Directed coherence of EEG on ICSS rats with methamphetamine-induced hyperactivity and stereotyped behavior.

Methamphetamine (MAP) can reinforce intracranial self-stimulation (ICSS) in rats, that is, reward-seeking behavior. However, the ICSS can be inhibited by the stereotyped behavior induced by MAP. This study was designed to observe the mutual information flow between prefrontal cortex (PFC) and ventral tegmental area (VTA) using directed coherence (DC) analysis during the hyperactivity and stereotyped behavior induced by administration of MAP (a derivative of amphetamine). The DC from PFC to VTA increased at 5-7 Hz in the hyperactivity as compared to the stereotypy. In contrast, enhanced information flow from VTA to PFC was observed in the stereotypy as compared to the hyperactivity. We found a reciprocal information flow between PFC and VTA corresponding to the hyperactivity and stereotyped behavior that was induced by administration of MAP.

Methamphetamine induces cytosolic Ca2+ oscillations in the VTA dopamine neurons.

Methamphetamine (METH) induces a schizophrenia-like psychosis. The dopamine neurons in the ventral tegmental area (VTA) have been implicated in schizophrenia and drug abuse. The present study investigated direct effects of METH on VTA dopamine neurons. We treated adult SD rats with METH (5 mg/kg/day) or saline for 7 days, isolated single VTA neurons, and monitored neuronal activities by measuring cytosolic Ca2+ concentration ([Ca2+]i) in immunocytochemically identified dopamine neurons. Acutely administered METH increased [Ca2+]i in dopamine neurons from METH- and saline-treated rats and induced oscillations of [Ca2+]i in dopamine neurons only from METH-treated rats. The METH-induced [Ca2+]i oscillations were inhibited by Ca(2+)-free conditions and Ca2+ channel blockers. The results indicate that acute METH increases [Ca2+]i in VTA dopamine neurons and that subchronic METH treatment sensitizes them to this drug, resulting in induction of [Ca2+]i oscillations. The activation of VTA dopamine neurons may be related to psycho-stimulant effects of METH.

Reciprocal information flow between prefrontal cortex and ventral tegmental area in an animal model of schizophrenia.

The medial prefrontal cortex (PFC) is anatomically and functionally connected with the ventral tegmental area (VTA), the neuronal source of mesocorticolimbic system that is pathophysiologically related to schizophrenia-like symptoms. Methamphetamine (MAP) was applied to examine the functional relationship between PFC and VTA in an animal model of schizophrenia. Hyperactivity and stereotyped behavior were observed accompanied by a distinctive direction of information flow. In hyperactivity, information flow in the direction from PFC to VTA was dominant. Contrarily, dominant information flow from VTA to PFC was found in stereotyped behavior. These results indicate that dysfunctional interaction between PFC and VTA is the neuronal basis of MAP-induced schizophrenia-like psychosis. The information flow and its direction can be useful tool to explain the neurogenesis of these abnormal behaviors.

Peripheral and central distribution of major branches of the facial taste nerve in the carp.

The major pathways of the peripheral facial taste system in the carp, Cyprinus carpio, are the maxillary (Max), mandibular (Mand), palatine (Pal) and recurrent nerve rami. The peripheral distribution of the sensory fibers of these branches (B) was determined by means of electrophysiological techniques. Max.B., Mand.B. and Pal.B., each of which arises from the gasserian-geniculate ganglionic complexes, were found to innervate respectively, the upper lip and the adjacent skin, the internal and external surface of the lower lip region, and the upper lip and the anterior palate, ipsilaterally. The recurrent nerve sends fibers mainly via dorsal and ventral branches of the posterior lateral line nerve (NPLL), and a pectoral branch of the occipito-spinal nerve. The dorsal and ventral branches of NPLL innervate respectively, the dorsal fin and the adjacent body surface, and the remainder of the body surface. The pectoral branch supplies the pectoral fin. The central connections of the above branches were also examined by using the techniques of transganglionic tracing with horseradish peroxidase (HRP). HRP was applied to each of the branches, and its penetration of the brainstem was carefully followed. Labeled fibers were observed only in the ipsilateral region of the brainstem. When Max.B or Mand.B. was treated with HRP, labeled fibers were observed in the facial sensory root and in the descending trigeminal root. When Pal.B. was treated, however, they were traced only to the facial sensory root; thus indicating that the former two branches are trigeminofacial complexes and the latter is a pure facial nerve. Labeled fibers for NPLL were found in the facial sensory root as well as in bundles projecting to the lateral line areas. The facial fibers of Max.B. and Mand.B. innervate respectively in the dorsal-intermediate portion of the rostral half of the facial lobe, and in the ventral portion of the caudal half of the lobe. Those of Pal.B. however, cover a large area of the lobe anteroposteriorly except for the dorsal and ventral portions. The recurrent fibers of NPLL and the pectoral B. end in the dorsal-medial portion of the caudal half of the lobe. Thus the results of this study show that there is a topographical relation between the receptive field of the 6 peripheral nerve branches and their locus of representation in the facial lobe. Similarly, that the gustatory system through Pal.B. is represented on the facial lobe in a disproportionately large area compared to that of the other 5 branches.

Effects of D1 and D2 dopamine receptor antagonists on cocaine-induced self-stimulation and locomotor activity in rats.

To clarify the involvement of D1 and D2 dopamine systems in intracranial self-stimulation (ICSS) and locomotor activity in rats, we studied the acute effects of cocaine and the interaction between cocaine and dopamine antagonists with respect to these behaviors. Although cocaine (5.0, 10.0, or 20.0 mg/kg) dose-dependently increased locomotor activity, it augmented the rate of ICSS only at 5.0 mg/kg. The failure of high doses of cocaine to augment purpose-oriented behavior such as ICSS may result from its induction of a manic-like state. The D1 dopamine receptor antagonist SCH23390 (0.02, 0.1, or 0.5 mg/kg) or the D2 antagonist nemonapride (0.04, 0.2, or 1.0 mg/kg) significantly decreased cocaine augmentation of ICSS. The higher two doses of either antagonist also produced a significant decrease in cocaine-induced locomotor activity. We therefore suspect that cocaine's augmentative effect on those behaviors, especially ICSS, requires activation of both D1 and D2 dopamine receptors.