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Biomedical subjects

B D Waterhouse

Publications and source records attributed to B D Waterhouse.

At least 19 recordsLinked to original sources
PubMed2004

A matter of focus: monoaminergic modulation of stimulus coding in mammalian sensory networks.

Although the presence of neuromodulators in mammalian sensory systems has been noted for some time, a groundswell of evidence has now begun to document the scope of these regulatory mechanisms in several sensory systems, highlighting the importance of neuromodulation in shaping feature extraction at all levels of neural processing. The emergence of more sophisticated models of sensory encoding and of the interaction between sensory and regulatory regions of the brain will challenge sensory neurobiologists to further incorporate a concept of sensory network function that is contingent on neuromodulatory and behavioral state.

Action Potentials↗
PubMed2001

Topographic organization and neurochemical identity of dorsal raphe neurons that project to the trigeminal somatosensory pathway in the rat.

The primary goals of this study were to: 1) examine the distribution of neurons within the dorsal raphe (DR) nucleus that project to cortical and subcortical sites along the trigeminal somatosensory pathway in rat; 2) determine the extent to which different regions within this ascending sensory system receive collateral projections from the same DR neuron; and 3) identify the putative transmitters contained within these DR projection neurons. Long-Evans hooded rats received pressure injections of various combinations of retrograde fluorescent tracers; into the whisker-related regions of the primary somatosensory cortex (barrel field cortex [BC]), ventral posterior medial thalamus (VPM), and principal nucleus of the trigeminal complex (PrV). The distribution of retrogradely labeled neurons within the DR was examined by fluorescence microscopy. The major finding was that cortically projecting neurons were located within the midline regions of the rostral portion of the DR, whereas cells projecting to subcortical trigeminal somatosensory structures were distributed bilaterally in the lateral wing regions of the DR as well as in the midline portions of the nucleus. Single neurons that send axon collaterals to multiple cortical and subcortical trigeminal somatosensory targets were observed in the dorsomedian and ventromedian regions of the DR. DR neurons that projected to cortical and subcortical sites contained serotonin but not tyrosine hydroxylase, the marker enzyme for catecholamine transmitters. Taken together, these findings provide further evidence of neurochemical specificity and functional anatomical organization within the DR efferent projection system.

Animals↗
PubMed2001

Evidence that dopamine-beta-hydroxylase immunoreactive neurons in the lateral reticular nucleus project to the spinal cord in the rat.

The existence of noradrenergic projections from the lateral reticular nucleus (LRt) to the dorsal quadrant of cervical, thoracic, or lumbar spinal cord was investigated using a combined method of WGA-apo-HRP-gold retrograde tracing and dopamine-beta-hydroxylase (DBH) immunocytochemistry. Preliminary retrograde tracing studies indicated that LRt neurons projecting to cervical, thoracic, or lumbar spinal cord were characteristically located near the perimeter of the LRt. Double-labeling experiments demonstrated that a portion of these peripherally-located, spinal-projecting neurons were DBH-immunoreactive. Double-labeled neurons were also located at the parvocellular division of the contralateral LRt in the thoracic injection cases. Double-labeled neurons were not observed at the subtrigeminal division in cervical, thoracic, or lumbar injection case. The results suggest the possibility that the noradrenergic LRt-spinal pathway might be involved in a variety of pain processing and cardiovascular regulatory functions in the rat.

Afferent Pathways↗
PubMed2000

Effects of intravenous cocaine administration on cerebellar Purkinje cell activity.

The goal of the present study was to investigate the effects of intravenous cocaine administration on cerebellar Purkinje cell firing. Extracellular neuron activity was recorded and cells were locally excited with spaced microiontophoretic pulses of glutamate. Glutamate-evoked and spontaneous discharges were compared before and immediately following cocaine administration. Cocaine injections (1. 0 and 0.25 mg/kg, i.v.) induced a reversible suppression of both spontaneous activity and glutamate-evoked excitation. Procaine was ineffective in producing similar actions. Cocaine only inhibited glutamate-induced excitation in animals pre-treated with reserpine (5 mg/kg, i.p.). Propranolol injections (10 mg/kg, i.p.) were ineffective in blocking cocaine-induced inhibitions. Yohimbine (5 mg/kg, i.p.) pre-treatment abolished cocaine-induced suppressions of either spontaneous or glutamate-evoked excitation. Therefore, cocaine administration decreases Purkinje cell spontaneous and glutamate-evoked discharges by a mechanism involving alpha(2)-adrenoceptor activation. It is suggested that by changing the normal function of the cerebellum cocaine can produce drug-related alterations in overt behavior and cognition.

