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Biomedical subjects

Y Ben-Ari

Publications and source records attributed to Y Ben-Ari.

At least 325 records · Page 18Linked to original sources
PubMed1979

Morphine withdrawal syndrome: differential participation of structures located within the amygdaloid complex and striatum of the rat.

The participation of amygdaloid and striatal structures in the various signs of morphine withdrawal syndrome (MWS) has been investigated using two complementary approaches: intracerebral application of naloxone in various nuclei of dependent rats and effects of various lesions and transections on systemically induced MWS. In morphine dependent rats local application of naloxone (10 micrograms in 0.1 microliter solution) in the vicinity of either the central nucleus of the amygdala or the lateral anterior nucleus but not in adjacent amygdaloid or striatal nuclei elicited the jump sign. Diarrhea was more frequently elicited by application of naloxone in the striatum or centromedial amygdala than the basolateral parts of the complex. In contrast, there was no specific anatomical correlates to the remaining signs including wet shakes, paw tremor, teeth chattering and chewing. Bilateral electrolytic lesion of the central amygdala or combined transection of the stria terminalis and so-called ventral amygdalofugal pathway eliminated the jump without affecting the remaining signs. In contrast a large bilateral destruction of the entire striatrum did not significantly affect the various signs. Bilateral transection of the stria terminalis reduced only the occurrence of the wet shakes. Also, a transection of the medial forebrain bundle considerably reduced the 3 main signs, i.e. jump, wet shakes and diarrhea. These results suggest that, in analogy to the acute actions of morphine, MWS should not be considered as a unitary phenomenon but as an ensemble of signs which probably reflect the intense activation induced by naloxone in a number of brain sites consequent to the abrupt interruption of opioid actions in a dependent animal. The significance of these results is discussed with reference to previous anatomical, biochemical and behavioural studies performed on the amygdala.

Amygdala↗
PubMed1979

Afferent connections to the amygdaloid complex of the rat and cat. I. Projections from the thalamus.

By the use of the retrograde transport of horseradish peroxidase (HRP), the projections from the thalamus to the amygdala were investigated in the rat and cat, with main emphasis on the former species. HRP was injected stereotactically by microiontophoresis in the various amygdaloid nuclei. Several control procedures including the use of different approaches for the introduction of the micropipette were undertaken to eliminate the possibility of misinterpretation due to uptake of the protein by adjacent structures or fibers en passant. The paraventricular and paratenial nuclei of the thalamus were found to project throughout the entire amygdaloid complex. The medial geniculate complex and the basal nucleus of the ventromedial complex (the thalamic taste relay) mainly project to the centromedial part of the amygdala. The basolateral nucleus is the main recipient of a hitherto undescribed bilateral thalamo-amygdaloid pathway originating in the interanteromedial nucleus. The parafasciculare nucleus projects to the central nucleus of the amygdala; in the cat mainly to the lateral subdivision of the central nucleus. The findings are discussed in relation to previous anatomical and electrophysiological studies centered on the amygdaloid complex. Special reference is made to the possible role of the thalamo-amygdaloid connections in the conveyance of sensory information to the amygdala.

Afferent Pathways↗
PubMed1979

Choline acetyltransferase and acetylcholinesterase containing projections from the basal forebrain to the amygdaloid complex of the rat.

The origin of the cholinergic innervation to the amygdaloid complex was investigated with the use of acetylcholinesterase (AChE) histochemistry and choline acetyltransferase (ChAT) assay of microdissected nuclei. Visualization of AChE-positive neurones in the ventral forebrain was facilitated by pretreatment of rats with 1.5 mg/kg di-isopropyl phosphofluoridate (DFP). The AChE-positive neurones in the ventral forebrain are distributed in a continuous system from the septum through the lateral preoptic area to the entopeduncular nucleus caudally. Knife cuts or kainic acid injections (1.5 microgram/l microliter) placed in the lateral preoptic area resulted in substantial depletion of the AChE and ChAT content of the amygdala nuclei. Kainic acid injections (1.5 microgram/l microliter) in the diagonal band area or cuts through the stria terminalis dorsally did not significantly modify the AChE staining or ChAT content of the amygdala (although diagonal band injections partially depleted the hippocampus of ChAT). Knife cuts severing both the so-called ventral pathway and the stria terminalis did not produce significantly greater ChAT depletion in the amygdala than those produced by the knife cuts or kainic acid injections in the lateral preoptic area. Parasagittal knife cuts undercutting the lateral pyriform cortex also failed to modify the AChE or ChAT content of the amygdala, but they depleted the undercut cortex of both ChAT and AChE; AChE-positive material accumulated ventrally and medially to the knife cut. It is suggested that the major source of the cholinergic innervation of the amygdala is the magnocellular AChE-positive neurones in the lateral preoptic area and adjacent regions of the ventral forebrain.

