Neuroscience networks: data-sharing in an information age.
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Biomedical subjects
Publications and source records attributed to Thomas R Insel.
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Mother-reared (MR) and nursery-reared (NR) male rhesus monkeys exhibit profound and persistent differences in social and emotional behavior. Compared to MR animals, NR monkeys show reduced reciprocal social behaviors and increased agonistic behavior and high levels of stereotypy. Cerebrospinal fluid oxytocin (CSF OT) in NR monkeys was significantly reduced compared to MR monkeys measured at 18, 24, and 36 months of age. Correlations between OT and individual social behavioral profiles measured across rearing conditions also revealed a significant association between OT and the expression of affiliative social behaviors including allogrooming and reciprocal intermale mounting at each age examined. In contrast, CSF vasopressin levels did not differ according to rearing history, but did correlate with fearful behaviors independent of rearing history. Differential rearing was not associated with differences in basal or stress-related plasma cortisol, although these levels did progressively decline as monkeys matured. MR but not NR monkeys were able to use a social companion to buffer their response to a stressor, but OT levels did not appear to be sensitive to the presence of a social companion in either group. These results are consistent with earlier reports from studies of rodents suggesting an important role for central OT pathways in the development of social affiliation.
There is a considerable literature on the neurobiology of reward, based largely on studies of addiction or substance abuse. This review considers the possibility that the neural circuits that mediate reward evolved for ethologically relevant cues, such as social attachment. Specifically, mesocorticolimbic dopamine appears important for maternal behavior in rats and pair bonding in monogamous voles. It is not yet clear that dopamine in this pathway mediates the hedonic properties of social bond formation or whether dopamine's role is more relevant to developing associative networks or assigning salience to social stimuli. The neuropeptides oxytocin (OT) and vasopressin (AVP) appear to be critical for linking social signals to the mesocorticolimbic circuit.
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All social relationships are dependent on an organism's ability to remember conspecifics. Social memory may be a unique form of memory, critical for reproduction, territorial defense, and the establishment of dominance hierarchies in a natural context. In the laboratory, social memory can be assessed reliably by measuring the reduction in investigation of a familiar partner relative to novel conspecifics. The neurohypophyseal neuropeptides oxytocin and vasopressin have been shown to influence a number of forms of social behavior, including affiliation, aggression, and reproduction. This article reviews vasopressin and oxytocin effects on social cognition, particularly the acquisition and retention of social recognition in rats and mice. Studies in rats have demonstrated that vasopressin in specific neural pathways, such as the lateral septum, is necessary for social recognition. As vasopressin facilitates recall when given after an initial encounter, the peptide appears important for the consolidation not the acquisition of a social memory. Although oxytocin has complex effects on social memory in rats, mice with a null mutation of the oxytocin gene are completely socially amnestic without other cognitive deficits evident. As oxytocin given centrally before but not after the initial encounter restores social recognition in these mutant mice, the neuropeptide appears critical for the acquisition rather than the consolidation phase of memory. Oxytocin's effects on social memory are mediated via a discrete cell population in the medial amygdala. These findings support the hypothesis that vasopressin and oxytocin are essential for social memory, although they appear to influence different cognitive processes and may modulate different neural systems. (c) Elsevier Science.
Vaginocervical stimulation (VS) significantly elevated the concentration of oxytocin (OT) in spinal cord superfusates of 8 intact urethane-anesthetized rats measured 10-15 min after VS (median [interquartile range]: 1.7 [1.00-3.37] pg/ml) compared to that measured 10-15 min before VS (1.1 [1.01-1.40] pg/ml). When VS was administered once (n = 8), it produced a 55% increase over baseline values; when administered a second time 45 min later (n = 6), it produced only a 22% increase over pre-VS values. The effects of estrogen on the VS-induced release of OT were then investigated using ovariectomized rats that were treated either with estradiol benzoate (EB; 10 microg/100 g bw) (n = 6) or with an oil vehicle (n = 6) subcutaneously for 3 days. The EB treatment significantly elevated the basal levels of OT released into spinal cord superfusates above vehicle control levels. Within 5-10 min after the onset of VS, OT concentrations in the superfusates were significantly higher in EB-treated than in vehicle-treated rats. The vehicle-treated rats did not show a significant elevation in OT concentration following VS. To rule out the possibility that the posterior pituitary gland was the source of this OT, the effect of hypophysectomy (HYPOX) was assessed on the VS-induced release of OT into spinal cord superfusates and plasma. The concentration of OT in spinal cord superfusates of both the HYPOX (n = 5) and intact rats (n = 6) increased significantly from 5.8 [4.4-6.5] pg/ml pre-VS to 7.9 [6.7-10.3] pg/ml immediately after VS, and from 4.4 [3.8-5] pg/ml pre-VS to 5.1 [4.6-5.7] pg/ml immediately after VS, respectively. There was no significant difference in baseline levels of OT in cerebrospinal fluid between the two groups. By contrast, plasma OT levels, while significantly elevated in response to VS from 3.42 [2.9-5.34] pg/ml baseline to 7.25 [5.33-15.77] pg/ml in the intact group, failed to respond significantly to VS in the HYPOX group (n = 5). The present findings provide evidence of a direct estrogen-dependent release of OT within the spinal cord in response to VS, presumably via descending oxytocinergic neurons.