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

Abstract

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.

Keywords: Adenosine; Caffeine; LTP; hippocampus; plasticity; synaptic.

Figure 1

(A) Caffeine‐treated rats consumed significantly (P < 0.05) less water compared to controls. (B) No significant (P > 0.05) differences were observed in average body weight. (C) Representative evoked field potential traces in control and (D) caffeine‐treated rats. (E) No significant (P > 0.05) differences in the average I/O curves were observed.

Figure 2

LTP was reliably and robustly induced and maintained up to at least 24 h in both caffeine‐treated and control animals. LTP was significantly lower (P < 0.05) in caffeine‐treated rats compared with controls at all the times tested, except at 9–11 min and 48 h posttetanization.