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Delta-9-tetrahydrocannabinol disrupts hippocampal neuroplasticity and neurogenesis in trained, but not untrained adolescent Sprague-Dawley rats.

Ryan W J Steel, John H Miller, Dalice A Sim, Darren J Day

Brain Research February 22, 2014 DOI: 10.1016/j.brainres.2013.12.034 (opens in new tab)

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Characteristics Experimental animal study Peer reviewed
Population Adolescent (P28-P42) Sprague-Dawley rats, both untrained and trained (15 days of training)
Intervention THC
Dose 6 mg/kg i.p.
Duration 15 days of training with daily treatment
Measures CB1R, PSD95, synapsin-I, synapsin-III, Ki67, DCX, PSA-NCAM, BrdU labelling
Topics Cannabis Neuroplasticity
Keywords Adolescent Hippocampus Plasticity Spatial learning
Key findings Training increased hippocampal neuroplasticity marker levels in control rats but not in THC-treated rats, while THC-treated trained rats showed reduced immature neuronal marker levels. Hippocampal proliferation and survival of BrdU-labelled cells were unaffected by THC. No THC effects occurred without training, indicating the effects reflect specific impairment of training-induced responses.

Abstract

Cannabis is the most widely used illicit drug, and disruption of learning and memory are commonly reported consequences of cannabis use. We have previously demonstrated a spatial learning impairment by ∆(9)-tetrahydrocannabinol (THC) in adolescent Sprague-Dawley rats (Steel et al., 2011). The molecular mechanisms underlying behavioural impairment by cannabis remain poorly understood, although the importance of adaptive changes in neuroplasticity (synaptic number and strength) and neurogenesis during learning are accepted. Here we aimed to identify any effects of THC on the early induction of these adaptive processes supporting learning, so we conducted our analyses at the mid-training point of our previous study. Both untrained and trained (15 days of training) adolescent (P28-P42) Sprague-Dawley rats were treated daily with THC (6 mg/kg i.p.) or its vehicle, and changes in the levels of markers of hippocampal neuroplasticity (CB1R, PSD95, synapsin-I, synapsin-III) and neurogenesis (Ki67, DCX, PSA-NCAM, BrdU labelling) by training were measured. Training of control animals, but not THC-treated animals increased neuroplasticity marker levels. However training of THC-treated animals, but not control animals reduced immature neuronal marker levels. Levels of hippocampal proliferation, and survival of the BrdU-labelled progeny of these divisions were unaffected by THC in trained and untrained animals. These data show a smaller neuroplastic response, and a reduction of new-born neuronal levels not attributable to effects on proliferation or survival by THC-treatment during training. Importantly no effects of THC were seen in the absence of training, indicating that these effects represent specific impairments by THC on training-induced responses.

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