Action Potentials↗
PubMed2000

Norepinephrine exhibits two distinct profiles of action on sensory cortical neuron responses to excitatory synaptic stimuli.

Located within the central gray of the caudal pons, the locus coeruleus (LC) is the sole source of norepinephrine (NE) projections to the forebrain. NE is released both tonically and phasically from axonal varicosities in LC efferent target circuits. NE has been shown to produce a diverse set of actions, including suppression of spontaneous and stimulus evoked discharge, augmentation of synaptically evoked excitation, and inhibition and gating of otherwise subthreshold synaptic inputs. Utilizing an extracellular in vitro tissue slice preparation and microiontophoretic techniques, the dose-dependent actions of NE on glutamate-evoked discharges of layer II/III and layer V sensory cortical neurons were investigated. Noradrenergic effects were further examined in terms of cell and adrenoceptor specificity. The results indicate two exclusive modulatory actions of NE: 1) ejection current-dependent suppression of glutamate evoked discharge, and 2) ejection current-dependent facilitation of glutamate-evoked discharge followed by suppression of the maximal facilitated response. These effects were observed in both normal and low Ca(2+) / high Mg(2+) bathing media, suggesting a postsynaptic site for NE's actions. The facilitation of glutamate evoked discharge was selectively mimicked by the alpha-1 agonist, phenylephrine, whereas the dose-dependent suppression was mimicked by the beta-agonist isoproterenol. These results suggest that the suppressant and facilitating actions of NE are mediated by beta and alpha-1 receptors, respectively. In general, these results are consistent with previous demonstrations of NE modulatory actions on central neurons, but indicate that in the cerebral cortex these effects are both cell- and receptor-specific.

Adrenergic alpha-Agonists↗
PubMed2000

Differential modulatory effects of norepinephrine on synaptically driven responses of layer V barrel field cortical neurons.

The effects of norepinephrine (NE) and the alpha-1 agonist phenylephrine (PE) on synaptically evoked responses of electrophysiologically identified pyramidal neurons in layer V of rat somatosensory cortex were studied in brain slices using intracellular recording techniques. When added to the bathing medium NE (10 microM) tended to increase the synaptic responsiveness of regular spiking neurons and decrease the responsiveness of intrinsic burst neurons. NE had mixed effects on layer V cells which were characterized as intermediate types between regular spiking and intrinsic burst neurons. PE exerted a similar spectrum of actions on layer V cortical neurons. For both adrenergic agents the greatest facilitating effect was observed on responses to low intensity synaptic stimulation. These results suggest that NE exerts different modulatory actions on different electrophysiologically-defined classes of layer V sensory cortical neurons.

Action Potentials↗
PubMed1999

Origin, distribution, and morphology of galaninergic fibers in the rodent trigeminal system.

The neuropeptide galanin (Gal) is found throughout the central nervous system. Of particular interest is the fact that Gal is present within the majority of noradrenergic locus coeruleus (LC) neurons. However, very few, if any, Gal-immunoreactive fibers have been identified in many of the major efferent targets of LC, including sensory neocortex and dorsal thalamus. The goal of the present study was to examine the Gal fiber innervation of the rodent trigeminal somatosensory system and its connection to the LC. Our results show that at least two different morphological profiles of Gal-immunoreactive fibers are present within relay nuclei along the ascending trigeminal pathway. Numerous small caliber Gal-immunoreactive fibers with bouton-like swellings were noted within the barrel cortex, the ventroposterior medial (VPM) nucleus, the posterior medial (POm) nucleus, the zona incerta (ZI), the reticular nucleus (nRT) of the thalamus, and the principal (PrV) and spinal (SpV) nuclei of the trigeminal complex. Immunoreactive fibers were prevalent in, but not restricted to, layer I of the barrel cortex. Within the somatosensory thalamus, the density of Gal-immunoreactive fibers was higher in POm than in VPM. Laminae I and II of SpV and the nRT and ZI also contained dense, large-diameter Gal-immunoreactive fibers. These large-diameter Gal-immunoreactive fibers did not co-contain dopamine beta-hydroxylase (DBH). In contrast, virtually every small-caliber Gal-immunoreactive fiber colocalized with DBH. To determine whether Gal-immunoreactive fibers originated from LC, we combined immunohistochemical procedures with fluorescent tracing techniques. After retrograde tracer injections into several trigeminal relay nuclei, we observed that approximately 50% of the labeled LC neuronal population was immunoreactive for Gal. Our results suggest an extensive Gal-immunoreactive fiber innervation of the rodent trigeminal system, much of which may originate from LC neurons in the brainstem.

