The neocortical projection to the inferior colliculus in the albino rat

Summary The purpose of the present study was to define the field of termination of the neocortical projection to the inferior colliculus in rat. The study was based on fiber degeneration following large lesions of the cerebral cortex, and anterograde transport of wheat germ agglutinin horseradish peroxidase ejected inotophoretically into more restricted neocortical loci. Neocortical fibers were found to supply the dorsal and external cortices of the inferior colliculus. The central nucleus, in contrast, did not receive such fibers. The results speak in favor of three separate projections, one partly bilateral to the deeper part of the dorsal collicular cortex, a second ipsilateral to the superficial part of this subdivision, and a third ipsilateral to the external collicular cortex.     

Intrathecal apamin selectively facilitates activity in ascending axons of rat spinal cord evoked by stimulation of afferent C fibers in sural nerve

Intrathecally administered apamin was tested for its effect on activity in ascending axons of the spinal cord using decerebrate rats with low spinal cord transection. Afferent Aβ, Aδ or C fibers were stimulated in the sural nerve, and the response evoked in ascending axons was recorded below the transection. Apamin (5 ng) produced an increase in C fiber-evoked activity which developed about 30 min after injection and persisted for more than 60 min after injection. Apamin (5, 20 and 50 ng) did not change the activity in ascending axons which responded only to stimulation of afferent Aβ and Aδ fibers.The results indicate that apamin facilitates synaptic transmission from high-threshold afferent C fibers to secondary neurons.     

Control of quantal transmitter release at frog's motor nerve terminals

Motor terminals on the cutaneous pectoris muscle of the frog were depolarized by current pulses through the recording macro-pathch-clamp electrode and the resulting quantal release was measured (excitation blocked with TTX). Above a threshold release increased very steeply with depolarization until saturation was approached. The dependence of release on duration of depolarization was even steeper: doubling pulse duration often produced more than 100-fold release (early facilitation) Distributions of delays of quantal release after the depolarization pulse were determined for wide ranges of depolarizations and pulse durations. The shape of these distributions was little affected by large changes in average release; increasing the temperature from 0°C to 10°C about halved the time scale of the distributions. Lengthening the depolarization from 0.5 to 6 ms produced a latency shift: the distributions of delays were shifted by almost the increase in pulse duration. At 5–6 ms pulse duration a few releases occurred during the final millisecond of the pulse. It is suggested that the time course of the phasic release is not controlled by the time course of changes in intracellular calcium concentration, but by an activator which is produced about proportional to supra-threshold pulse amplitude and duration, and that this activator effects release with a cooperativity of 6–7. An additional depolarization produced repressor is responsible for the minimum delay.Supported by the Deutsche Forschungsgemeinschaft     

Memory encoding and retrieval on the ascending and descending limbs of the blood alcohol concentration curve

Rationale Little is known about acute effects of alcohol on memory encoding and retrieval on different limbs (ascending and descending) of the blood alcohol concentration (BAC) curve. Objectives This extensive experiment was designed to examine alcohol's effects on memory encoding and retrieval throughout a protracted drinking episode. Methods In a 9-h session, male participants consumed either alcohol (1 ml/kg) or placebo (n=32/32) over a period of 90 min and learned various materials in different memory tasks before, during, and after consuming the drinks, while their BAC levels were monitored. A week later, in a similar session, they were tested on learned materials before, during, and after drinking. Mood was assessed throughout both sessions. Results Alcohol impaired recall of words more than recognition, and cued recall most severely. Perceptual priming and picture recognition were not affected by alcohol. Alcohol impaired encoding in cued recall, recognition of completed word fragments, and free recall regardless of limb, but impaired retrieval in word recognition only during the ascending BAC. Alcohol increased negative mood on the descending limb during the first session, and on the ascending limb during the second session. Conclusions Under naturalistic drinking conditions, alcohol's effects on memory depend on task, memory process, and limb of the BAC curve. The differential effects of alcohol on retrieval during the ascending and descending limbs demonstrate the importance of examining the differential effects on the two limbs.     

The rise and fall of priming: how visual exposure shapes cortical representations of objects

How does the amount of time for which we see an object influence the nature and content of its cortical representation? To address this question, we varied the duration of initial exposure to visual objects and then measured functional magnetic resonance imaging (fMRI) signal and behavioral performance during a subsequent repeated presentation of these objects. We report a novel 'rise-and-fall' pattern relating exposure duration and the corresponding magnitude of fMRI cortical signal. Compared with novel objects, repeated objects elicited maximal cortical response reduction when initially presented for 250 ms. Counter-intuitively, initially seeing an object for a longer duration significantly reduced the magnitude of this effect. This 'rise-and-fall' pattern was also evident for the corresponding behavioral priming. To account for these findings, we propose that the earlier interval of an exposure to a visual stimulus results in a fine-tuning of the cortical response, while additional exposure promotes selection of a subset of key features for continued representation. These two independent mechanisms complement each other in shaping object representations with experience.     

Altered motor cortex excitability in tinnitus patients: a hint at crossmodal plasticity

Idiopathic tinnitus is a frequent and often debilitating auditory phantom perception of largely unknown pathological conditions. In electrophysiological and functional neuroimaging studies, affected subjects have shown excessive spontaneous activity in the central auditory system. To further investigate the underlying central nervous component, we assessed motor cortex excitability in 19 patients with chronic tinnitus by means of transcranial magnetic stimulation (TMS). When results were compared with data from 19 healthy controls matched for age and sex, we found significantly enhanced intracortical facilitation in tinnitus patients. These findings parallel excitability changes after limb amputation and experimental deafferentation. Our results give further support to crossmodal interactions involving neuroplastic changes in some forms of tinnitus and may help to better understand mechanisms of maladaptive cortical reorganisation involved in phantom perceptions.     

