A model for the organization of language in the adult humans brain is derived from electrical stimulation mapping of several language-related functions: naming, reading, short-term verbal memory, mimicry of orofacial movements, and phoneme identification during neurosurgical operations under local anesthesia. A common peri-Sylvian cortex for motor and language functions is identified in the language dominant hemisphere, including sites common to sequencing of movements and identification of phonemes that may represent an anatomic substrate for the “motor theory of speech perception.” This is surrounded by sites related to short-term verbal memory, with sites specialized for such language functions as naming or syntax at the interface between these motor and memory areas. Language functions are discretely and differentially localized in association cortex, including some differential localization of the same function, naming, in multiple languages. There is substantial individual variability in the exact location of sites related to a particular function, a variability which can be partly related to the patient's sex and overall language ability and which may depend on prior brain injury and, perhaps subtly, on prior experience. A common “specific alerting response” mechanism for motor and language functions is identified in the lateral thalamus of the language–dominant hemisphere, a mechanism that may select the cortical areas appropriate for a particular language function.

Ethologists and others studying animal behavior in a “cognitive” spirit are in need of a descriptive language and method that are neither anachronistically bound by behaviorist scruples nor prematurely committed to particular “information-processing models.” Just such an interim descriptive method can be found in intentional system theory. The use of intentional system theory is illustrated with the case of the apparently communicative behavior of vervet monkeys. A way of using the theory to generate data - including usable, testable “anecdotal” data - is sketched. The underlying assumptions of this approach can be seen to ally it directly with “adaptationist” theorizing in evolutionary biology, which has recently come under attack from Stephen Gould and Richard Lewontin, who castigate it as the “Panglossian paradigm.” Their arguments, which are strongly analogous to B. F, Skinner's arguments against “mentalism,” point to certain pitfalls that attend the careless exercise of such “Panglossian” thinking (and rival varieties of thinking as well), but do not constitute a fundamental objection to either adaptationist theorizing or its cousin, intentional system theory.

Without disputing the experimental evidence that subjects have available most of the content of brief displays for a fraction of a second, or that visual stimuli Persist after their physical termination for a similar time, I argue that this evidence is irrelevant to perception. Specifically, the notion of an icon as a brief storage of information persisting after stimulus termination cannot possibly be useful in any typical visual information-processing task except reading in a lightning storm. Since the visual world that provides the stimuli for perception is continuous and not chopped up by tachistoscopes, and since our eyes and heads are rarely motionless, no realistic circumstances exist in which having a frozen iconic storage of information could be helpful. Rather, the presence of such an icon interferes with perception. This paper examines instances of normal perception, and then reviews experimental evidence on temporal integration, saccadic suppression, masking, and the photoreceptor basis of visual persistence, to further demonstrate that a storage of excitation cannot be a useful device for storing information. Finally, I note that little would have to be changed in our theories of visual perception or information processing if we simply forgot all about the icon and iconic memory as an early stage of processing.

Problems with current hypotheses of catecholamine involvement in antidepressant action are reviewed. The theories examined include those that attribute a key role to increased brain norepinephrine (NE) availability or to the desensitization of brain beta adrenergic receptors. Although these hypotheses are consistent with a great deal of relevant laboratory and clinical data there arc an increasing number of findings that cannot be explained by them. These contradictions include findings on the lag time between pharmacological and therapeutic effects of antidepressants, the actions of propranolol and thyroid hormones on depression, the relationship between cortisol secretion and depression, the net effect of chronic antidepressants on noradrenergic neurotransmission, and the functions of cyclic AMP in the CNS. To reconcile the discordant data in these areas of research, a new formulation, the output hypothesis, which is derived from the foregoing theories, is proposed. The new hypothesis assumes that depression or adverse behavioral effects of stress results when the output of brain cells bearing noradrenergic receptors is too low to meet increased demand resulting from stress or other biologically disruptive events. According to this view antidepressants act by a mechanism akin to adaptation to chronic stress in which there is a prolonged increase in postsynaptic noradrenergic receptor activation in the brain. The prolonged increase is necessary for NE to induce, via the beta adrenoceptor–cAMP system, trophic or long-term metabolic effects that increase the output of catecholamine effector cells to a level commensurate with demand.