Acetylcholinesterase↗
PubMed1979

[Primary and secondary cerebral lesions produced by kainic acid injections in the rat].

Systematic (i. p.) or intra-amygdaloid injections of kainic acid elicit typical generalised convulsive seizures with typical electrographic correlates. Depending on the survival time and the amount of neurotoxin administered, secondary pathological damage is invariably found in various brain structures removed from the injection site such as various hippocompal fields, midline thalamic nuclei and neocortical layers III and VI. Various lines of evidence are reported which suggest that the secondary pathological damage is not due to the spread of the neurotoxin but to the epileptic status it induces.

Amygdala↗
PubMed1978

[Epileptogenic action of intra-amygdaloid injection of kainic acid].

Intra-amygdaloid unilateral application of low doses of kainic acid rapidly elicits, in both chronic and acute conditions, secondarily generalized convulsive seizures which often culminate in fatal true status epilepticus unless appropriate anti-epileptic drugs are provided. Spontaneous recurrent seizures are observed for several hours starting approximately 10 min. after the application of kainic acid. In addition to the primary degeneration in the amygdaloid complex, a secondary cell loss is seen in CA3 area of the dorsal hippocampus. It is suggested that this procedure may constitute a particularly suitable model for the study of true focalized status epilepticus.

Amygdala↗
PubMed1977

Histamine synthesizing afferents within the amygdaloid complex and bed nucleus of the stria terminalis of the rat.

The regional distribution of histidine decarboxylase (HD) activity has been studied in the amygdaloid complex and the bed nucleus of the stria terminalis (BST) of the rat. The central and medial nuclei of the amygdala had 2-fold higher HD activity levels than the remaining nuclei of the complex. HD activity was exceptionally high in the BST, particularly in its ventral part. A lesion of the stria terminalis had no effect on this distribution whereas a combined lesion of the stria terminalis and the so-called ventral pathway induced a decrease of approximately 60% in all the amygdaloid nuclei, but not in the BST. On the other hand, a lesion of the medial forebrain bundle (MFB) induced a similar decrease in both the amygdaloid nuclei and the BST. These results confirm that HD-containing fibres are present in the MFB. On the one hand these project massively to the BST and on the other penetrate in the amygdala ventromedially along the ansa peduncularis and preferentially innervate the more medially located nuclei.

Afferent Pathways↗
PubMed1977

Regional distribution of choline acetyltransferase and acetylcholinesterase within the amygdaloid complex and stria terminalis system.

The distribution of "marker" enzymes for cholinergic neurons has been studied in 10 subdivisions of the amygdaloid complex of the rat brain. Choline acetyltransferase activity was measured using a radiochemical method in samples dissected from fresh serial sections. Acetylcholinesterase was studied using a histochemical procedure. Both enzymes had similar patterns of distribution within the amygdaloid complex and were most concentrated in the posterior lateral and basolateral nuclei and in the nucleus of the lateral olfactory tract. These enzymes were much less concentrated in the cortical, medial, central, and basomedial nuclei. Large differences in acetylcholinesterase staining were found within the lateral posterior and the basolateral nuclei and within the pyriform cortex. Biochemical studies showed a parallel distribution of choline acetyltransferase within these nuclei. The results indicate that cholinergic neural elements in the amygdala are concentrated primarily in the basolateral complex and suggest that this region may be innervated by cholinergic fibers traveling in the ventral amygdalo-fugal pathway.

Acetylcholinesterase↗
PubMed1977

Electrical stimulation of preganglionic nerve increases tyrosine hydroxylase activity in sympathetic ganglia.

The effect of synaptic stimulation on tyrosine hydroxylase [tyrosine 3-monooxygenase: L-tyrosine, tetrahydropteridine:oxygen oxidoreductase (3-hydroxylating), EC 1.14.16.2] activity in the rat superior cervical ganglion was studied. The preganglionic cervical sympathetic trunk was stimulated unilaterally at 10 Hz for 30 min. Forty-eight hours later tyrosine hydroxylase activity was 33% higher on the stimulated than on the control side. The enzyme activity restimulated than on the control side. The enzyme activity remained elevated in the stimulated ganglia for 2 days. No change was observed in total ganglion protein. Comparable increases in tyrosine hydroxylase activity were observed in anesthetized and conscious animals.

Afferent Pathways↗