Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0848237 (acute stress)
 4,619 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects of morphine, hypoxaemia or hypercapnia on gastric acid secretion, gastric mucus synthesis and the gastric mucosa were studied in conscious rats with pyloric occlusion. Hypoxaemia and hypercapnia were induced by morphine 32 mg/kg given i.p., or each condition was produced separately by adjusting the composition of respired air in the chamber where the animals were kept during the experimental period. Hypoxia significantly enhanced gastric mucus synthesis whereas hypercapnia significantly reduced gastric acid secretion. These effects were significantly alleviated by atropine pretreatment. Morphine-treated rats exhibited decreased gastric acid secretion, increased gastric mucus synthesis and a higher mean ulcer index but only the reduced gastric acid output was significantly prevented by atropine. It is suggested that the effect of morphine on gastric acid secretion may result from its respiratory depressant action and consequent acute stress production. However, the mechanisms by which morphine can increase mucus synthesis and produce ulceration remain obscure.
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PMID:Effects of morphine, hypoxaemia and hypercapnia on the rat stomach. 375 55

Synaptic plasticity in the ventral tegmental area (VTA) is modulated by drugs of abuse and stress and is hypothesized to contribute to specific aspects of addiction. Both excitatory and inhibitory synapses on dopamine neurons in the VTA are capable of undergoing long-term changes in synaptic strength. While the strengthening or weakening of excitatory synapses in the VTA has been widely examined, the role of inhibitory synaptic plasticity in brain reward circuitry is less established. Here, we investigated the effects of drugs of abuse, as well as acute stress, on long-term potentiation of GABAergic synapses onto VTA dopamine neurons (LTP(GABA)). Morphine (10 mg/kg i.p.) reduced the ability of inhibitory synapses in midbrain slices to express LTP(GABA) both at 2 and 24 h after drug exposure but not after 5 days. Cocaine (15 mg/kg i.p.) impaired LTP(GABA) 24 h after exposure, but not at 2 h. Nicotine (0.5 mg/kg i.p.) impaired LTP(GABA) 2 h after exposure, but not after 24 h. Furthermore, LTP(GABA) was completely blocked 24 h following brief exposure to a stressful stimulus, a forced swim task. Our data suggest that drugs of abuse and stress trigger a common modification to inhibitory plasticity, synergizing with their collective effect at excitatory synapses. Together, the net effect of addictive substances or stress is expected to increase excitability of VTA dopamine neurons, potentially contributing to the early stages of addiction.
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PMID:Drugs of abuse and stress impair LTP at inhibitory synapses in the ventral tegmental area. 2060 69