The distribution of the calcium binding proteins parvalbumin and calbindin D-28k was examined in the claustrum of the rat by means of immunohistochemistry. The two proteins displayed a different and largely complementary pattern of distribution. Parvalbumin-immunostaining was intense in the neuropil of the dorsal claustrum and virtually absent in the neuropil of the ventral claustrum; parvalbumin-immunoreactive neuronal cell bodies were relatively numerous in the dorsal claustrum and were detected only occasionally in the ventral region. On the other hand, calbindin-immunostaining was prevalent in the ventral claustrum; very few calbindin-positive neurons were seen in the dorsal sector of the nucleus, whereas they were relatively more numerous in the ventral claustrum. The cell bodies of the majority of the claustral parvalbumin- or calbindin-immunoreactive neurons were oval or round, but immunostained polymorphous neurons were also observed. The surface of the immunopositive dendritic branches was smooth, with no evidence of spines. Fluorescent retrograde tracing was combined with immunohistofluorescence to determine whether the parvalbumin-containing claustral cells project to the frontoparietal cortex. Neurons labelled after large fluorogold injections in frontoparietal cortical fields were highly intermingled in the dorsal claustrum with parvalbumin-immunoreactive cells but the two neuronal populations were separate. These data show that parvalbumin-immunoreactive claustral neurons do not project to the frontoparietal cortex. In addition, although these cells may project to other cortical or subcortical targets, the present findings suggest that they may represent, at least in part, local circuit claustral neurons, corresponding to the aspiny intrinsic neurons described in the rat claustrum in studies based on Golgi impregnation.

Animals↗

PubMedDate not supplied

The influence of chronic moderate ethanol administration on NADPH-diaphorase (nitric oxide synthase) activity in rat brain.

Nitric oxide synthase (NOS), the enzyme with reduced nicotinamide-adenine dinucleotide phosphate (NADPH)-diaphorase activity, generates nitric oxide (NO) which is an important bioregulatory molecule in the nervous, immune, and cardiovascular systems. NOS is linked to non-adrenergic non-cholinergic (NANC) neuronal pathways and modulation of the N-methyl-D-aspartate receptors, yet its modification by ethanol has been little explored. A possible modification by chronic ethanol administration of activity and/or localization of NADPH-diaphorase (NO-synthase) in rat brain may thus provide the pathogenic basis of alcohol-induced brain injury. When female Wistar rats were treated chronically with ethanol for 50 days, the NADPH-diaphorase staining of granular neurons and neurons located in the molecular layer of the cerebral cortex was significantly reduced. Chronic ethanol consumption led to a significant reduction in NADPH-diaphorase staining in the superficial layers of the superior colliculus. The number of NADPH-diaphorase-positive neurons was significantly reduced (P < 0.001) in the stratum zonale and stratum griseum superficiale (by 42.3-65.6% of control values). This could alter synaptic processes in the highly organized structures involved in oculomotor and somatic motor coordination and thus contribute to the motor disturbances which are associated with alcohol abuse.

Analysis of Variance↗

PubMedDate not supplied

Neocortical projections to the amygdala. (An experimental study with the Nauta method).

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Amygdala↗