Ketamine Induces Dopamine-Dependent Depression of Evoked Hippocampal Activity in the Nucleus Accumbens in Freely Moving Rats

Ketamine, at a Dose that Disrupts Motor Behavior and Latent Inhibition, Enhances Prefrontal Cortex Synaptic Efficacy and Glutamate Release in the Nucleus Accumbens

“…Our group has previously shown in freely moving rats that ketamine, used at the same dose as in the present study, induced a depression of glutamatergic transmission between the hippocampus and the NAc (Hunt et al, 2005) and, on the contrary, a potentiation of synaptic efficacy between the basolateral amygdala and the NAc . Taken together with the present electrophysiological results, these data indicate that blockade of NMDA receptors induces a profound disruption of information processing in the NAc, facilitating selectively information flow from the prefrontal cortex and amygdala.…”

“…It is possible that glutamatergic mechanisms might also participate to the acquisition of latent inhibition. Dysfunction of glutamatergic inputs to the accumbens by ketamine (Hunt et al, 2005;Kessal et al, 2005 and present results) might therefore underlie the disruption of latent inhibition observed with this compound in our conditioned-fear paradigm.…”

“…This has been partially demonstrated by recent studies using the pharmacological ketamine model of schizophrenia. Indeed, this NMDA antagonist depresses synaptic efficacy between the hippocampus and the NAc (Hunt et al, 2005), while it enhances synaptic transmission between the basolateral amygdala and the NAc . Such an investigation for the projection from the PFC to the NAc would be of particular interest.…”

Serotonergic lesions of the dorsal hippocampus differentially modulate locomotor hyperactivity induced by drugs of abuse in rats: implications for schizophrenia

“…Thus, enhanced motor activation following ketamine or phencyclidine treatment in DHL rats may result from NMDA receptor antagonist-mediated disinhibition of accumbal activity via a dysregulated glutamatergic hippocampal-accumbens circuit (Kelley and Domesick 1982;Walaas and Fonnum 1980). Ketamine directly affects the hippocampal-accumbens pathway (Hunt et al 2005) and electrical stimulation of the CA1 in the dorsal hippocampus results in locomotor activation (Ma et al 1998). In a manner directly related to NMDA receptor blockade, ketamine enhances neuronal activity in the dorsal hippocampus, unlike D-amphetamine (Duncan et al 1999).…”

The Brain Cytoplasmic RNA BC1 Regulates Dopamine D2Receptor-Mediated Transmission in the Striatum

“…For example, reduced sensitivity of striatal D 2 DR occurs in a mouse model of familial Parkinson's disease (Goldberg et al, 2005), whereas increased sensitivity seems to mediate striatal neuron dysfunction and degeneration in Huntington's disease (Charvin et al, 2005). Furthermore, reduced D 2 DR activity in the striatum has been implicated in the maintenance of cocaine self-administration (Nader et al, 2006), and increased sensitivity of these receptors plays a role in schizophrenia (Hunt et al, 2005) and anxiety (Ponnusamy et al, 2005).…”