Timing of the repetitive movements that constitute any rhythmic behavior is regulated by intrinsic properties of the central nervous system rather than by sensory feedback from moving parts of the body. Evidence of this permits resolution of the long-standing controversy over the neural basis of rhythmic behavior and aids in the identification of this mechanism as a general principle of neural organization applicable to all animals with central nervous systems.

https://science.sciencemag.org/content/sci/210/4469/492.full.pdf

Neural basis of rhythmic behavior in animals

Melatonin, the major hormone produced by the pineal gland, displays characteristic daily and seasonal patterns of secretion. These robust and predictable rhythms in circulating melatonin are strong synchronizers for the expression of numerous physiological processes in photoperiodic species. In mammals, the nighttime production of melatonin is mainly driven by the circadian clock, situated in the suprachiasmatic nucleus of the hypothalamus, which controls the release of norepinephrine from the dense pineal sympathetic afferents. The pivotal role of norepinephrine in the nocturnal stimulation of melatonin synthesis has been extensively dissected at the cellular and molecular levels. Besides the noradrenergic input, the presence of numerous other transmitters originating from various sources has been reported in the pineal gland. Many of these are neuropeptides and appear to contribute to the regulation of melatonin synthesis by modulating the effects of norepinephrine on pineal biochemistry. The aim of this review is firstly to update our knowledge of the cellular and molecular events underlying the noradrenergic control of melatonin synthesis; and secondly to gather together early and recent data on the effects of the nonadrenergic transmitters on modulation of melatonin synthesis. This information reveals the variety of inputs that can be integrated by the pineal gland; what elements are crucial to deliver the very precise timing information to the organism. This also clarifies the role of these various inputs in the seasonal variation of melatonin synthesis and their subsequent physiological function.

Generation of the Melatonin Endocrine Message in Mammals: A Review of the Complex Regulation of Melatonin Synthesis by Norepinephrine, Peptides, and Other Pineal Transmitters

Neuronal Transcriptome of Aplysia: Neuronal Compartments and Circuitry

While a role has been well established for excitotoxic necrosis in the pathogenesis of traumatic or ischemic damage to the CNS, accumulating evidence now suggests that apoptosis may also be a prominent contributor. In this review we focus on the role of glutamate and attendant intracellular calcium influx in triggering or modifying excitotoxic necrosis and apoptosis, raising the possibility that calcium influx may affect these two death pathways in opposite directions. Incorporating consideration of both pathways will probably be needed to develop the most effective neuroprotective treatments for CNS injury.

Neuronal apoptosis after CNS injury: the roles of glutamate and calcium.

We identified candidate neurons in the cerebral ganglion that regulate feeding responses mediated by the buccal ganglion Backfilling the cerebral-buccal connectives revealed that each cerebral hemi-ganglion contains approximately 20 neurons that project axons to the buccal ganglion Three M-cluster neurons (CBI-1, CBI-2, CBI-3) and one E- cluster neuron (CBI-4) were identified as cerebral-to-buccal interneurons (CBIs) based on position, morphology, synaptic connections, and ability to drive buccal motor programs (BMPs) CBI-1 responds to touch of the tentacles, lips, and buccal mass It receives monosynaptic EPSPs from interganglionic, cerebral-to-buccal mechanoafferent (ICBM) neurons and monosynaptically excites buccal cells, some of which are also excited by the ICBMs Tonic firing of CBI- 1 usually evokes a single cycle of BMP activity CBI-1 phase-shifts the rhythmic BMP driven by firing a dopaminergic neuron in the buccal ganglion CBI-1 itself exhibits dopamine-like histofluorescence following formaldehyde-glutaraldehyde fixation CBI-2 is excited by food stimuli applied to the lips Constant-current intracellular stimulation of CBI-2 produces phasic firing of the cell that reliably evokes a rhythmic BMP that incorporates buccal and cerebral motor neurons, putative pattern-generating and pattern-initiating neurons, and neuromodulatory cells (metacerebral cells) CBI-4 also evokes a rhythmic BMP, but the details of its actions and synaptic effects differ from that of CBI-2 CBI-3 does not evoke a BMP, even though it is excited by food stimuli applied to the lips, and it makes monosynaptic connections (both excitatory and inhibitory) to many follower cells of the other CBIs Firing of CBI-3 phase-delays the BMP driven by CBI-2 Since its activity is incorporated into BMPs and it provides direct inputs to elements of the feeding circuitry, it may play a role in pattern generation The distinctive features of the CBIs suggest that the consummatory phase of feeding may be controlled by a population of interneurons that subserve different roles

https://www.jneurosci.org/content/jneuro/11/11/3630.full.pdf

Steven M. Fredman

Papers

Cerebral ganglion of Aplysia: Cellular organization and origin of nerves

Neural control of locomotion in Aplysia: Role of the Central Ganglia

Motor program for pedal waves during Aplysia locomotion is generated in the pedal ganglia

Processing of chemosensory and mechanosensory information in identifiable Aplysia neurons

Synaptic connections in the cerebral ganglion of Aplysia.