than socially-tested ones, suggesting that social interaction may promote endogenous brain opioid release.

Animals↗
PubMed1980

Brief social isolation, pain responsiveness, and morphine analgesia in young rats.

Vocalizations induced by brief tail-shock were measured in young rats that were either socially or individually housed. A single day of isolation increased tail-shock-induced vocalizations, and in animals isolated 3--4 days, morphine (4 mg/kg) was less effective in reducing vocalizations than in socially housed animals. The data suggest that social contact can sustain endogenous analgesic processes in the body.

Analgesia↗
PubMed1980

Opioid blockade and social comfort in chicks.

When young animals are separated from their normal social environment in groups they distress vocalize (DV) less than when isolated alone. Opioid blockade with naloxone (1 mg/kg peripherally, and 1 microgram centrally) increased crying more in group tested chicks than individually tested ones. The serotonin receptor blocking agent methysergide and the cholinergic blocking agent atropine sulfate produced similar effects. The testing of birds in mirrored environments also produced a reduction of DV's, and all three receptor blocking agents augmented DV's more in mirrored environments than in mirrorless ones. However, in studies evaluating changes in this comfort response by facilitation of opiate, serotonin (5 HT), and acetylcholine (ACh) activity (with morphine, quipazine and pilocarpine, respectively), only morphine was found to magnify the comforting effect of mirrors. The effects of naloxone on contact comfort, and the acquisition and expression of imprinting were further evaluated, and opioid blockade reduced all these measures of social comfort. It is concluded that endogenous opioid activity (and to a lesser extent, 5 HT and ACh) contribute to the comfort which animals derive from their social environment.

Animals↗
PubMed1980

Endogenous opioids and social behavior.

Evidence for the hypothesis that brain-opioids mediate social affect and social attachments is summarized. Opiates and opioids are very effective in reducing social separation-induced distress vocalizations (DVs), in puppies, young guinea pigs and chicks, while opiate antagonists can increase DVs. In studies of specific social behaviors in rodents, morphine (at doses 1 mg/kg and below) decreases proximity maintenance time in socially housed animals, increased play, decreases maternal aggression but has no effect on pup retrieval. Naloxone reduces play and disrupts pup-retrieval, but has no consistent effect on proximity maintenance time of socially housed animals. In young rats tested in social learning situations, morphine delays and naloxone hasten extinction. These data are consistent with the proposition that brain opioids modulate social emotions and behaviors.

Aggression↗
PubMed1980

Opiates and homing.

Beginning at 15 days of age. Long-Evans rat pups were trained to run toward their home cage in a T-maze task. Morphine (.5-1.0 mg/kg sc) slowed initial acquisition running times but did not change the number of trials required to learn the position habit. Morphine markedly impeded extinction of the homing behavior. Opiate-treated animals ran as accurately and as quickly toward home on the 12th day of extinction as on the first (10 trials given per day). Conversely, naloxone (1 mg/kg sc) reduced resistance to extinction. The morphine effect was not state-dependent since the drug also impeded extinction in animals that had acquired the task under saline. The morphine effect was blocked by naloxane, which indicates that the increased resistance to extinction was due to an opiate receptor effect. These results indicate that morphine has a strong capacity to sustain a social habit in the absence of reinforcement.

Animals↗
PubMed1979

Morphine reduces social cohesion in rats.

The effect of low (1 mg/kg) doses of morphine on maintenance of physical proximity were evaluated in paired rats observed in a 4 square foot test arena. Morphine reliably reduced proximity maintenance time, and this was apparently not due to sedation, since the effect was unmodified by doses of amphetamine which substantially increased motor activity. The effects of naloxone were inconsistent on this measure of social motivation. In general, the results are consistent with the theoretical proposition that a brain neurochemical change which might lead to social attraction is the activation of endogenous opioid systems. When opiate activity is exogenously sustained, animals exhibit a subnormal tendency to be gregarious.

Amphetamine↗