Wide-field conditioning effects on small-field neurons in the posterior sigmoid gyrus of domestic cats

Single neurons were isolated in four different recording sites in sensorimotor cortex of the domestic cat, all sites being topographically related to the contralateral forepaw. Conditioning-testing interactions were made on 409 small-field neurons, the testing input being the contralateral forepaw (also the ipsilateral forepaw in the case of bilateral-field neurons) and the conditioning input being any paw that was ineffective in exciting the neuron. About 29% of the neurons showed inhibitory interactions and 23% showed facilitatory interactions. Of these, about 5.5% showed both effects, according to the conditioning site. Nearly 54% of the neurons failed to show any interaction effects. Most of the latter were isolated in the two posterior recording sites, located in somatosensory area I; the interaction effects were found predominantly in the two anterior recording sites, located in agranular tissue. Neurons that responded only to contralateral forepaw stimulation (sa neurons) and showed facilitatory interactions from the other three paws had response properties characteristic of neurons that respond to all four paws (m neurons). The sa neurons that showed inhibitory interactions from the other three paws did not differ significantly in response properties from those that showed no interaction effects. These findings are relevant to current criteria for the classification of sensorimotor cortex neurons and lead to remarks on the possible thalamic routes that mediate the interaction effects.     

Relationship between the pericardial and pleural spaces in cross-sectional imaging

Sixty patients, including 15 with large pericardial effusions, five with large left pleural effusions, and nine with both, were studied prospectively with two-dimensional echocardiography to verify the relation of percardial effusions and posterior paramediastinal pleural effusions to the descending thoracic aorta. It was found that large pericardial effusions lie anterior to the descending aorta both at the level of the left atrium and the left ventricle, whereas large posterior paramediastinal pleural effusions lie posterior, lateral, or posterolateral to the descending aorta. A retrospective study of 148 M-mode echocardiograms showed similar findings; but the descending thoracic aorta was less reliably identified, and the lateral position of pleural effusions with respect to the aorta could not be evaluated.     

The effects of cerebellar stimulation on the motor cortical excitability in neurological disorders: A review

The cerebellum regulates execution of skilled movements through neural connections with the primary motor cortex. A main projection from the cerebellum to the primary motor cortex is a disynaptic excitatory pathway relayed at the ventral thalamus. This dentatothalamocortical pathway receives inhibitory inputs from Purkinje cells of the cerebellar cortex. These pathways (cerebellothalamocortical pathways) have been characterized extensively using cellular approaches in animals. Advances in non-invasive transcranial activation of neural structures using electrical and magnetic stimulation have allowed us to investigate these neural connections in humans. This review summarizes various studies of the cerebellothalamocortical pathway in humans using current transcranial electrical and magnetic stimulation techniques. We studied effects on motor cortical excitability elicited by electrical or magnetic stimulation over the cerebellum by recording surface electromyographic (EMG) responses from the first dorsal interosseous (FDI) muscle. Magnetic stimuli were given with a round or figure eight coil (test stimulation) for primary motor cortical activation. For cerebellar stimulation, we gave high-voltage electrical stimuli or magnetic stimuli through a cone-shaped coil ipsilateral to the surface EMG recording (conditioning stimulation). We examined effects of interstimulus intervals (ISIs) with randomized condition-test paradigm, using a test stimulus given preceded by a conditioning stimulus by ISIs of several milliseconds. We demonstrated significant gain of EMG responses at an ISI of 3 ms (facilitatory effect) and reduced responses starting at 5 ms, which lasted 3-7 ms (inhibitory effect). We applied this method to patients with ataxia and showed that the inhibitory effect was only absent in patients with a lesion at cerebellar efferent pathways or dentatothalamocortical pathway. These results imply that this method activates the unilateral cerebellar structures. We confirmed facilitatory and inhibitory natures of cerebellothalamocortical pathways in humans. We can differentiate ataxia attributable to somewhere in the cerebello-thalamo-cortical pathways from that caused by other pathways.     

Evidence that descending serotonergic systems protect spinal cord plasticity against the disruptive effect of uncontrollable stimulation

Prior work has demonstrated that spinal cord neurons, isolated from the brain through a spinal transection, can support learning. Spinally transected rats given legshock whenever one hindlimb is extended learn to maintain the shocked leg in a flexed position, minimizing net shock exposure. This capacity for learning is inhibited by prior exposure to an uncontrollable stimulus (e.g., intermittent tailshock). The present experiments examined whether spinal cord neurons are more vulnerable to the adverse effects of uncontrollable stimulation after spinal cord injury. Experiment 1 confirmed that uncontrollable shock inhibits subsequent learning in transected rats. Rats that received uncontrollable stimulation prior to transection did not exhibit this effect, suggesting that brain systems exert a protective effect. Experiment 2 showed that this protective effect was removed if subjects received a dorsolateral funiculus lesion prior to shock exposure. Subsequent experiments were designed to determine the identity of the neurochemical systems that protect spinal plasticity. Intrathecal application of serotonin (5-HT) or a 5-HT 1A/7 agonist (8-OH DPAT) in transected rats had a protective effect that blocked the adverse effect of uncontrollable stimulation (Experiment 3). The alpha-2 noradrenergic agonist, clonidine, also protected plasticity (Experiment 4), but this effect was linked to cross-reactivity at the 5-HT 1A receptor (Experiment 5). Microinjection of a 5HT 1A antagonist (WAY 100635) into the spinal cord before intact rats received uncontrollable stimulation blocked the brain-dependent protection of spinal cord neurons. The findings indicate that serotonergic systems normally protect spinal cord plasticity from the deleterious effects of uncontrollable stimulation.