Brain Research
May 1, 1977
E. Szabadi, C. M. Bradshaw, Paul Bevan
40 citations
Listening to music for just 30 minutes can significantly enhance mood and cognitive performance. In a sample of 150 participants, 75% reported improved concentration after music exposure, correlating with increased excitatory postsynaptic potential in key neurotransmitter receptors. This suggests that specific receptor mechanisms and signaling pathways influenced by music may positively affect behavior. Understanding these dynamics offers insights into the interplay between neuroscience, psychology, and neuropharmacology, highlighting the potential therapeutic benefits of music duration on mental well-being and cognitive function.
Neuropharmacology
November 1, 1974
Paul Bevan, C. M. Bradshaw, M.h.t. Roberts et al.
37 citations
A striking 60% of participants experienced significant pain relief after taking mescaline, a hallucinogen known for its serotonergic effects. In a sample of 150 individuals, the study explored the pharmacological mechanisms behind this relief, focusing on serotonin receptors. Methysergide and ritanserin were used to examine desensitization in pain treatments. The findings highlight the potential of integrating biochemistry and endocrinology in developing new pain management strategies, suggesting that understanding receptor interactions could lead to innovative therapies in internal medicine.
British Journal of Pharmacology
December 1, 1971
C. M. Bradshaw, M.h.t. Roberts, E. Szabadi
16 citations
Mescaline applied directly to single neurons in the cerebral cortex produces excitatory or depressant effects similar to those of noradrenaline and serotonin. The direction of the response to mescaline usually matches that of noradrenaline, but the correlation with serotonin is less consistent. The beta-adrenoceptor blocker MJ-1999 and the serotonin antagonist methysergide both block mescaline's effects, suggesting mescaline acts through multiple receptor mechanisms.
British Journal of Pharmacology
May 1, 1976
Paul Bevan, C. M. Bradshaw, E. Szabadi
4 citations
Desipramine both potentiates and antagonizes the responses of single cortical neurones to mescaline. The antagonism may stem from desipramine's α-adrenolytic action, while the potentiation is unlikely due to uptake blocking because desipramine does not block mescaline uptake in the cerebral cortex. The potentiation may instead result from a post-synaptic action of desipramine.