Biomedical subjects

J Bolz

Publications and source records attributed to J Bolz.

57 records · Page 4Linked to original sources

PubMed1980

Evoked potentials, expectancy wave, and skin resistance in depressed patients and healthy controls.

Averaged evoked potentials, expectancy waves and number and amplitude of skin resistance responses to auditory stimuli are found to be significantly smaller in a group of 18 patients with primary depression than in 27 healthy controls. AEP amplitude attenuation is shown not to be an averaging artifact, due to varying response latencies. There are no simple relations between electrocortical and electrodermal parameters, but patients display more significant correlations between these two sets of variable than controls. Amplitude attenuations are interpreted as hyporesponsivity resulting from depressive inhibition. The narrower coupling of variables in the depressed group is viewed as a limitation in physiological plasticity.

Acoustic Stimulation↗

PubMedDate not supplied

Generation of end-inhibition in the visual cortex via interlaminar connections.

To understand the mechanisms by which the receptive field properties of visual cortical cells are generated, one must consider both the thalamic input to the cortex and the intrinsic cortical connections. In the cat striate cortex, layer 4 is the main recipient of input from the lateral geniculate nucleus, yet the cells in that layer possess several receptive field properties that are distinct from the geniculate input, including orientation specificity, binocularity, directionality and end-inhibition, the last of which allows cells to respond to edges of a restricted length. These properties could be generated by connections within the layer, by its input from the claustrum or by the massive projection that layer 4 receives from layer 6. In the present study, we attempted to determine the functional role of the layer 6 to layer 4 projection by reversible inactivation of layer 6 using the inhibitory transmitter gamma-aminobutyric acid (GABA). After inactivating layer 6, cells in layer 4 lost end-inhibition. Cells in layer 2 + 3, which receive their principal input from layer 4, were similarly affected. The elimination of end-inhibition was specific, other receptive field properties, such as direction selectivity or orientation specificity, remaining intact.

Animals↗

PubMedDate not supplied

Substance P-immunoreactive retinal ganglion cells and their central axon terminals in the rabbit.

Retinal ganglion cells are the projection neurons that link the retina to the brain. Peptide immunoreactive cells in the ganglion cell layer (GCL) of the mammalian retina have been noted but their identity has not been determined. We now report that, in the rabbit, 25-35% of all retinal ganglion cells contain substance P-like (SP) immunoreactivity. They were identified by either retrograde transport of fluorescent tracers injected into the superior colliculus, or by retrograde degeneration after optic nerve section. SP immunoreactive cells are present in all parts of the retina and have medium to large cell bodies with dendrites that ramify extensively in the proximal inner plexiform layer. Their axons terminate in the dorsal lateral geniculate nucleus, superior colliculus and accessory optic nuclei, and these terminals disappear completely after contralateral optic nerve section and/or eye enucleation. In the dorsal lateral geniculate nucleus large, beaded, immunoreactive axons and varicosities make up a narrow plexus just below the optic tract, where they define a new geniculate lamina. The varicosities make multiple synaptic contacts with dendrites of dorsal lateral geniculate nucleus projection neurons and presumptive interneurons in complex glomerular neuropil. This is direct evidence that some mammalian retinal ganglion cells contain substance P-like peptides and strongly suggests that, in the rabbit, substance P (or related tachykinins) may be a transmitter or modulator in a specific population or populations of retinal ganglion cells.

Animals↗