Two different mirror neuron networks: The sensorimotor (hand) and limbic (face) pathways.

The vast majority of functional studies investigating mirror neurons (MNs) explored their properties in relation to hand actions, and very few investigated how MNs respond to mouth actions or communicative gestures. Since hand and mouth MNs were recorded in two partially overlapping sectors of the ventral precentral cortex of the macaque monkey, there is a general assumption that they share a same neuroanatomical network, with the parietal cortex as a main source of visual information. In the current review, we challenge this perspective and describe the connectivity pattern of mouth MN sector. The mouth MNs F5/opercular region is connected with premotor, parietal areas mostly related to the somatosensory and motor representation of the face/mouth, and with area PrCO, involved in processing gustatory and somatosensory intraoral input. Unlike hand MNs, mouth MNs do not receive their visual input from parietal regions. Such information related to face/communicative behaviors could come from the ventrolateral prefrontal cortex. Further strong connections derive from limbic structures involved in encoding emotional facial expressions and motivational/reward processing. These brain structures include the anterior cingulate cortex, the anterior and mid-dorsal insula, orbitofrontal cortex and the basolateral amygdala. The mirror mechanism is therefore composed and supported by at least two different anatomical pathways: one is concerned with sensorimotor transformation in relation to reaching and hand grasping within the traditional parietal-premotor circuits; the second one is linked to the mouth/face motor control and is connected with limbic structures, involved in communication/emotions and reward processing.

Frequency and topography in monkey electroencephalogram during action observation: possible neural correlates of the mirror neuron system.

The observation of actions executed by others results in desynchronization of electroencephalogram (EEG) in the alpha and beta frequency bands recorded from the central regions in humans. On the other hand, mirror neurons, which are thought to be responsible for this effect, have been studied only in macaque monkeys, using single-cell recordings. Here, as a first step in a research programme aimed at understanding the parallels between human and monkey mirror neuron systems (MNS), we recorded EEG from the scalp of two monkeys during action observation. The monkeys were trained to fixate on the face of a human agent and subsequently to fixate on a target upon which the agent performed a grasping action. We found that action observation produced desynchronization in the 19-25 Hz band that was strongest over anterior and central electrodes. These results are in line with human data showing that specific frequency bands within the power spectrum of the ongoing EEG may be modulated by observation of actions and therefore might be a specific marker of MNS activity.

Effects of the intravitreal administration of dopaminergic ligands on the b-wave amplitude of the rabbit electroretinogram.

In the retina of mammals, dopamine (DA) is generally released by amacrine cells and is known to alter the physiology of most retinal cells. It is well known that DA reduces the amplitude of the b-wave of the electroretinogram (ERG) in rabbit. However, the specific receptor subtypes that mediate this action have not yet been elucidated. To do this, we recorded flash ERGs before and after the intravitreal injection of D1-like DA receptor agonists (SKF38393, A77693) and antagonist (SCH23390), and of D2-like agonist (R(-)-propylnorapomorphine hydrochloride; NPA) and antagonist ((S)-(-)-sulpiride). Contralateral control eyes were injected with the vehicle only. Both D1 agonists provoked a reduction of the ERG b-wave amplitude (34.0% and 59.2% of the pre-injection level, respectively). The D2-like agonist NPA had no significant effects on ERG components. Unexpectedly, both D1- and D2-like antagonists also reduced the b-wave amplitude (28.9% and 59.8%). Overall, these data suggest that the previously described effect of DA on the rabbit ERG b-wave came from activation of D1-like receptors. On the basis of the effects observed with D2-like antagonist, a subtle contribution of D2-like presynaptic receptors cannot be ruled out.

Effects of angiotensin II on visual evoked potentials in the superior colliculus of juvenile rats.

There are age-related changes in the relative expression of the AT(1)and AT(2)receptors of angiotensin II (Ang II) in brain regions such as the superior colliculus, a midbrain visual structure where both receptor subtypes are found. We investigated the effects of Ang II on gross visual activity in the colliculus of anesthetized rats aged between 15 and 35 post-natal days. Microinjection of Ang II in the superficial layers yielded a strong reduction in the amplitude of visual evoked potentials in a dose-related manner. Injection of the peptide in more ventral collicular layers did not modify the potential confirming the discrete localization of the angiotensinergic receptors in the superficial layers. Preliminary data indicated that the co-injection of Ang II with Losartan or PD 123319 yielded a partial blockade of Ang II suppressive effects, indicating that both AT(1)and AT(2)receptors are likely to be involved in mediating these responses. Overall, this study shows that the inhibitory nature of Ang II action is similar in juvenile and adult animals (Merabet et al. 1994 and Merabet et al. 1997)