CENTRAL CONTROL OF RECEPTORS AND SENSORY TRANSMISSION SYSTEMS 



747 



m sec 



peaks of facilitation, holds for the thalamic relay of 

 c\'oked responses during barbiturate anesthesia or 

 following lesions placed in the brain-stem reticular 

 formation. These alterations result from the 'release' 

 from a tonic inhibitory reticular influence which evi- 

 dently modulates the thalamic relay nuclei during 

 wakefulness (48). Other evidence indicates that stim- 

 ulation of the brain-stem reticular formation will 

 affect the lateral geniculate as well as retinal relays of 

 photically-evoked responses (39). Apparently evoked 

 responses to the same flash signal may be augmented 

 in the retina and yet depressed in the thalamus. 



Altogether, these experiments suggest that each of 

 the major stations which relay afferent impulses 

 within the spinal cord, medulla and thalamus appears 

 to be susceptible to interference by inhibitory influ- 

 ences, and that these influences are tonically active 

 in the unanesthetized animal. 



FIG. 5. Sensorimotor cortex inHuence on trigeminal relay 

 and brain-stem reticular formation responses to infraorbital 

 nerve stimulation. Curarized cats without central anesthesia. 

 A. Bulbar recording from left spinal fifth tract. Afferent tri- 

 geminal response following stimulation of the left infraorbital 

 nerve (/) before, (2) during, (j) 3 sec. after and (^) 6 sec. after 

 repetitive stimulation of right sensorimotor cortex (100 per 

 sec. for 3 sec). In this record the trigeminal response is com- 

 posed mainly of a secondary wave, the primary spike being 

 hardly visible as an initial notch. B. Recording from the right 

 side of the midbrain reticular formation. Reticular response 

 evoked by infraorbital stimulation (i) before, (2) 13 sec. after 

 and (3) about 20 sec. after repetitive stimulation of right sen- 

 sorimotor cortex (100 per sec. for 3 sec). [From Hernandez- 

 Peon & Hagbarth (36).] 



the inhibitory effect is probaljly taking place at the 

 level of the central (dorsal cochlear nucleu.s) relay. 



Thalamic Relays 



Recently the brain-stem reticular formation has 

 been found capable of altering synaptic transmission 

 through thalamic relay nuclei. In animals without 

 central anesthesia, test-evoked responses being con- 

 veyed through the somatosensory relay (from the 

 medial lemniscus to the internal capsule) develop a 

 shortened latency and duration and a reduced ampli- 

 tude during brain-stem activation (48). The peaks of 

 facilitation that otherwise appear during recovery 

 following a relayed volley are likewi.se obliterated. 

 The converse, i.e. a long latency, high amplitude and 

 prolonged duration response followed by succes.sive 



CEPHALIC INTERACTION SYSTEMS 



Cortuipiial Prnjulum Systtmi 



In addition to the primary somcsthetic sensory re- 

 sponses which are highly resistant to deep anesthesia, 

 there are the so-called 'secondary' responses which 

 have longer latency, are more widespread and are 

 somewhat less resistant to anesthesia (5, 20). These 

 have been shown to be independent of the classical 

 medial lemniscus pathway and to be dependent 

 upon structures lying in the medial part of the 

 cephalic brain-stem (14, 62). These secondary re- 

 sponses are recorded well beyond the ijoundaries of 

 the classical somesthetic receiving cortex and may 

 even be of higher amplitude in the surrounding asso- 

 ciation cortex (33, 42, 43, 76, 77, 79). 



A number of additional studies have extended the 

 analysis of the somesthetic secondary response and 

 have found what appear to be analogous .secondary 

 responses relating to the auditory and visual systeins 

 as well. Recent studies, illustrated in figure 6, of 

 Buser & Borenstein may be taken as exemplary of 

 current insight into these mechanisms (i i)." Primary 



- Recent work confirms that the 'secondary discharge' of 

 Forbes & Morison (20), observed in rather deeply anesthetized 

 cats, probably involves a different mechanism from that re- 

 sponsible for the 'reponses sensorielles secondaires' of Buser cSi. 

 Borenstein (11), observed in animals lacking central anesthesia. 

 Drs. Evarts and Fleming (personal communication) have 

 established that by recording from implanted electrodes in the 

 visual receiving cortex of the cat they can demonstrate a dis- 



