PubMed Health⌕ Search

PubMed · 6427810

The death instinct.

Abstract

The death instinct has always been a controversial concept, insufficient to account for actual dying, and usually taken to be fused with aggression. After dislodging it from the shadow of aggression in order to evaluate its function, the instinct turns out to be one of the components that form the death motivation. Human beings develop a complex motivation for death, one that is more than biology (instincts) or physics (entropy). It includes (a) the death instinct, the primary analogue; (b) sequellae of the universal experience of object-loss, with identification and fantasies of a restorative reunion; (c) guilt over hostile attitudes toward the lost object, with depression, longings for atonement , and self-punishment; (d) compliance with reality, like that of old age or grave sickness. Examined in light of the complementary series of Freud's aetiological equation, the death instinct turns into a precondition of the composition motivation. Death motivation is a comprehensive concept, since patients express various of its aspects during their psychoanalyses , and it facilitates a metapsychological understanding and refines the accuracy of interpretation.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

U Lowental. 1983. The death instinct.. https://pubmed.ncbi.nlm.nih.gov/6427810/

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

Reduced aggression in mice lacking GABA transporter subtype 1.

Dysregulation of the brain GABAergic system has been implicated in the pathophysiology of violence and aggression. As a key regulator of central GABAergic activity, dysfunction of the GABA transporter subtype 1 (GAT1) represents a potential mechanism mediating pathologic aggression. We provide evidence that GAT1-/- mice and GAT1+/- mice exhibit lower aggressive behavior both in home cage resident-intruder test and neutral arena resident-intruder test, compared to wild-type mice (GAT1+/+). The pharmacologic effects of the GAT1 inhibitor, tiagabine and the GABA(A) receptor antagonist, bicuculline have been assessed in GAT1+/+ mice: tiagabine inhibits attacks but bicuculline induces attacks. Compared to GAT1+/- and +/+ mice, the GAT1-/- mice displayed a normal circadian pattern of home cage activity, but more activity overall. Meanwhile, reduced testosterone concentration was found in GAT1-/- mice compared to GAT1+/+ mice but not in GAT1+/+ mice treated with tiagabine, suggesting that testosterone is not directly involved in GAT1 mediated aggressive behavior regulation. These results showed that GAT1 is an important target involved in the regulation of aggressive behavior in mice, and long-term dysfunction of GAT1 may also result in the alteration of testosterone secretion.

Aggression↗

Significant increase in the aggressive behavior of transgenic mice overexpressing peripheral progastrin peptides: associated changes in CCK2 and serotonin receptors in the CNS.

The gastrin precursor peptide, progastrin (PG), is secreted from enteroendocrine cells in the intestine and increased in patients with hypergastrinemia and colorectal cancers. In recent years, we and others have demonstrated an important role of PG peptides in colorectal carcinogenesis, and were surprised to note significant changes in the behaviors of transgenic mice overexpressing PGs. In the present studies, we examined emotional behaviors of transgenic mice overexpressing PG in the intestinal and peripheral circulation. Aggression, locomotor activity and anxiety-like behaviors of the homozygous transgenic (Tg/Tg) mice and the wild-type (WT) littermates were examined by intruder/resident test, open field and elevated plus maze, respectively. A significant increase in the aggression, locomotor activity, and anxiety-like behaviors was detected in the Tg/Tg vs WT mice. As CCK, CCK(2) receptors (CCK(2)R), and 5-HT(1A) receptors (5-HT(1A)R) in the CNS play an important role in these behaviors, possible changes in the expression of CCK and CCK(2)R and the density of CCK(2)R and 5-HT(1A)R were determined by either real-time RT-PCR or autoradiography of ligand binding assays. The results suggest that the expressions of CCK and CCK(2)R were increased in the hypothalamus, and the density of CCK(2)R were increased in the hypothalamus and amygdala of Tg/Tg vs WT mice. Similarly, the density of 5-HT(1A)R was increased in the hypothalamus. Our results suggest that an upregulation of the CCK response system and 5-HT(1A)R in the hypothalamus of Tg/Tg mice may mediate the alterations in the observed behaviors of these mice.

Aggression↗

Neurons expressing serotonin-1B receptor in the basolateral nuclear group of the amygdala in normally behaving and aggressive dogs.

The present study aimed to quantify neurons expressing the serotonin-1B receptor and evaluate numerical differences in normally behaving and pathologically aggressive dogs in order to assess whether the serotonin-1B receptor is involved in pathological canine aggression. Because previous studies have reported structural alterations in the basolateral nuclear group (BNG) of the amygdaloid body of aggressive dogs, this structure was selected as region of interest in the present study. Indirect immunohistochemistry was applied to visualise the serotonin-1B-receptor-positive neurons. Immunoreactivity was located predominantly within the neuronal cell bodies and adjacent neuronal processes. In the aggressive dogs the BNGs contained a significantly higher number of serotonin-1B-receptor-positive neurons compared to the normally behaving dogs. This number was strongly correlated with the total number of neurons per BNG, which was also significantly increased in aggressive dogs compared to normal dogs. The percentage of neurons expressing the serotonin-1B receptor did not differ significantly between both groups. No significant asymmetries were observed for the number and percentage of serotonin-1B-receptor-positive neurons. Potential relationships between the present findings and the etiology of aggressive behaviour, the neuroprotective role of the serotonin-1B receptor and receptor dysfunction are discussed.

Aggression↗