**3.7 EEG recording**

Rats were equipped with neocortical electrodes to record EEG from cerebral cortex while an other electrode was implanted into the dorsal hippocampus to register hippocampal theta activity, since previous work has shown the last brain area to be involved in object recognition [Prickaerts et al., 2002; Broadbent et al., 2004].

In intact as well as in NBM-lesioned rats, EEG activity, derived from neocortex and hippocampus, was continuously monitored and recorded when animals were exposed to familiar and novel environments.

Neural Basis of Object Recognition 15

analysis showed a strong increase in total as well as delta and theta power (*p*<0.001 vs sham). **C.** and **D.** depict EEG spectrum power recorded in NBM lesioned animal after systemic administration of saline (C) or AC1 (D). The cholinergic agonist dramatically modified EEG power when compared with EEG baseline activity. A significant (*p*<0.001) fall in total voltage power, as well as in the power of lower frequency bands (0.25-3 and 4-7 Hz) is here highlighted. No EEG effect was reported after saline administration. Sham group showed no significant difference in EEG activity when compared with intact animals (data not shown). Each experiment: n =7. AC1 (12.5 mg/kg i.p.), saline (2 ml i.p.). Ordinates show the voltage power expressed in arbitrary values, abscissae show the frequency range (0.25-

Fig. 7. Theta and alpha EEG power recorded in neocortex of rat subjected to lesion of the

theta power (\**p*<0.001 vs NBM lesion; #p<0.001 vs baseline). Values in mean + SEM.

In NBM lesioned animals, theta power resulted dramatically increased while alpha power was reduced (\**p*<0.001 vs sham). Treatment with AC1 was able to reverse the neocortical EEG activity producing a significant increase in alpha power and a marked reduction in

The effects of these new compounds on learning and memory consolidation were investigated by hippocampal activity and in novel object recognition. Using the spectral analysis of the EEG, theta band (4-7 Hz) was directly recorded in rats by hippocampal depth electrode (Fig. 8). Theta oscillation was continuously monitored and recorded before and during exploration. In control animals, exploratory behaviour was correlated with an increase in hippocampal theta oscillation activity. In NBM-lesioned rats, no change in hippocampal theta frequency oscillations was observed during familial and novel

16 Hz).

NBM during ORT performance.

**3.8 Hippocampal activity and ORT** 

recognition (Fig. 9).

For statistical purpose, bipolar signals, derived from each neocortical area in both brain hemispheres as well as in the hippocampus, were analysed. qEEG analysis was performed on the theta range both in the hippocampus and on the whole EEG spectrum in the cerebral cortex. Five artifact-free epochs, of 10 s each, selected from EEG baseline and that recorded during the performance in behavioural tasks, were processed using Fast Fourier Transform (FFT) as previously described [Rispoli et al., 2004b]. Statistical analysis of the data was performed on the EEG signal amplitude (V).

Neocortical EEG architecture and hippocampal theta activity was dramatically changed in NBM-lesioned rats when compared with sham-operated and intact animals. In NBMlesioned animals, EEG baseline activity resulted significantly increased in total power (Fig. 6); in detail, quantitative analysis of EEG spectrum showed a marked raise in theta power; while neocortical high voltage spindle (HVS) appeared. No significant EEG difference was reported in sham group when compared with intact control one. No significant EEG change was also reported in lesioned animals during behavioural performance.

In NBM lesioned animals, during object recognition performance, our compounds produced desynchronisation and evidenced a marked decrease in the energy of the whole EEG power; a further analysis of the EEG spectrum showed a significant reduction of theta energy (Fig. 7). Incidence of HVS activity was also significantly reduced in NBM-lesioned animals. Moreover, in this AD model statistical analysis revealed very significant correlation between EEG changes and ORT performance.

Fig. 6. Quantitative EEG and Spectral Analysis.

A typical example of neocortical EEG activity recorded in sham-operated (**A**) and NBMlesioned animals (**B**). In NBM-lesioned animals, EEG architecture was altered; in fact, qEEG 14 Advances in Object Recognition Systems

For statistical purpose, bipolar signals, derived from each neocortical area in both brain hemispheres as well as in the hippocampus, were analysed. qEEG analysis was performed on the theta range both in the hippocampus and on the whole EEG spectrum in the cerebral cortex. Five artifact-free epochs, of 10 s each, selected from EEG baseline and that recorded during the performance in behavioural tasks, were processed using Fast Fourier Transform (FFT) as previously described [Rispoli et al., 2004b]. Statistical analysis of the data was

Neocortical EEG architecture and hippocampal theta activity was dramatically changed in NBM-lesioned rats when compared with sham-operated and intact animals. In NBMlesioned animals, EEG baseline activity resulted significantly increased in total power (Fig. 6); in detail, quantitative analysis of EEG spectrum showed a marked raise in theta power; while neocortical high voltage spindle (HVS) appeared. No significant EEG difference was reported in sham group when compared with intact control one. No significant EEG change

In NBM lesioned animals, during object recognition performance, our compounds produced desynchronisation and evidenced a marked decrease in the energy of the whole EEG power; a further analysis of the EEG spectrum showed a significant reduction of theta energy (Fig. 7). Incidence of HVS activity was also significantly reduced in NBM-lesioned animals. Moreover, in this AD model statistical analysis revealed very significant correlation between

A typical example of neocortical EEG activity recorded in sham-operated (**A**) and NBMlesioned animals (**B**). In NBM-lesioned animals, EEG architecture was altered; in fact, qEEG

was also reported in lesioned animals during behavioural performance.

performed on the EEG signal amplitude (V).

EEG changes and ORT performance.

Fig. 6. Quantitative EEG and Spectral Analysis.

analysis showed a strong increase in total as well as delta and theta power (*p*<0.001 vs sham). **C.** and **D.** depict EEG spectrum power recorded in NBM lesioned animal after systemic administration of saline (C) or AC1 (D). The cholinergic agonist dramatically modified EEG power when compared with EEG baseline activity. A significant (*p*<0.001) fall in total voltage power, as well as in the power of lower frequency bands (0.25-3 and 4-7 Hz) is here highlighted. No EEG effect was reported after saline administration. Sham group showed no significant difference in EEG activity when compared with intact animals (data not shown). Each experiment: n =7. AC1 (12.5 mg/kg i.p.), saline (2 ml i.p.). Ordinates show the voltage power expressed in arbitrary values, abscissae show the frequency range (0.25- 16 Hz).

Fig. 7. Theta and alpha EEG power recorded in neocortex of rat subjected to lesion of the NBM during ORT performance.

In NBM lesioned animals, theta power resulted dramatically increased while alpha power was reduced (\**p*<0.001 vs sham). Treatment with AC1 was able to reverse the neocortical EEG activity producing a significant increase in alpha power and a marked reduction in theta power (\**p*<0.001 vs NBM lesion; #p<0.001 vs baseline). Values in mean + SEM.
