Neuronal Bases of Systemic Organization of Behavior.

Despite the years of studies in the field of systems neuroscience, functions of neural circuits and behavior-related systems are still not entirely clear. The systems description of brain activity has recently been associated with cognitive concepts, e.g. a cognitive map, reconstructed via place-cell activity analysis and the like, and a cognitive schema, modeled in consolidation research. The issue we find of importance is that a cognitive unit reconstructed in neuroscience research is mainly formulated in terms of environment. In other words, the individual experience is considered as a model or reflection of the outside world and usually lacks a biological meaning, such as describing a given part of the world for the individual. In this chapter, we present the idea of a cognitive component that serves as a model of behavioral interaction with environment, rather than a model of the environment itself. This intangible difference entails the need in substantial revision of several well-known phenomena, including the long-term potentiation.The principal questions developed here are how the cognitive units appear and change upon learning and performance, and how the links between them create the whole structure of individual experience. We argue that a clear distinction between processes that provide the emergence of new components and those underlying the retrieval and/or changes in the existing ones is necessary in learning and memory research. We then describe a view on learning and corresponding neuronal activity analysis that may help set this distinction.

Preclinical model of transcorneal alternating current stimulation in freely moving rats.

PURPOSE: Transcorneal alternating current stimulation (tACS) has become a promising tool to modulate brain functions and treat visual diseases. To understand the mechanisms of action a suitable animal model is required. However, because existing animal models employ narcosis, which interferes with brain oscillations and stimulation effects, we developed an experimental setup where current stimulation via the eye and flicker light stimulation can be applied while simultaneously recording local field potentials in awake rats. METHOD: tACS was applied in freely-moving rats (N = 24) which had wires implanted under their upper eye lids. Field potential recordings were made in visual cortex and superior colliculus. To measure visual evoked responses, rats were exposed to flicker-light using LEDs positioned in headset spectacles. RESULTS: Corneal electrodes and recording assemblies were reliably operating and well tolerated for at least 4 weeks. Transcorneal stimulation without narcosis did not induce any adverse reactions. Stable head stages allowed repetitive and long-lasting recordings of visual and electrically evoked potentials in freely moving animals. Shape and latencies of electrically evoked responses measured in the superior colliculus and visual cortex indicate that specific physiological responses could be recorded after tACS. CONCLUSIONS: Our setup allows the stimulation of the visual system in unanaesthetised rodents with flicker light and transcorneally applied current travelling along the physiological signalling pathway. This methodology provides the experimental basis for further studies of recovery and restoration of vision.

Fast transmission from the dopaminergic ventral midbrain to the sensory cortex of awake primates.

Motivated by the increasing evidence that auditory cortex is under control of dopaminergic cell structures of the ventral midbrain, we studied how the ventral tegmental area and substantia nigra affect neuronal activity in auditory cortex. We electrically stimulated 567 deep brain sites in total within and in the vicinity of the two dopaminergic ventral midbrain structures and at the same time, recorded local field potentials and neuronal discharges in cortex. In experiments conducted on three awake macaque monkeys, we found that electrical stimulation of the dopaminergic ventral midbrain resulted in short-latency (~35 ms) phasic activations in all cortical layers of auditory cortex. We were also able to demonstrate similar activations in secondary somatosensory cortex and superior temporal polysensory cortex. The electrically evoked responses in these parts of sensory cortex were similar to those previously described for prefrontal cortex. Moreover, these phasic responses could be reversibly altered by the dopamine D1-receptor antagonist SCH23390 for several tens of minutes. Thus, we speculate that the dopaminergic ventral midbrain exerts a temporally precise, phasic influence on sensory cortex using fast-acting non-dopaminergic transmitters and that their effects are modulated by dopamine on a longer timescale. Our findings suggest that some of the information carried by the neuronal discharges in the dopaminergic ventral midbrain, such as the motivational value or the motivational salience, is transmitted to auditory cortex and other parts of sensory cortex. The mesocortical pathway may thus contribute to the representation of non-auditory events in the auditory cortex and to its associative functions.

Predictive value of changes in electroencephalogram and excitatory postsynaptic field potential for CA1 damage after global ischaemia in rats.

Recordings of the electroencephalogram (EEG) are regularly used to asses the severity of transient global ischaemia in rats. Here, we investigated whether the EEG obtained from electrodes placed in the hippocampus does indeed give valuable information about the consequences of an ischaemic event. Furthermore, we evaluated how evoked synaptic responses from the same electrodes placed in the hippocampal CA1 area changed with time and in relation to damage. We performed transient two vessel-occlusion with hypobaric hypotension in rats to induce selective, delayed neuronal death in CA1. Beforehand, the animals had been chronically implanted with electrodes. Stimulating electrodes had been placed into the Schaffer collaterals and recording electrodes into the CA1 area. EEG was recorded from shortly before ischaemia until up to 40 min post-ischaemia. Field excitatory post-synaptic potentials (fEPSP) were recorded before ischaemia or sham-operation and 2 and 7 days afterwards. We found a significant negative correlation between the duration of the EEG amplitude decrease (flattening) and the number of surviving neurons in CA1, which were quantified by histology after 7 days post-ischaemia. However, substantial neuronal damage was only seen when the time of flattening was more than 12 min and outlasted the time of ischaemia. The impairment of synaptic function, measured as the decrease of fEPSP slope 2 days post-ischaemia correlated with the later maturated structural damage in CA1. The fEPSP remained decreased until day 7 post-ischaemia. Animals with no damage (sham condition) showed a transient decrease of the fEPSP slope. In conclusion, our data show that the duration of EEG-flattening predicts the extent of neuronal damage. However, EEG-flattening just during the period of clamping both common carotid arteries--albeit an essential precondition for substantial CA1 cell loss to occur--is not sufficient to predict damage. The degree of impairment of evoked synaptic function of CA1 neurons (fEPSP) 2 days after ischaemia predicts the final extent of damage with significant probability.