NORADRENERGIC MODULATION OF RETINOGENICULATE TRANSMISSION IN THE CAT

1. Relay neurones were extracellularly recorded from the A-layers of the dorsal lateral geniculate nucleus (dLGN) of the anaesthetized cat. The noradrenergic influence on retinogeniculate transmission was investigated through microiontophoretic techniques in a total of 140 dLGN relay cells using three experimental approaches: (i) the effects of agonists for alpha1-, alpha2- and beta-adrenoceptors were separately analysed; (ii) the noradrenergic influence was related to the global state of activity of the relay neurones, which was associated with discrete patterns of the electroencephalogram (EEG); (iii) distinct phases of visual responses evoked from the area of the retinal receptive field, and of binocular and lateral inhibitory responses, were evaluated before, during and after the action of noradrenergic agonists. 2. The spontaneous generation of high-frequency bursts of spikes in dLGN relay neurones, associated with periods of highly synchronized, delta-like patterns of the EEG, was selectively suppressed by the beta-adrenoceptor agonist isoprenaline or the alpha1-adrenoceptor agonist phenylephrine. Single action potentials, occurring at a low frequency between bursts, were significantly less affected. Depending upon the ejection level of the adrenoceptor agonists, burst activity was suppressed by 23-73 %, compared with a reduction in single spike firing in the range 7-24 %. The suppression of burst firing occurred in all functional types of dLGN relay neurones (X, Y; on, off), enhanced burst activity was observed in less than 1 % of the cells. 3. On-going tonic sequences of action potentials (around 15 Hz), occurring during periods of EEG activity characterized by lower amplitudes and higher frequencies, were separately affected by adrenoceptor agonists. Isoprenaline had no significant effect, phenylephrine induced a global reduction of spike firing with no obvious relation to the ejection level, and the alpha1-adrenoceptor agonist clonidine inhibited action potential generation in a near dose-dependent manner. 4. Visual response properties were investigated during periods of less synchronized states of EEG activity. Responses to visual stimulation of the retinal receptive field centre were not significantly influenced by isoprenaline, while phenylephrine or clonidine attenuated the phasic and the tonic response component in all functional types of relay neurones and independent of the stimulus contrast being used. At low ejection levels, slight facilitatory effects were observed with isoprenaline (65 % of neurones that were tested) or phenylephrine (15 %). The inhibitory influence of the antagonistic surround area of the receptive field appeared unaltered during action of isoprenaline or phenylephrine. 5. Binocular and long-range lateral inhibition were selectively modulated by adrenoceptor agonists in more than 90 % of the neurones that were tested. Application of isoprenaline resulted in a significant decrease (average 7 spikes s-1) in amplitude and duration of the late phases of inhibitory responses, thereby reducing the relative strength of late inhibition by about 45 %. By contrast, phenylephrine induced a significant increase (average 5 spikes s-1) in the strength of late inhibitory responses. 6. In a sample of neurones, the influences of adrenoceptor stimulation on visual responses during periods of delta-like, synchronized EEG activity were directly compared with those changes in visual responsiveness which were associated with the naturally occurring shift in the EEG to patterns of lower amplitudes and higher frequencies. The shift in the EEG was accompanied in the dLGN with a suppression of burst firing, a strong increase in the tonic component of visual responses from an average of 10 to an average of 45 spikes s-1, and a significant reduction averaging 67 % in the late phases of binocular and lateral inhibition. These changes were largely mimicked by microiontophoretic application of isoprenaline. 7. We conclude that the noradrenergic influence provides an important basis for the faithful transfer of visual signals through the dLGN during periods of increased arousal by preventing burst discharges and controlling the late phases of globally organized inhibitory mechanisms without interfering with the antagonistic centre-surround organization of the receptive field area. The suppressant influence of alpha2-adrenoceptors may reflect the existence of a regulatory system, which limits the effects of the ascending brainstem system in the dLGN.