Afferent Pathways↗
PubMed1998

Projection patterns from the raphe nuclear complex to the ependymal wall of the ventricular system in the rat.

The goal of the present study was to characterize the anatomical and neurochemical relationships that the raphe nuclear complex maintains with respect to lateralized and centralized components of the ventricular system. From this investigation, we 1) determined the ipsilateral vs. contralateral distribution of raphe efferents to the ependymal wall of the lateral ventricle, 2) assessed the degree of collateralization of individual ependymal projection neurons to other sites along the ventricular path, 3) compared the topography of raphe neurons that project to the ventricular lining as well as the lumen of the fourth and lateral ventricles, and 4) evaluated the neurochemical identity of raphe neurons that innervate the ventricular system. After tracer injections into the lateral ventricle, labeled cells were distributed evenly on both sides of the midline in the dorsomedial subregion of the intermediate dorsal raphe nucleus. Further rostrally, labeled cells were clustered bilaterally above the medial longitudinal fasciculi and extended into the median raphe nucleus. Injections that involved the ependymal wall of the lateral ventricle resulted in prominent ipsilateral labeling within the dorsal raphe nucleus, just ventral to the cerebral aqueduct. Most of the labeled cells in this latter group had collateral projections to other sites along the ventricular path. Most of the ventricle projection cells contained serotonin but not nicotinamide adenine dinucleotide phosphate diaphorase. These findings indicate that the raphe nuclear complex is topographically organized with respect to the ventricular system. Selected subsets of serotoninergic dorsal raphe neurons may influence discrete segments of the ventricular system independently as well as coordinate functions throughout the system through axon collaterals to other sites along the ventricular neuraxis.

Animals↗
PubMed1998

Systemically administered cocaine alters stimulus-evoked responses of thalamic somatosensory neurons to perithreshold vibrissae stimulation.

Previous studies have shown that systemically administered cocaine can transiently alter responses of primary somatosensory cortical neurons to threshold level stimulation of peripheral receptive fields. The goal of the present investigation was 2-fold: (1) characterize the effects of systemic cocaine on stimulus-evoked responses of the ventral posterior medial (VPM) thalamic neurons which relay somatosensory information to the cortex and (2) determine the time course and magnitude of changes in monoamine levels within the somatosensory thalamus following systemic administration of cocaine. Extracellularly recorded responses of single VPM thalamic neurons to whisker stimulation were monitored before and after cocaine administration in halothane anaesthetized rats. Each cell was first characterized by assessing its response profile to a range of perithreshold level deflections of the optimal whisker on the contralateral face. Drug effects on stimulus-response curves, response magnitude and latency were determined from quantitative analysis of spike train data. The results indicate that cocaine elicits a predictable augmentation or attenuation of the sensory response magnitude, with the direction of the change inversely related to the initial magnitude of the stimulus-evoked discharge. In addition, cocaine consistently reduced the response time of somatosensory thalamic neurons to peripheral receptive field stimulation. At the same dose and over the same time period, cocaine also produced marked elevation of norepinephrine and serotonin levels within the ventrobasal thalamus, as determined by in vivo microdialysis. These results suggest that cocaine-induced increases in norepinephrine and serotonin are responsible for drug-related modulation of the transfer of sensory signals through primary thalamocortical relay circuits.

Animals↗
PubMed1998

Phasic activation of the locus coeruleus enhances responses of primary sensory cortical neurons to peripheral receptive field stimulation.

