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H C Pape

Publications and source records attributed to H C Pape.

133 records · Page 8Linked to original sources
PubMed1987

Lateral excitation in the cat lateral geniculate nucleus.

Visual responses were elicited by global phase reversal stimuli in cells of the cat dorsal lateral geniculate nucleus (dLGN) after small retinal lesions had been centered on each receptive field. After acute lesions of different sizes exclusively lateral inhibition was found. When GABAergic inhibition was blocked by continuous microiontophoretic application of bicuculline lateral excitation emerged in dLGN cells partially deafferented by small and medium size acute retinal lesions, but not in those affected by large lesions. This indicates the presence of excitatory retinal inputs at the periphery of the dLGN cell dendrites which are normally suppressed by strong, long-ranging lateral inhibitory processes. After chronic deafferentation, the remaining excitatory inputs increase in effectiveness and lateral excitation is seen without blockade of inhibition. The maximal lateral spread of excitation (300 micron) in the dLGN is distinctly smaller than the extent of lateral inhibition (1000 micron).

Animals↗
PubMed1987

Local cortical lesions abolish lateral inhibition at direction selective cells in cat visual cortex.

Many cells in the cat visual cortex display a strong selectivity for the direction of motion of an optimally oriented stimulus. Postsynaptic inhibition has been suggested to generate this direction selectivity in simple cells, but the intracortical pathways involved have not been identified. While continuously recording from simple cells in layers 4 and 6, we have inactivated the superficial cortical layers in small regions 0.4-2.5 mm from the cortical column under study by using heat lesions, localized cooling or gamma-aminobutyric acid (GABA) microiontophoresis. When inactivation affected cortical regions retinotopically representing motion in the non-preferred direction towards the receptive field, the responses to movement in this direction increased, and the recorded cells lost direction selectivity due to loss of inhibition. Our results indicate that direction selectivity of simple cells involves asymmetric inhibition of predictable cortical topography.

Animals↗
PubMed1987

Contributions of inhibitory mechanisms to the shift responses of X and Y cells in the cat lateral geniculate nucleus.

1. Adult cats were anaesthetized with a mixture of halothane, nitrous oxide and oxygen to record from single neurones of the dorsal lateral geniculate nucleus (d.l.g.n.) with five-barrel glass micro-electrodes. Periphery effects (shift effects) were elicited by large-field phase-reversing gratings presented in the visual field outside the conventional receptive field area. 2. A range of transient excitatory responses was found in X and Y cells. Y cells had phasic shift effects with significantly higher amplitudes and shorter durations (mean 52 impulses/s, 135 ms) than those observed in the tonic shift effects of X cells (mean 24 impulses/s, 169 ms). All Y cells and most X cells responded to stimulation of remote retinal regions. About 7% of the X cells displayed no shift effect. 3. Micro-ionophoresis of the gamma-aminobutyric acid (GABA) antagonist bicuculline, acetylcholine (ACh) and L-glutamate specifically influenced the shift effects of X and Y cells. 4. During continuous application of the GABA antagonist bicuculline the differences in maximal response rates and amplitudes of X and Y cells were eliminated. The maintained activity raised predominantly in X cells and the early peak rates increased more in X- than in Y-cell shift effects, leading to equal average peak rates of 100 and response amplitudes of about 85 impulses/s in both cell classes. The characteristic time courses of X- and Y-cell responses were not affected. 5. Micro-ionophoretic application of ACh caused a combination of excitatory and disinhibitory effects. Maintained activity as well as early parts of stimulus-evoked responses were similarly raised in X and Y cells. In addition, the Y-cell shift effects became less phasic by elevation of the late response part. Sodium pentobarbitone, used to block ACh excitation, suppressed the ACh-induced effects in the early phase of the X- and Y-cell shift effects and the increase of maintained activity in Y-cells, while the effect on the late part of Y-cell responses persisted. Elevation of background activity partially remained in X cells, and the X-cell responses became tonically prolonged at the same time. 6. L-Glutamate increased the activity of X and Y cells without changing the characteristic shift-effect properties of both cell classes. 7. It is concluded that different short- and long-lasting inhibitory mechanisms shape the responses of d.l.g.n. neurones to stimulation outside the conventional receptive field.(ABSTRACT TRUNCATED AT 400 WORDS)

Acetylcholine↗
PubMed1986

Binocular interactions in the lateral geniculate nucleus of the cat: GABAergic inhibition reduced by dominant afferent activity.

