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Biomedical subjects

J Panksepp

Publications and source records attributed to J Panksepp.

At least 91 records · Page 5Linked to original sources
PubMed1978

Effects of morphine and naloxone on separation distress and approach attachment: evidence for opiate mediation of social affect.

In order to determine the relationship between endorphins and social attachment, the effects of morphine (an opiate agonist) and naloxone (an opiate antagonist) on various indices of attachment in guinea pigs were studied. In infants, crying or separation-induced distress vocalizations were significantly decreased by single injections of low morphine doses (0.25, .050 and 0.75 mg/kg) in a dose-dependent manner. Naloxone (1mg/kg1 reliably increased separation distress vocalizations in both juvenile and adult guinea pigs. Therefore, similar to opiate withdrawal symptoms, separation distress appeared to be alleviated by morphine and potentiated by naloxone. As for approach attachment, offspring/maternal proximity-maintenance time was significantly decreased by morphine (1.0, 2.5 and 5.0 mg/kg), suggesting that opiates may be capable of replacing a function normally subserved by endorphins in reinforcing attachments. These data support the hypothesis that an endorphin-based addiction-like process may underlie the maintenance of social attachments, and that separation distress may reflect a state of endogenous "endorphin withdrawal".

Aged↗
PubMed1978

The biology of social attachments: opiates alleviate separation distress.

The possibility that brain opiate systems participate in the control of social affect was assessed by determining capacity of low doses of exogenous opiates (0.125-0.50 mg/kg oxymorphone, and 0.10-0.50 mg/kg morphine sulfate) to reduce distress vocalizations of socially isolated puppies. Low doses of opiates were capable of profoundly reducing crying as well as the motor agitation they exhibit during brief periods of social isolation. Since reductions in crying could be obtained with morphine in the absence of any gross behavioral disturbances, the possibility is entertained that brain opiates may function to control the intensity of emotions arising from social separation. Possible parallels between the biological nature of narcotic addiction and the formation of social bonds are discussed.

Animals↗
PubMed1977

(-)-Hydroxycitrate and conditioned aversions.

The capacity of various salts of (-)-hydroxycitrate to produce conditioned rejection of a 0.25% saccharin solution was evaluated. The ethylenediamine salt of (-)-hydroxycitrate produced strong conditioned rejection of saccharin under both deprivation and nondeprivation conditions, but this effect was less than produced by equimolar doses of lithium chloride. The sodium salt of hydroxycitrate produced no conditioned rejection of saccharin in water deprived rats but did so in nondeprived animals. In these experiments, food intake was reduced by (-)-hydroxycitrate only during the first hour following administration of the drug. The magnitude of appetite rejection did not correspond to the degree of conditioned rejection, lending support to the conclusion that the food intake reduction was not merely a consequence of aversive effects of the drug.

Animals↗
PubMed1975

Medial and lateral hypothalamic oxygen consumption as a function of age, starvation and glucose administration in rats.

In fed rats, in vitro oxygen consumption of the ventromedial hypothalamus (VMH) was found to be reliably higher than that of the lateral hypothalamus (LHA), and this differential effect was abolished by prior food deprivation. Neither body weight (236-569 g) nor age (50-180 days old) was important in determining the magnitude of differential respiration of these hypothalamic subareas. VMH respiration was found to be especially responsive to intragastric administration of glucose-oxygen consumption increasing 94% above baseline levels in VMH, with only a 28% increment occurring in the LHA. Using various delays between loading of glucose and testing, the VMH-LHA ratio in oxygen consumption was found to be inversely related to food intake. Implications of these findings to the nature of hypothalamic control of feeding are discussed.

Age Factors↗
PubMed1975

Mathematical analysis of energy regulatory pattens of normal and diabetic rats.

Analysis of feeding patterns indicated that diabetic (alloxan) hyperphagia is characterized by doubling of meal sizes with no change in feeding frequency. Correlation of meal sizes and intermeal intervals did not provide any systematic relationships for either normal or diabetic rats. When equations of the general form Y = A + Bcos (X) were fit to successive satiety ratios (postmeal interval/meal size), the diabetic rats showed significantly lower A coefficients, reflecting a lower average level of satiety, as well as significantly lower B coefficients, reflecting less systematic variability in the satiating value of food around the average level. It is concluded that the major regulatory deficit in diabetic animals is a chronic reduction in the long-term signal of body nutrient repletion.

Animals↗
PubMed1975

Central metabolic and humoral factors involved in the neural regulation of feeding.

Evidence is summarized for the theory that long-term regulation of energy balance is elaborated by an interface between matabolism and brain activity within the medial hypothalamus, while short-term satiety effects are a more direct consequence of dampened activity in lateral hypothalamic feeding circuits. Possible relationships of these functions to autonomic control circuits are discussed.

Adipose Tissue↗