Caffeine consumption disrupts hippocampal long‐term potentiation in freely behaving rats

Caffeine consumption disrupts hippocampal long‐term potentiation in freely behaving rats

Caffeine, one of the most commonly consumed psychoactive substances in the world, has long been known to alter neurological functions, such as alertness, attention, and memory. Despite caffeine's popularity, systematic investigations of its effects on synaptic plasticity in the brain are still...

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Bibliographic Details
Published in:Physiological reports Vol. 6; no. 5; pp. e13632 - n/a
Main Authors: Blaise, J. Harry, Park, Jee E., Bellas, Nicholas J., Gitchell, Thomas M., Phan, Vy
Format: Journal Article
Language:English
Published: United States John Wiley & Sons, Inc 01-03-2018
John Wiley and Sons Inc
Subjects:
Adenosine
Animals
Caffeine
Caffeine - adverse effects
Caffeine - pharmacology
Central Nervous System Stimulants - adverse effects
Central Nervous System Stimulants - pharmacology
Dentate gyrus
Drinking water
Electrophysiological recording
Hippocampal plasticity
Hippocampus
Hippocampus - drug effects
Hippocampus - physiology
Learning
Long-Term Potentiation
LTP
Male
Memory
Neuroscience
Original Research
plasticity
Rats
Rats, Sprague-Dawley
Rodents
Synapses
synaptic
Synaptic plasticity
Synaptic transmission
Toxins, Pollutants and Chemical Agents
LTP
plasticity
Adenosine
hippocampus
synaptic
Caffeine
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Summary:Caffeine, one of the most commonly consumed psychoactive substances in the world, has long been known to alter neurological functions, such as alertness, attention, and memory. Despite caffeine's popularity, systematic investigations of its effects on synaptic plasticity in the brain are still lacking. Here we used a freely behaving rodent model of long‐term potentiation (LTP), a frequently studied form of synaptic plasticity, to assess the effects of caffeine consumption on hippocampal plasticity. LTP, which is a persistent increase in the strength of synaptic connections between neurons, is a cellular mechanism widely considered to underlie the processes of learning and memory. A group of 10‐week‐old Sprague–Dawley rats were administered caffeine (1 g/L) in their drinking water 3 weeks prior to collection of electrophysiological data. Another group of age‐matched animals received tap water and served as controls. Stimulating and recording electrodes were chronically implanted in the perforant pathway (PP) and dentate gyrus (DG) region of the hippocampus, respectively, to permit stable electrophysiological recordings of synaptic transmission at this synapse. Population spike amplitude (PSA) measures of LTP induction and duration were acquired in vivo while animals were freely behaving using a well‐established electrophysiological recording protocol. Results indicate caffeine‐treated rats (n = 9) had a significantly (P < 0.05) reduced level of LTP induction compared with controls (n = 10). More studies are needed to identify the exact mechanism through which caffeine alters LTP induction in this freely behaving model of synaptic plasticity. We used a freely behaving rodent model of long‐term potentiation (LTP) to assess the effects of caffeine consumption on hippocampal synaptic plasticity. Results indicate caffeine‐treated rats (n = 9) had a significantly (P < 0.05) reduced level of LTP induction compared with controls (n = 10).
Bibliography:This work was funded by ‘Faculty Research Committee Grant’, Trinity College, Hartford CT, USA.
Funding Information
ISSN:2051-817X
DOI:10.14814/phy2.13632