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Recent, convergent evidence places the anterior thalamic nuclei at the heart of diencephalic amnesia. However, the reasons for the severe memory loss in diencephalic amnesia remain unknown. A potential clue comes from the dense, reciprocal connections between the anterior thalamic nuclei and retrosplenial cortex, another region vital for memory. We now report a loss of synaptic plasticity [long-term depression (LTD)] in rat retrosplenial cortex slices months following an anterior thalamic lesion. The loss of LTD was lamina-specific, occurring only in superficial layers of the cortex and was associated with a decrease in GABA(A)-mediated inhibitory transmission. As retrosplenial cortex is itself vital for memory, this distal lesion effect will amplify the impact of anterior thalamic lesions. These findings not only provide novel insights into the functional pathology of diencephalic amnesia and have implications for the aetiology of the posterior cingulate hypoactivity in Alzheimer's disease, but also show how distal changes in plasticity could contribute to diaschisis.

We have investigated properties of GABAergic synaptic transmission in perirhinal cortex evoked by stimulation of temporal and entorhinal cortex sides. GABA A IPSCs were isolated by blockade of glutamatergic transmission in slices of adult perirhinal cortex; IPSC decay was best fitted with two exponentials. Interestingly, temporal IPSCs had a larger slow component of decay (P < 0.05) compared to entorhinal IPSCs. Depression of IPSCs by the GABA B receptor agonist baclofen was greater (P < 0.05) in the temporal input (79 ′ 4% depression) than the entorhinal input (65 ′ 3% depression). Furthermore, baclofen abolished the slow component of IPSC decay in both inputs. Activity-dependent depression of IPSCs at 5 Hz was greater (P < 0.05) in the temporal input [paired pulse ratio (PPR) 0.5 ′ 0.04] compared to that in the entorhinal input (PPR 0.67 ′ 0.02, n = 10). The differences in paired pulse depression between the inputs were removed by the GABA B receptor antagonist CGP55845A. This study demonstrates several differences in GABA transmission between temporal and entorhinal inputs including the differential activation of presynaptic GABA B receptors and differential regulation of inhibitory synaptic transmission. These properties may be important in the control of neuronal activity within perirhinal cortex.

We have investigated properties of GABAergic synaptic transmission in perirhinal cortex evoked by stimulation of temporal and entorhinal cortex sides. GABAA IPSCs were isolated by blockade of glutamatergic transmission in slices of adult perirhinal cortex; IPSC decay was best fitted with two exponentials. Interestingly, temporal IPSCs had a larger slow component of decay (P0.05) compared to entorhinal IPSCs. Depression of IPSCs by the GABAB receptor agonist baclofen was greater (P0.05) in the temporal input (79 +/- 4% depression) than the entorhinal input (65 +/- 3% depression). Furthermore, baclofen abolished the slow component of IPSC decay in both inputs. Activity-dependent depression of IPSCs at 5 Hz was greater (P0.05) in the temporal input [paired pulse ratio (PPR) 0.5 +/- 0.04] compared to that in the entorhinal input (PPR 0.67 +/- 0.02, n = 10). The differences in paired pulse depression between the inputs were removed by the GABAB receptor antagonist CGP55845A. This study demonstrates several differences in GABA transmission between temporal and entorhinal inputs including the differential activation of presynaptic GABAB receptors and differential regulation of inhibitory synaptic transmission. These properties may be important in the control of neuronal activity within perirhinal cortex.