Single cells were recorded in layers A and A1 of the cat dorsal lateral geniculate nucleus (dLGN) with multibarrel micropipettes. Interocular inhibition ("binocular inhibition") was elicited by phase-reversing gratings presented monocularly to the nondominant eye. This inhibition was blocked by microiontophoretic application of bicuculline and thus proven to be GABAergic. Cortical cooling enhanced the inhibition from the nondominant eye. After localized destruction of the receptive field area in the dominant eye, duration and strength of discharge depression were increased. It is concluded that afferent activity from the dominant eye reduces inhibition from the nondominant eye in the dLGN.

Animals↗
PubMed1986

Excitatory and differential disinhibitory actions of acetylcholine in the lateral geniculate nucleus of the cat.

Single neurones were recorded in the dorsal lateral geniculate nucleus (d.l.g.n.) of adult cats anaesthetized with a mixture of halothane, nitrous oxide and oxygen. The multibarrel-glass micro-electrodes were filled with sodium acetate, L-glutamate, acetylcholine (ACh), gamma-aminobutyric acid (GABA) and bicuculline. In normally innervated, spontaneously active d.l.g.n. cells, ACh and L-glutamate elicited increased firing rates. After elimination of the excitatory input from the retina by retinal photocoagulation, the effects of ACh and L-glutamate were similar. This proves that both drugs have direct excitatory effects on d.l.g.n. cells and that disinhibition is not the most prominent influence of ACh in the d.l.g.n. The excitatory action of ACh on relay cells in the d.l.g.n. was strongly influenced by barbiturates. Sub-narcotic levels of sodium pentobarbitone completely abolished the excitation by ACh while the response to L-glutamate remained unchanged. Excitation, centre-surround antagonism and periphery effects were elicited by spots of light and by large field phase-reversing gratings with and without central sparing of the receptive field area. Binocular inhibition was elicited with the phase-reversing grating presented to the non-dominant eye. After localized destruction of the retinal receptive field area, retinogeniculate excitation ceased and an isolated lateral inhibition was observed in the acutely deafferented d.l.g.n. cells. The time course and strength of this inhibition was disclosed by raising the background discharge with microiontophoretically applied L-glutamate. With increasing size of retinal lesions the strength of isolated lateral inhibition decreased exponentially. A maximal intrageniculate range of more than 1000 microns was derived from computations of the lateral extent of deafferentation in the d.l.g.n. The inhibition acted beyond the classic surround inhibition of d.l.g.n. cells and thus was named long-range lateral inhibition. Microiontophoretically applied GABA elicits a strong inhibitory effect at the d.l.g.n. cells which is antagonized by bicuculline. Centre-surround antagonism, binocular inhibition and long-range inhibition were blocked by bicuculline and thus proven to be GABAergic. Each class of inhibition was differentially influenced by microiontophoretically applied ACh. Long-range inhibition was disinhibited, centre-surround antagonism was enhanced, and binocular inhibition was not significantly changed. In contrast to ACh excitation, the disinhibitory action of ACh was not suppressed by pentobarbitone.(ABSTRACT TRUNCATED AT 400 WORDS)

Acetylcholine↗
PubMedDate not supplied

Identification of genes expressed in the amygdala during the formation of fear memory.

In this study we describe changes of gene expression that occur in the basolateral complex of the mouse amygdala (BLA) during the formation of fear memory. Through the combination of a behavioral training scheme with polymerase chain reaction-based expression analysis (subtractive hybridization and virtual Northern analysis) we were able to identify various gene products that are increased in expression after Pavlovian fear conditioning and are of potential significance for neural plasticity and information storage in the amygdala. In particular, a key enzyme of monoamine metabolism, aldehyde reductase, and the protein sorting and ubiquitination factor Praja1, showed pronounced and learning-specific induction six hours after fear conditioning training. Aldehyde reductase and Praja1, including a novel alternatively spliced isoform termed Praja1a, were induced in the BLA depending on the emotional stimulus presented and showed different expression levels in response to associative conditioning, training stress, and experience of conditioned fear. Stress and fear were further found to induce various signal transduction factors (transthyretin, phosphodiesterase1, protein kinase inhibitor-alpha) and structural reorganization factors (e.g., E2-ubiquitin conjugating enzyme, neuroligin1, actin, UDP-galactose transporter) during training. Our results show that the formation of Pavlovian fear memory is associated with changes of gene expression in the BLA, which may contribute to neural plasticity and the processing of information about both conditioned and unconditioned fear stimuli.

Aldehyde Reductase↗