In the present study we examined the effects of phasic activation of the nucleus locus coeruleus (LC) on transmission of somatosensory information to the rat cerebral cortex. The rationale for this investigation was based on earlier findings that local microiontophoretic application of the putative LC transmitter, norepinephrine (NE), had facilitating actions on cortical neuronal responses to excitatory and inhibitory synaptic stimuli and more recent microdialysis experiments that have demonstrated increases in cortical levels of NE following phasic or tonic activation of LC. Glass micropipets were used to record the extracellular activity of single neurons in the somatosensory cortex of halothane-anesthetized rats. Somatosensory afferent pathways were activated by threshold level mechanical stimulation of the glabrous skin on the contralateral forepaw. Poststimulus time histograms were used to quantitate cortical neuronal responses before and at various time intervals after preconditioning burst activation of the ipsilateral LC. Excitatory and postexcitatory inhibitory responses to forepaw stimulation were enhanced when preceded by phasic activation of LC at conditioning intervals of 200-500 ms. These effects were anatomically specific in that they were only observed upon stimulation of brainstem sites close to (>150 micron) or within LC and were pharmacologically specific in that they were not consistently observed in animals where the LC-NE system had been disrupted by 6-OHDA pretreatment. Overall, these data suggest that following phasic activation of the LC efferent system, the efficacy of signal transmission through sensory networks in mammalian brain is enhanced.

Animals↗
PubMed1997

Lateralization and functional organization of the locus coeruleus projection to the trigeminal somatosensory pathway in rat.

The primary goals of this study were to (1) examine the distribution of locus coeruleus (LC) neurons, which project to cortical and subcortical sites along the trigeminal somatosensory pathway in rats, and (2) determine the extent to which different regions within this ascending sensory system receive collateral projections from the same LC neuron. Long-Evans hooded rats received unilateral pressure injections of different combinations of retrograde fluorescent tracers into whisker-related regions of primary (SI) and secondary (SII) somatosensory cortices, the ventrobasal (VB) and posterior group (POm) nuclei of the thalamus, and the principalis nucleus of the trigeminal complex (PrV). Coronal sections (40-100 microm) through the LC were examined by fluorescence microscopy, and the distribution of retrogradely labeled cells was recorded. The major finding was that whisker-related regions of the cortex receive efferent projections from neurons concentrated in the caudal portion of the ipsilateral LC, whereas subcortical trigeminal somatosensory structures receive bilateral input from both LC nuclei. Despite the bilateral nature of the LC projection to subcortical sites, the majority of LC efferents to VB and POm thalamus originate in the ipsilateral LC nucleus, whereas projections to PrV originate primarily from the contralateral LC. An additional finding was that a relatively large proportion of LC cells, which project to a single somatosensory structure, also send axon collaterals to other relay sites along the same ascending somatosensory pathway. Taken together, these results suggest that the LC-noradrenergic system maintains a more selective relationship with functionally related efferent targets than has been previously appreciated.

Animals↗
PubMed1996

Monoaminergic substrates underlying cocaine-induced enhancement of somatosensory-evoked discharges in rat barrel field cortical neurons.

Previously, we have described a selective potentiating effect of systemically administered cocaine (0.25-1.0 mg/kg i.v.) on long-latency excitatory responses (E2) of rat "barrel field" cortical neurons to mystacial vibrissae stimulation. The rat trigeminal system receives both norepinephrine (NE) and serotonin (5-HT)-containing afferents, but only minimal input from dopaminergic sources. The goal of the present study was to determine which of these monoamine systems was responsible for the previously observed facilitating action of cocaine on E2 responses of barrel field cortical neurons. Two approaches were used: 1) evaluation of cocaine effects on cortical neuron responses to whisker stimulation in NE- or 5-HT-depleted animals and 2) assessment of the effects of selective monoamine uptake blockers on cortical neuron responses to whisker deflection. Extracellular recordings were obtained from spontaneously active neurons in the barrel field cortex of halothane-anesthetized rats. Spontaneous activity and cellular responses to mechanical displacement of a single whisker were monitored before and after systemic (i.v.) administration of either cocaine or one of the following selective uptake blockers, fluoxetine (5-HT), desipramine (NE) and GBR12909 (dopamine). Cocaine-induced increases in the E2 response were observed in N-(2-chloroethyl)-N-ethyl-2-bromobenzylamine (DSP4, noradrenergic neurotoxin)-treated animals, but were reduced or abolished in p-chlorophenylalanine-treated (5-HT depletion) rats. Fluoxetine and desipramine, but not GBR12909, produced cocaine-like potentiation of the E2 response to whisker stimulation. These results point to a 5-HT-dependent mechanism as the substrate underlying cocaine's facilitating effects on long-latency somatosensory cortical neuron responses to receptive field stimulation.

Animals↗
PubMed1995

Effects of systemic and local ethanol on responses of rat cerebellar Purkinje neurons to iontophoretically applied gamma-aminobutyric acid.

