Long-lasting effects of neonatal pentobarbital administration on spatial learning and hippocampal synaptic plasticity

Acute pentobarbital treatment impairs spatial learning and memory and hippocampal long-term potentiation in rats

“…Although the influence of pentobarbital on learning and memory is still debated, increasing numbers of studies have shown that pentobarbital application results in memory deficits in different animal models [4][5][6][7]. Consistent with these reports, we found that direct intrahippocampal infusion of pentobarbital (20 min before the first trial on each training day) significantly impaired hippocampus-dependent spatial learning in the Morris water maze test ( Fig.…”

“…Although we examined only the acute effects of pentobarbital on spatial learning and memory in the present study, pentobarbital might also exert a longterm influence on learning and memory. Indeed, a recent report supports this view with the finding that the neonatal administration of pentobarbital leads to long-lasting spatial learning deficits [7]. However, it remains unclear whether pentobarbital application in adults has a chronic effect on learning and memory.…”

“…The systemic administration of pentobarbital can produce memory dissociation in rats [5] and disrupt short-term memory and attention in monkeys performing an operant behavioral test battery [6]. A recent study also showed that neonatal treatment with pentobarbital leads to impairments of spatial memory that persists even into adulthood [7].…”

“…Unfortunately, reports of the effects of pentobarbital on learning and memory are contradictory. Some studies have shown no interference with learning and memory [3], whereas others have shown that pentobarbital application might impair memory [4][5][6][7]. For example, Kirk and colleagues reported that pentobarbital quantitatively impairs the memory acquisition processes involved in short-term recall performance [4].…”

Neonatal ketamine exposure causes impairment of long-term synaptic plasticity in the anterior cingulate cortex of rats

“…A possible explanation is that GABAergic interneurons provide an inhibitory input to the axon initial segment soma and proximal dendrites of glutamatergic pyramidal neurons, thereby regulating the output activity of these glutamatergic neurons. In the absence of GABAergic inhibition, hyperexcitability of pyramidal neurons would thus lead to impairment of LTP due to their occlusion or saturation (Tachibana et al, 2011). Thus, we propose that neurotoxic injury of GABAergic neurons resulting from neonatal ketamine exposure would directly lead to disruption of cortical inhibition and indirectly cause disinhibition of glutamatergic signaling, both contributing to excessive cortical excitability that in turn impairs the induction of LTP.…”