Cortical modules

Varga V, Szekely AD, Csillag A, Sharp T, Hajos M. Evidence for a role of GABA intemeurones in the cortical modulation of rnidbrain 5-hydroxytryptamine neurones. Neuroscience 2001 106 783-792. 

Obviously, the question of the geometric distribution of dendritic clusters needs to be examined further, and any modular theory of cortical function based on the concept that the apical dendritic clusters are the axes of functional cortical modules, or minicolumns, has to take into account that there is biological variation in the composition of the modules, as shown by studies like those of Lev and White (1997) and Vercelli et al. (2004). 

White EL, Peters A (1993) Cortical modules in the posteromedial barrel subfield (SmI) of the mouse. J Comp Neurol 334 86-96. 

Another theory for the action of stimulant diugs in ADHD involves effects on nonstiiatal monoamine systems. Frontal cortical dopamine, norepinephrine, and serotonin are clearly important in cognitive functioning and impulse control. These neurotransmitters directly modulate reward-related behaviors associated with the striatal dopamine system. Moreover, the amygdala may be pharmacologically influenced leading to enhanced... 

Anderson RE, Tan WK, Martin HS, Meyer FB. Effects of glucose and Pa02 modulation on cortical intracellular acidosis, NADH redox state, and infarction in the ischemic penumbra. Stroke 1999 30(1) 160-170. 

Cortical function is modulated by many other neurotransmitters. However, their role in the pathophysiology of epilepsy and in the action of antiepileptic drugs is not yet well known. 

Goldapple, Kimberly, Zindel Segal, Carol Garson, Mark Lau, Peter Bieling, Sidney Kennedy and Helen Mayberg, Modulation of Cortical-Limbic Pathways in Major Depression Treatment-Specific Effects of Cognitive Behavior Therapy , Archives of General Psychiatry 61, no. 1 (2004) 34-41... 

Noradrenaline acts on three types of receptor. The ai receptors mediate the main excitatory effects of noradrenaline upon wake-active neurons in the dorsal raphe, basal forebrain, and elsewhere (Vandermaelen Aghajanian, 1983 Nicoll, 1988 Fort et al., 1995 Brown et al., 2002). The a2 receptors mediate inhibitory effects of noradrenaline, e.g. on noradrenaline neurons themselves and on cholinergic brainstem neurons (Williams et al., 1985 Williams Reiner, 1993). The (3-receptors modulate neurons in a more subtle fashion, increasing excitability via blockade of afterhyperpolarizations in hippocampal and cortical neurons (Haas Konnerth, 1983). Activation of (3-receptors also promotes synaptic plasticity via activation of the cyclic-AMP-dependent kinase (PKA) and cyclic AMP response element binding protein (CREB) signal transduction pathway (Stanton Sarvey, 1987 Cirelli et al., 1996). 

ACh regulates the cortical arousal characteristic of both REM sleep and wakefulness (Semba, 1991, 2000 Sarter Bruno, 1997, 2000). Medial regions of the pontine reticular formation (Figs. 5.2 and 5.7) contribute to regulating both the state of REM sleep and the trait of EEG activation. Within the medial pontine reticular formation, presynaptic cholinergic terminals (Fig. 5.1) that release ACh also are endowed with muscarinic cholinergic receptors (Roth et al, 1996). Autoreceptors are defined as presynaptic receptors that bind the neurotransmitter that is released from the presynaptic terminal (Kalsner, 1990). Autoreceptors provide feedback modulation of transmitter release. Autoreceptor activation... 

With this in mind, the search for molecular markers that define populations of neurons in areas important for arousal is clearly warranted. In this chapter we describe the identification of four peptidergic systems that modulate different aspects of the sleep-wakefulness cycle. The success of this strategy demonstrates the need for new markers of neuronal cell types, which may define populations of neurons critical for our understanding of cortical activity and sleep. 

Cortistatin a cortical neuropeptide with sleep-modulating activity... 

Cortistatin was discovered as a result of the effort to characterize cortex-specific gene expression modulated by synaptic activity. It was named after its cortical expression and sequence homology to somatostatin (de Lecea et a ., 1996). The characterization of this peptide is yet another example of the use of reverse genetics to study the molecular components of the sleep machinery. 

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