The goals of this study were: (1) to determine the effects of acute systemic or local application of ethanol (ETOH) on the response of cerebellar Purkinje cells (P-cells) to iontophoretically applied gamma-aminobutyric acid (GABA) and (2) to characterize the effects of Ro15-4513, a putative antagonist of ETOH-GABA interactions, on ETOH-induced changes in GABA responsiveness. Male Sprague-Dawley rats (230-370 g) were anesthetized with halothane and implanted with intraperitoneal catheters for administration of ETOH (1.0-2.0 g/kg), before the recording session. Extracellular activity of single P-cells was recorded with the central barrel of a five-barrel micropipette, the other barrels of which were used for microiontophoresis of GABA and electro-osmosis of ETOH at the recording site. Spontaneous discharge and response of P-cells to GABA were monitored during a pre-ETOH control and for 1-1.5 h after systemic or electro-osmotic administration of ETOH. Transient suppression of spontaneous P-cell discharge was usually observed within 4-8 min of systemic ETOH injection. This effect lasted 2-4 min in 10 out of 19 rats tested. GABA-mediated inhibitory responses of cerebellar P-cells were increased by 45-50% relative to pre-ETOH values at 10 and 90 min post-ETOH injection. Prior administration of the imidazobenzodiazepine Ro15-4513 (4-6 mg/kg) failed to antagonize either the ETOH-induced enhancement of GABA-mediated inhibition or the transient inhibition of spontaneous P-cell activity rat cerebellar P-cell produced by ETOH. In these studies, electro-osmotically applied ETOH produced a potent suppression of spontaneous P-cell activity which precluded further augmentation of unit responses to GABA. These results show that doses of systemically administered ETOH which are mildly intoxicating in the awake, behaving animal, enhance the inhibitory action of GABA on cerebellar P-cell discharge.

Action Potentials↗
PubMed1995

Effects of systemic and local ethanol on responses of rat cerebellar Purkinje neurons to iontophoretically applied norepinephrine and gamma-aminobutyric acid.

The goal of the present study was to determine the effect of acute ethanol (ETOH), administered intraperitoneally or electro-osmotically, on norepinephrine (NE) induced increases in gamma-aminobutyric acid (GABA) mediated inhibition of single cerebellar Purkinje neurons (P-cells). Male Sprague-Dawley rats (230-370g) were anesthetized with halothane and implanted with an intraperitoneal catheter for systemic administration of ETOH (1.0-1.5 g/kg) prior to the recording session. Extracellular activity of single P-cells was recorded before and after iontophoresis of GABA and NE using five-barrel glass micropipettes. GABA was administered at the recording site by microiontophoretic pulses before, during and after continuous iontophoretic application of NE. Spontaneous discharge, GABA responses and NE-GABA interactions in P-cells were monitored for each experiment before and 1-1.5 h following systemic administration of ETOH. As in our previous reports administration of NE, at low ejection currents (10-60 nA), augmented GABA mediated suppression of P-cell spontaneous discharge. Between 10 and 60 min after injection of ETOH, this NE induced augmentation of GABA inhibition was further potentiated. This potentiation involved increases in both the magnitude and the duration of the GABA inhibition observed after NE alone. NE-induced augmentation of GABA inhibition persisted for 2-13 min longer after ETOH administration than in the pre-ETOH control period. Local electro-osmotic application of ETOH, which resulted in strong depression of spontaneous activity and caused small increases in GABA-mediated inhibition, did not directly potentiate NE-induced augmentation of GABA action. These results indicate that NE-mediated augmentation of GABA inhibition of P-cell activity is potentiated following systemic, but not local, ETOH administration.

Action Potentials↗
PubMed1995

Noradrenergic enhancement of GABA-induced input resistance changes in layer V regular spiking pyramidal neurons of rat somatosensory cortex.

