1: Neuroscience 1997 Jun;78(4):1229-38
Caffeine reduces the efficacy of electroreceptor cell synapses: an
electrophysiological single-unit in vivo study.
Peters RC, Versteeg E, Bretschneider F, Brans RJ, Went A
Utrecht University, Comparative Physiology, The Netherlands.
Ampullary electroreceptor organs of catfish, Ictalurus melas, were exposed
apically to caffeine solutions at concentrations of 0, 5, 7.5, 10, and 15 mM.
Recording sinusoidally-modulated activity of single-unit afferents reveals a
dose-dependent decrease in mean afferent activity and sensitivity. A rebound
effect of average activity occurs after caffeine is washed out. After 25 min
exposure to 15 mM caffeine the peak of the gain curve shifts from 8 Hz to 4 Hz.
The corresponding phase characteristic shows an increased phase lag with a
maximum shift of 35 degrees at 20 Hz. The latency between stimulus and response
increases from 12 to 19 ms; the recovery time after onset of the pulse decreases
with 60 ms. The most probable explanation for the recorded effects is that
caffeine reduces the availability of intracellular Ca2+ by blocking of the
inositol triphosphate receptors in the endoplasmic reticulum. This in turn would
affect many intracellular properties and processes. The unavailability of Ca2+
could reduce the synaptic efficacy and increase latency by suppressing fusion of
synaptic vesicles with the presynaptic membrane and by depressing vesicle
transport. The change in frequency response corresponds in part to reduction of
the apical membrane surface area of the receptor cells, and in part to the
increased latency. Accumulation of glutamate-containing vesicles could account
for the higher mean activity and modulation amplitude in the lower frequency
range after caffeine is washed out. Caffeine might act postsynaptically by
inducing hyperpolarization of the terminals of the primary afferents.
PMID: 9174089
1: Psychophysiology 2000 Sep;37(5):583-95
Effects of nicotine and caffeine, separately and in combination, on EEG
topography, mood, heart rate, cortisol, and vigilance
Gilbert DG, Dibb WD, Plath LC, Hiyane SG
Department of Psychology, Southern Illinois University at Carbondale,
62901-6502, USA. dgilbert@siu.edu
[Record supplied by publisher]
Effects of nicotine and caffeine, separately and in combination, were assessed
in 12 male habitual smokers in a repeated-measures design. Caffeine (0-mg vs.
two 150-mg doses administered in a decaffeinated/sugar-free cola drink
post-baseline and 90 min later) was crossed with nicotine (ad libitum own dosing
vs. 1.0-mg machine-delivered dose vs. 0.05-mg machine-delivered dose).
Participants smoked a total of five cigarettes at 30-min intervals over a 2-hr
period. Caffeine and nicotine had large effect sizes on electroencephalogram
(EEG) power; however, these effects were modulated by the eyes open versus
closed condition, the other drug, and electrode site. EEG effects of open versus
closed eyes tended to be of the same size and direction as those of nicotine and
caffeine. However, whereas nicotine increased EEG power in some higher frequency
bands in some conditions, caffeine decreased EEG power across almost all
conditions. Serum cortisol concentration, vigor, and pleasantness were increased
by nicotine, but not by caffeine. Level of depressive mood depended on an
interaction of caffeine and nicotine. Vigilance performance was enhanced
significantly by caffeine and was increased almost significantly by nicotine.
The findings were interpreted in terms of common and differential mechanisms of
the two drugs.
PMID: 11037035
2: Life Sci 1995;57(19):PL285-92
24h withdrawal following repeated administration of caffeine attenuates brain
serotonin but not tryptophan in rat brain: implications for caffeine-induced
depression.
Haleem DJ, Yasmeen A, Haleem MA, Zafar A
Department of Biochemistry, University of Karachi, Pakistan.
Caffeine injected at doses of 20, 40 and 80 mg/kg increased brain levels of
tryptophan, 5-hydroxytryptamine (5-HT) and 5-hydroxyindole acetic acid (5-HIAA)
in rat brain. In view of a possible role of 5-HT in caffeine-induced depression
the effects of repeated administration of high doses of caffeine on brain 5-HT
metabolism are investigated in rats. Caffeine was injected at doses of 80 mg/kg
daily for five days. Control animals were injected with saline daily for five
days. On the 6th day caffeine (80 mg/kg) injected to 5 day saline injected rats
increased brain levels of tryptophan, 5-HT and 5-HIAA. Plasma total tryptophan
levels were not affected and free tryptophan increased. Brain levels of 5-HT and
5-HIAA but not tryptophan decreased in 5 day caffeine injected rats injected
with saline on the 6th day. Plasma total and free tryptophan were not altered in
these rats. Caffeine-induced increases of brain tryptophan but not 5-HT and
5-HIAA were greater in 5 day caffeine than 5 day saline injected rats. The
findings are discussed as repeated caffeine administration producing adaptive
changes in the serotonergic neurons to decrease the conversion of tryptophan to
5-HT and this may precipitate depression particularly in conditions of caffeine
withdrawal.
PMID: 7475912
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