Previous in vivo studies have shown that microiontophoretic application of norepinephrine (NE) and isoproterenol (ISO) can enhance gamma-aminobutyric acid (GABA)-induced depressant responses of rat somatosensory cortical neurons. In the present investigation we have examined the transmembrane electrophysiological events which are associated with interactions between NE and GABA in layer V pyramidal neurons of rat barrel field cortex. Intracellular recordings were made from electrophysiologically identified cells in a superfused cortical tissue slice preparation before, during and after bath or microdrop application of GABA, NE and ISO, alone or in combination. GABA application produced a small depolarization from resting membrane potential associated with a reduction (22%) in input resistance. NE and ISO (10-100 microM) also produced in some cases small membrane depolarizations (1-4 mV) but little concomitant changes in input resistance. Simultaneous application of NE with GABA potentiated amino acid-induced changes in input resistance in 4 cases and antagonized (n = 4) or had no effect (n = 4) on GABA-associated membrane events in 8 other cases. When the alpha-blocker, phentolamine (20 microM), was added to the medium, NE-induced enhancement of the GABA response was observed in 3 of 5 cases (60%), suggesting both, a beta-adrenergic mediation and a possible alpha-receptor masking of this noradrenergic-potentiating action. Consistent with this interpretation was the finding that the beta-agonist, ISO (10-100 microM), produced net increases in GABA-induced input resistance changes in 64% of cases tested (9 of 14). The potentiating effect of NE and ISO was mimicked by the adenyl cyclase activator, forskolin (n = 2), and a membrane permeant analog of cyclic-AMP, 8-bromo-cyclic AMP (n = 3); and could also be demonstrated when the GABAA agonist muscimol (0.5-1 microM) was substituted for GABA. The reversal potential for GABA and GABA + NE remained the same. These findings suggest that previous demonstrations of NE-potentiating effects on GABA inhibition may be mediated by beta-receptor/cyclic-AMP-linked actions on mechanisms which regulate GABAA receptor-induced membrane conductance changes.

8-Bromo Cyclic Adenosine Monophosphate↗
PubMed1995

Systemically administered cocaine selectively enhances long-latency responses of rat barrel field cortical neurons to vibrissae stimulation.

Prominent among cocaine's psychostimulant actions are its abilities to heighten awareness of the sensory surround and induce sensory hallucinations. Although many studies have examined the cellular actions of cocaine in "reward" circuits of the brain, few have investigated the impact of cocaine on neuronal function in primary sensory circuits. The goal of this study was to characterize the effects of cocaine on somatosensory cortical neuronal responsiveness to peripheral activation of afferent synaptic pathways. Extracellular recordings were obtained from spontaneously active single units in the barrel field cortex of halothane-anesthetized rats. The spontaneous firing rate and cellular responses to mechanical displacement of a single whisker on the contralateral face were monitored before and after systemic administration of cocaine (0.25, 0.5, 1.0 and 2.0 mg/kg i.v.). Control responses to whisker stimulation consisted of an initial excitatory burst (E1), a postexcitatory suppression of activity (I) and a secondary excitatory discharge (E2). Cocaine effects on spontaneous discharge were minimal at low doses up to and including 1.0 mg/kg, whereas suppression of spontaneous activity was observed at doses above 2.0 mg/kg. After cocaine injection, E1 responses were unchanged or within +/- 30% of control; however, E2 responses were routinely enhanced 50% to 600% above control levels. I responses were increased in magnitude and/or duration. Such facilitation of E2 and I responses was observed at doses as low as 0.25 mg/kg but most consistently at doses of 0.5 to 1.0 mg/kg. Suppression of evoked responses was observed at doses above 2.0 mg/kg. Cocaine's effects on spontaneous and evoked discharge were rapid in onset. Peak effects occurred at 6 min postinjection and recovery to control patterns of discharge were observed by 20 min postinjection. These results indicate that cocaine consistently exerts a facilitating effect on specific late components of cortical neuron responses to sensory stimuli. Although the neural substrates responsible for this effect have not been identified, such findings demonstrate a clear effect of cocaine on sensory signal transmission at dosages that can support behavioral reinforcement.

Animals↗
PubMed1994

Noradrenergic modulation of cat area 17 neuronal responses to moving visual stimuli.

Orientation and velocity tuning curves were obtained from neurons in cat primary visual cortex before, during and after the iontophoretic application of norepinephrine (NE). While no consistent effects on orientation tuning were observed, the most consistently observed effect of NE on velocity tuning was enhancement of the selectivity for stimulus speed and direction. This was evidenced by a narrowing of velocity tuning curves in 16/28 of the neurons we encountered as well as by an increase in the measured direction index for 13/28 cells. In contrast to NE, acetylcholine and gamma-amino-n-butyric acid (GABA) simply increased and decreased, respectively, the visually-evoked discharges, and in no case altered the shape of the velocity tuning curve. These data suggest that the spatiotemporal tuning of visual cortical neurons may be dependent not only on local interactions between visual afferents and target neurons, but in addition, depend on the activation state of the noradrenergic coeruleo-cortical projection system.

Animals↗